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1
Gumay, Ainun Rahmasari, Saekhol Bakri, and Astika Widy Utomo. "The Effect of Green Tea Leaf Extract on Spatial Memory Function and Superoxyde Dismutase Enzyme Activity in Mice with D-galactose Induced Dimentia." Sains Medika 8, no. 1 (April 4, 2017): 8. http://dx.doi.org/10.26532/sainsmed.v8i1.1050.
Повний текст джерелаАнотація:
Background:�Oxidative stress�and�inflammation�play�an important role in�pathogenesis of�brain aging�and neurodegenerative diseases such as�Alzheimer. Green tea�has been shown to have antioxidant, anti-inflammatory, anticancer, and neuroprotective�activity. Objectives: to determine the effect of green tea extract on�spatial memory function and superoxide dismutase�enzyme activity in mice with D-galactose induced dementiaMethods:�An experimental study using "post test only control group design".�Twenty male�BALB/c Mice aged 6-8�weeks were divided into�4�groups.�Negative control group�(NG)�was induced by subcutaneous injection of�D-galactose�(150�mg/kg BW)�once�daily for�6�weeks.�GT-90, GT-270,�GT-540�were induced by�D-galactose�and orally administered with 90, 270, and 540 mg/kg BW of�green tea extract�once daily for 6 weeks.�The spatial memory functions were assessed using Morris water maze and�SOD enzyme activities�were evaluated using ELISA.�One-way Anova and Kruskal-Wallis were used for statistical analysis.�Results: mean�percentage of latency time in the GT-90�(35.29�(SD=�2.69)%),�GT-270�(35.28 (SD= 2.62)%), and�GT-540�(35.62�(SD=5.05)%)�were�significantly�higher compared to that of NG�(20.38�(SD =�3.21)%), p�<0.05). SOD enzyme activity in the�GT-270�(0.78 (SD = 0.07) U/ml)�was�significantly�higher�compared to that of NG�(0.51 (SD = 0.01) U�ml), p= 0.004).Conclusion:�Green tea extract�may�improve�spatial memory�function�and�the activity of�superoxide dismutase�enzyme in mice�with D-galactose induced�dementia.
2
Marufah, Marufah, and M. Adib. "EKSTRAK BUAH PEPAYA (Carica papaya L.) MENINGKATKAN KADAR CATALASE DAN GLUTATHIONE HATI TIKUS YANG TERPAPARLEAD ACETATE." Jurnal SainHealth 2, no. 1 (March 28, 2018): 8. http://dx.doi.org/10.51804/jsh.v2i1.170.8-12.
Повний текст джерелаАнотація:
Pollution is an entry or inclusion living things, subtances, energy, and or other components into environment and or change of environment compositions because of human activity or natural process with the result that decrease of quality to certain level that causes doesn’t work environment. Pollution can be caused many subtances that is heavy metal, i.e. lead acetate (Pb). Lead acetate affect physiological aberration, biochemical, and behavior. Heavy metal induction induce ROS production act as destructive oxidants. Body capability to oxidant neutralize serviced by superoxyde dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione (GSH), vitamin C, vitamin E, and other antioxidants in the cell. Antioxidants synthesized by plants, which is papaya (Carica papaya L.). Papaya (Carica papaya L.) effect on CAT and GSH levels was performed on male mice wistar strain. Mice induced by lead acetate 20 gr / Kg weight dose for 6 weeks, given papaya extract 100, 200, and 400 mg/Kg weight dose for 6 weeks. Further glutathione and catalase levels are measured on mice liver. This study proves, papaya extract increase catalase levels (p = 0,000) and glutathione levels (p = 0,000) on mice liver induced lead acetate. Papaya extract 400 mg/Kg/day most effective dose to increase catalase and glutathione levels on mice liver induced lead acetate.
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Curti, Valeria, Vincenzo Zaccaria, Arold Tsetegho Sokeng, Marco Dacrema, Irene Masiello, Anna Mascaro, Giuseppe D’Antona, and Maria Daglia. "Bioavailability and In Vivo Antioxidant Activity of a Standardized Polyphenol Mixture Extracted from Brown Propolis." International Journal of Molecular Sciences 20, no. 5 (March 12, 2019): 1250. http://dx.doi.org/10.3390/ijms20051250.
Повний текст джерелаАнотація:
Several lines of evidence demonstrate the antioxidant, anti-inflammatory and antimicrobial activities of propolis, mostly ascribed to its polyphenol content. However, little is known regarding the bioavailability of propolis in acute and prolonged settings of oral administration. In this study, we first determined the content of the main polyphenols in a brown propolis extract obtained using a patented extraction method (Multi Dinamic Extraction—M.E.D.) by RP-HPLC-UV-PDA-MSn analysis, followed by the bioavailability of galangin and chrysin, the most abundant polyphenols in the mixture (7.8% and 7.5% respectively), following acute (single bolus of 500 mg/kg containing about 3.65 mg of the polyphenol mixture) and prolonged (100, 250 and 500 mg/kg body for 30 days) oral administration in 30 male 8 weeks old C57BL/6 wild-type mice. In the acute setting, blood was taken at 30 s and 5, 10, 15, 20, 25, 30, 45, 60 and 120 min following the oral bolus. In the prolonged setting, blood samples were obtained after 10, 20 or 30 days of administration. At the end of treatment, expression of antioxidant enzymes (superoxyde dismutase, SOD-1; catalase, CAT; glutathione peroxidase, GSS) was evaluated in liver tissue. Following both acute and prolonged administration, neither galangin nor chrysin were detectable in the plasma of mice, whereas the glucuronide metabolite of galangine was detectable 5 min after acute administration. At the end of the prolonged treatment SOD-1 was found to have increased significantly, unlike CAT and GSS. Overall, these data suggest that oral administration of whole brown propolis extract is followed by rapid absorption and metabolization of galangin followed by adaptations of the antioxidant first line defense system.
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BROWN, David R., and Andreas BESINGER. "Prion protein expression and superoxide dismutase activity." Biochemical Journal 334, no. 2 (September 1, 1998): 423–29. http://dx.doi.org/10.1042/bj3340423.
Повний текст джерелаАнотація:
The function of the prion protein (PrPc) remains uncertain. It has been suggested that prion protein expression may aid cellular resistance to oxidative stress by influencing the activity of Cu/Zn superoxide dismutase (Cu,Zn SOD). The activity of Cu,Zn SOD was investigated in mice with different levels of PrPc expression. Increasing levels of PrPc expression were linked to increased levels of Cu,Zn SOD activity. Western-blot and Northern-blot analysis indicated that mice either lacking or overexpressing PrPc had levels of Cu,Zn SOD mRNA equivalent to those expressed in wild-type mice. Mice overexpressing the prion protein had lower levels of resistance to oxidative stress but higher expression levels of glutathione peroxidase, probably due to increased levels of hydrogen peroxide produced by increased Cu,Zn SOD activity. When cells were metabolically labelled with radioactive copper, increased radioactivity was immunoprecipitated with Cu,Zn SOD from mice with higher levels of PrPc. In addition, diethyldithiocarbamate, a copper chelator that inactivates Cu,Zn SOD by capturing copper from the molecule, is more able to inactivate Cu,Zn SOD expressed in animals with higher levels of PrPc. As recent studies have suggested that PrPc may regulate some aspect of copper metabolism, it is suggested that PrPc expression may regulate Cu,Zn SOD activity by influencing copper incorporation into the molecule.
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Carvalho-Queiroz, Claudia, Rosemary Cook, Ching C. Wang, Rodrigo Correa-Oliveira, Nicola A. Bailey, Nejat K. Egilmez, Edith Mathiowitz, and Philip T. LoVerde. "Cross-Reactivity of Schistosoma mansoni Cytosolic Superoxide Dismutase, a Protective Vaccine Candidate, with Host Superoxide Dismutase and Identification of Parasite-Specific B Epitopes." Infection and Immunity 72, no. 5 (May 2004): 2635–47. http://dx.doi.org/10.1128/iai.72.5.2635-2647.2004.
Повний текст джерелаАнотація:
ABSTRACT Schistosoma mansoni, an intravascular parasite, has evolved a number of immune evasion mechanisms to establish itself in the host, such as antioxidant enzymes. Our laboratory has demonstrated that the highest levels of certain antioxidant enzymes are found in adult worms, which are the least susceptible to immune killing. Vaccination of mice with naked DNA constructs containing the gene encoding Cu/Zn cytosolic superoxide dismutase (SmCT-SOD) showed significant levels of protection compared to a control group, and our data demonstrate that the adult worms are a target of the immune response that confers resistance in SmCT-SOD DNA-vaccinated mice. Because SmCT-SOD shows significant identity with the human homologue, we evaluated the reactivity of anti-SmCT-SOD antibodies derived from SmCT-SOD-immunized mice and rabbits and from S. mansoni-infected individuals to human superoxide dismutase (hSOD) and SmCT-SOD parasite-specific peptides to assess the potential for autoimmune responses from immunization with the recombinant molecule. In addition, we evaluated the ability of various SmCT-SOD adjuvant-delivered immunizations to induce cross-reactive antibodies. Both mouse and rabbit antibodies generated against SmCT-SOD recognized the denatured form of hSOD. The same antibodies did not recognize nondenatured hSOD. Sera from infected individuals with different clinical forms of schistosomiasis recognized SmCT-SOD but not hSOD. Antibodies from mice immunized with different SmCT-SOD-containing formulations of both DNA and protein were able to recognize SmCT-SOD-derived peptides but not soluble hSOD. All together, these findings serve as a basis for developing a subunit vaccine against schistosomiasis.
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Park, Jong Woong, Wen-Ning Qi, Yongting Cai, Igor Zelko, John Q. Liu, Long-En Chen, James R. Urbaniak, and Rodney J. Folz. "Skeletal muscle reperfusion injury is enhanced in extracellular superoxide dismutase knockout mouse." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (July 2005): H181—H187. http://dx.doi.org/10.1152/ajpheart.00458.2004.
Повний текст джерелаАнотація:
This study investigates the role of extracellular SOD (EC-SOD), the major extracellular antioxidant enzyme, in skeletal muscle ischemia and reperfusion (I/R) injury. Pedicled cremaster muscle flaps from homozygous EC-SOD knockout (EC-SOD−/−) and wild-type (WT) mice were subjected to 4.5-h ischemia and 90-min reperfusion followed by functional and molecular analyses. Our results revealed that EC-SOD−/− mice showed significantly profound I/R injury compared with WT littermates. In particular, there was a delayed and incomplete recovery of arterial spasm and blood flow during reperfusion, and more severe acute inflammatory reaction and muscle damage were noted in EC-SOD−/− mice. After 90-min reperfusion, intracellular SOD [copper- and zinc-containing SOD (CuZn-SOD) and manganese-containing (Mn-SOD)] mRNA levels decreased similarly in both groups. EC-SOD mRNA levels increased in WT mice, whereas EC-SOD mRNA was undetectable, as expected, in EC-SOD−/− mice. In both groups of animals, CuZn-SOD protein levels decreased and Mn-SOD protein levels remained unchanged. EC-SOD protein levels decreased in WT mice. Histological analysis showed diffuse edema and inflammation around muscle fibers, which was more pronounced in EC-SOD−/− mice. In conclusion, our data suggest that EC-SOD plays an important role in the protection from skeletal muscle I/R injury caused by excessive generation of reactive oxygen species.
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Mathias, Maxwell, Joann Taylor, Elizabeth Mendralla, and Marta Perez. "Neonatal Extracellular Superoxide Dismutase Knockout Mice Increase Total Superoxide Dismutase Activity and VEGF Expression after Chronic Hyperoxia." Antioxidants 10, no. 8 (August 1, 2021): 1236. http://dx.doi.org/10.3390/antiox10081236.
Повний текст джерелаАнотація:
Bronchopulmonary dysplasia (BPD) is a common lung disease affecting premature infants that develops after exposure to supplemental oxygen and reactive oxygen intermediates. Extracellular superoxide dismutase (SOD3) is an enzyme that processes superoxide radicals and has been shown to facilitate vascular endothelial growth factor (VEGF) and nitric oxide (NO) signaling in vascular endothelium. We utilized a mouse model of neonatal hyperoxic lung injury and SOD3 knockout (KO) mice to evaluate its function during chronic hyperoxia exposure. Wild-type age-matched neonatal C57Bl/6 (WT) and SOD3−/− (KO) mice were placed in normoxia (21% FiO2, RA) or chronic hyperoxia (75% FiO2, O2) within 24 h of birth for 14 days continuously and then euthanized. Lungs were harvested for histologic evaluation, as well as comparison of antioxidant enzyme expression, SOD activity, VEGF expression, and portions of the NO signaling pathway. Surprisingly, KO-O2 mice survived without additional alveolar simplification, microvascular remodeling, or nuclear oxidation when compared to WT-O2 mice. KO-O2 mice had increased total SOD activity and increased VEGF expression when compared to WT-O2 mice. No genotype differences were noted in intracellular antioxidant enzyme expression or the NO signaling pathway. These results demonstrate that SOD3 KO mice can survive prolonged hyperoxia without exacerbation of alveolar or vascular phenotype.
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Dirami, Ghenima, Donald Massaro, and Linda Biadasz Clerch. "Regulation of lung manganese superoxide dismutase: species variation in response to lipopolysaccharide." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 5 (May 1, 1999): L705—L708. http://dx.doi.org/10.1152/ajplung.1999.276.5.l705.
Повний текст джерелаАнотація:
Lipopolysaccharide (LPS) treatment increases survival of rats, but not of mice, during hyperoxia. Manganese superoxide dismutase (Mn SOD) in the lung plays a critical role in LPS-induced tolerance to hyperoxia in rats. Therefore, we now compared the response of lung Mn SOD with treatment of mice and rats with LPS. LPS treatment of rats increased Mn SOD activity and protein concentration, did not change its specific activity, increased Mn SOD mRNA concentration 35-fold, and elevated Mn SOD synthesis 50% without changing general protein synthesis. LPS treatment of mice did not alter any of these parameters except for a 16-fold increase in Mn SOD mRNA concentration. Mn SOD translational efficiency (synthesis/mRNA concentration) was diminished 93% in rat lung and 76% in mouse lung by treatment with LPS. However, the absolute translational efficiency was twofold higher in lungs of LPS-treated rats than in lungs of LPS-treated mice. The failure of LPS to raise Mn SOD activity in mouse lungs is due, at least in part, to a smaller increase in Mn SOD mRNA and lower translational efficiency in LPS-treated mice than in LPS-treated rats.
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Ookawara, Tomomi, Nobuo Imazeki, Osamu Matsubara, Takako Kizaki, Shuji Oh-Ishi, Chitose Nakao, Yuzo Sato, and Hideki Ohno. "Tissue distribution of immunoreactive mouse extracellular superoxide dismutase." American Journal of Physiology-Cell Physiology 275, no. 3 (September 1, 1998): C840—C847. http://dx.doi.org/10.1152/ajpcell.1998.275.3.c840.
Повний текст джерелаАнотація:
Protein content and mRNA expression of extracellular superoxide dismutase (EC-SOD) were investigated in 16 mouse tissues. We developed a double-antibody sandwich ELISA using the affinity-purified IgG against native mouse EC-SOD. EC-SOD could be detected in all of the tissues examined (lung, kidney, testis, brown fat, liver, adrenal gland, pancreas, colon, white fat, thymus, stomach, spleen, heart, skeletal muscle, ileum, and brain, in decreasing order of content measured as μg/g wet tissue). Lung showed a markedly higher value of EC-SOD than other tissues. Interestingly, white fat had a high content of EC-SOD in terms of micrograms per milligram protein, which corresponded to that of lung. Kidney showed the strongest expression of EC-SOD mRNA. Relatively strong expression of the mRNA was observed in lung, white fat, adrenal gland, brown fat, and testis. Heart and brain showed only weak signals, and no such expression could be detected in either digestive organs or skeletal muscle. Immunohistochemically, EC-SOD was localized mainly to connective tissues and vascular walls in the tissues examined. Deep staining in the cytosol was observed in the cortical tubular cells of kidney. These results suggest that EC-SOD is distributed systemically in mice and that the physiological importance of this enzyme may be a compensatory adaptation to oxidative stress, particularly in lung and kidney.
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Bowler, Russell P., Mike Nicks, Karrie Warnick, and James D. Crapo. "Role of extracellular superoxide dismutase in bleomycin-induced pulmonary fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 4 (April 1, 2002): L719—L726. http://dx.doi.org/10.1152/ajplung.00058.2001.
Повний текст джерелаАнотація:
Bleomycin administration results in well-described intracellular oxidative stress that can lead to pulmonary fibrosis. The role of alveolar interstitial antioxidants in this model is unknown. Extracellular superoxide dismutase (EC-SOD) is the primary endogenous extracellular antioxidant enzyme and is abundant in the lung. We hypothesized that EC-SOD plays an important role in attenuating bleomycin-induced lung injury. Two weeks after intratracheal bleomycin administration, we found that wild-type mice induced a 106 ± 25% increase in lung EC-SOD. Immunohistochemical staining revealed that a large increase in EC-SOD occurred in injured lung. Using mice that overexpress EC-SOD specifically in the lung, we found a 53 ± 14% reduction in bleomycin-induced lung injury assessed histologically and a 17 ± 6% reduction in lung collagen content 2 wk after bleomycin administration. We conclude that EC-SOD plays an important role in reducing the magnitude of lung injury from extracellular free radicals after bleomycin administration.
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Bowler, Russell P., John Arcaroli, Edward Abraham, Manisha Patel, Ling-Yi Chang, and James D. Crapo. "Evidence for extracellular superoxide dismutase as a mediator of hemorrhage-induced lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 4 (April 1, 2003): L680—L687. http://dx.doi.org/10.1152/ajplung.00191.2002.
Повний текст джерелаАнотація:
Hemorrhage results in excessive production of superoxide that is associated with severe lung injury. We examined whether the superoxide dismutase (SOD) mimetic manganese(III) mesotetrakis (di- N-ethylimidazole) porphyrin (AEOL 10150) could attenuate this lung injury and whether extracellular (EC)-SOD-deficient mice would have increased hemorrhage-induced lung injury. Compared with wild-type mice, EC-SOD-deficient mice had increased lung neutrophil accumulation, a 3.9-fold increase in myeloperoxidase activity, a 1.5-fold increase in nuclear factor (NF)-κB activation, and a 1.5-fold increase in lipid peroxidation 1 h after hemorrhage. Pretreatment with AEOL 10150 did not attenuate neutrophil accumulation but significantly reduced NF-κB activation and lipid peroxidation in both wild-type and EC-SOD-deficient mice. The increase in hemorrhage-induced neutrophil accumulation in the lungs of EC-SOD-deficient mice suggests that EC-SOD might play a role in mediating neutrophil recruitment to the lung.
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Faraci, F. M., M. L. Modrick, C. M. Lynch, L. A. Didion, P. E. Fegan, and S. P. Didion. "Selective cerebral vascular dysfunction in Mn-SOD-deficient mice." Journal of Applied Physiology 100, no. 6 (June 2006): 2089–93. http://dx.doi.org/10.1152/japplphysiol.00939.2005.
Повний текст джерелаАнотація:
We tested the hypothesis that the mitochondrial form of superoxide dismutase [manganese superoxide dismutase (Mn-SOD)] protects the cerebral vasculature. Basilar arteries (baseline diameter ∼140 μm) from mice were isolated, cannulated, and pressurized to measure vessel diameter. In arteries from C57BL/6 mice preconstricted with U-46619, acetylcholine (ACh; an endothelium-dependent vasodilator) produced dilation that was similar in male and female mice and abolished by an inhibitor of nitric oxide synthase. Vasodilation to ACh was not altered in heterozygous male or female Mn-SOD-deficient (Mn-SOD+/−) mice compared with wild-type littermate controls (Mn-SOD+/+). Constriction of the basilar artery to arginine vasopressin, but not KCl or U-46619, was increased in Mn-SOD+/− mice ( P < 0.05), and this effect was prevented by tempol, a scavenger of superoxide. We also examined responses of cerebral (pial) arterioles (branches of the middle cerebral artery, control diameter ∼30 μm) to ACh in anesthetized mice using a cranial window. Responses to ACh, but not nitroprusside (an endothelium-independent agonist), were reduced ( P < 0.05) in cerebral arterioles in Mn-SOD+/− mice, and this effect was prevented by tempol. Thus these are the first data on the role of Mn-SOD in cerebral circulation. In the basilar artery, ACh produced nitric oxide-mediated dilation that was similar in male and female mice. Under normal conditions in cerebral arteries, responses to ACh were not altered but constrictor responses were selectively enhanced in Mn-SOD+/− mice. In the cerebral microcirculation, there was superoxide-mediated impairment of responses to ACh.
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Veerareddy, Sukrutha, Christy-Lynn M. Cooke, Philip N. Baker, and Sandra T. Davidge. "Gender differences in myogenic tone in superoxide dismutase knockout mouse: animal model of oxidative stress." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 1 (July 2004): H40—H45. http://dx.doi.org/10.1152/ajpheart.01179.2003.
Повний текст джерелаАнотація:
Oxidative stress mediated by prooxidants has been implicated in the pathogenesis of vascular disorders. However, the effect of prooxidants on myogenic regulation of vascular function and the differential influence of gender is not known. SOD, an intracellular enzyme, restricts excess prooxidant levels and may limit vascular dysfunction. We therefore tested the effects of Cu,Zn SOD deficiency on vascular tone in both male and female SOD knockout (SOD−/−) mice. We hypothesized that myogenic tone would be enhanced in SOD−/− mice by excess prooxidants compared with wild-type control mice. Indeed, resistance-sized mesenteric arteries from SOD−/− mice exhibited enhanced myogenic tone compared with control mice. Myogenic tone was lower in female than male control mice. Interestingly, this gender effect was absent in SOD−/− mice, such that myogenic tone of mesenteric arteries from females was equated to that of arteries from males. Furthermore, the pathways that modulate myogenic tone were diverse. In both male and female control mice, inhibition of prostaglandin H synthase (PGHS) and nitric oxide synthase (NOS) pathways enhanced myogenic tone. In female SOD−/− mice, inhibition of PGHS and NOS pathways enhanced myogenic tone to a greater extent compared with control mice. Conversely, in male SOD−/− mice, NOS and PGHS inhibition did not alter tone and only inhibition of gap junctions enhanced myogenic tone. In conclusion, this study revealed enhanced myogenic tone in SOD−/− mice compared with control mice. Furthermore, Cu,Zn SOD deficiency particularly enhanced myogenic tone in female mice such that their vascular tone attained the level of male SOD−/− mice, possibly mediated by prooxidants.
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Nakao, Chitose, Tomomi Ookawara, Takako Kizaki, Shuji Oh-Ishi, Hiromi Miyazaki, Shuhkoh Haga, Yuzo Sato, Li Li Ji, and Hideki Ohno. "Effects of swimming training on three superoxide dismutase isoenzymes in mouse tissues." Journal of Applied Physiology 88, no. 2 (February 1, 2000): 649–54. http://dx.doi.org/10.1152/jappl.2000.88.2.649.
Повний текст джерелаАнотація:
The purpose of the present study was to investigate the effects of swimming training on the changes in three superoxide dismutase (SOD) isoenzymes in mice. The trained mice underwent a 6-wk swimming program (1 h/day, 5 days/wk) in water at 35–36°C. Immunoreactive extracellular SOD (EC-SOD), copper- and zinc-containing SOD (CuZn-SOD), and manganese-containing SOD (Mn-SOD) contents and their mRNA abundance were determined in serum, heart, lung, liver, kidney, and gastrocnemius muscle. EC-SOD content in liver and kidney was significantly increased with training. After training, CuZn-SOD content rose significantly only in kidney but decreased significantly in heart, lung, and liver. Mn-SOD content showed a significant increase in lung, kidney, and skeletal muscle but a significant decrease in liver. In most tissues, however, the changes in SOD isoenzyme contents were not concomitant with those in their mRNA levels. The results obtained thus suggest that, except for kidney, the responses in mouse tissues of three SOD isoenzymes (protein levels and mRNA abundance) to swimming training are different and that kidney may be one of the most sensitive organs to adapt to oxidative stress during physical training, although the mechanism remains vague.
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Ramiro-Diaz, Juan Manuel, Carlos H. Nitta, Levi D. Maston, Simon Codianni, Wieslawa Giermakowska, Thomas C. Resta, and Laura V. Gonzalez Bosc. "NFAT is required for spontaneous pulmonary hypertension in superoxide dismutase 1 knockout mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 9 (May 1, 2013): L613—L625. http://dx.doi.org/10.1152/ajplung.00408.2012.
Повний текст джерелаАнотація:
Elevated reactive oxygen species are implicated in pulmonary hypertension (PH). Superoxide dismutase (SOD) limits superoxide bioavailability, and decreased SOD activity is associated with PH. A decrease in SOD activity is expected to increase superoxide and reduce hydrogen peroxide levels. Such an imbalance of superoxide/hydrogen peroxide has been implicated as a mediator of nuclear factor of activated T cells (NFAT) activation in epidermal cells. We have shown that NFATc3 is required for chronic hypoxia-induced PH. However, it is unknown whether NFATc3 is activated in the pulmonary circulation in a mouse model of decreased SOD1 activity and whether this leads to PH. Therefore, we hypothesized that an elevated pulmonary arterial superoxide/hydrogen peroxide ratio activates NFATc3, leading to PH. We found that SOD1 knockout (KO) mice have elevated pulmonary arterial wall superoxide and decreased hydrogen peroxide levels compared with wild-type (WT) littermates. Right ventricular systolic pressure (RVSP) was elevated in SOD1 KO and was associated with pulmonary arterial remodeling. Vasoreactivity to endothelin-1 was also greater in SOD1 KO vs. WT mice. NFAT activity and NFATc3 nuclear localization were increased in pulmonary arteries from SOD1 KO vs. WT mice. Administration of A-285222 (selective NFAT inhibitor) decreased RVSP, arterial wall thickness, vasoreactivity, and NFAT activity in SOD1 KO mice to WT levels. The SOD mimetic, tempol, also reduced NFAT activity, NFATc3 nuclear localization, and RVSP to WT levels. These findings suggest that an elevated superoxide/hydrogen peroxide ratio activates NFAT in pulmonary arteries, which induces vascular remodeling and increases vascular reactivity leading to PH.
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Balendra, Vyshnavy, and Sandeep Kumar Singh. "Therapeutic potential of astaxanthin and superoxide dismutase in Alzheimer's disease." Open Biology 11, no. 6 (June 2021): 210013. http://dx.doi.org/10.1098/rsob.210013.
Повний текст джерелаАнотація:
Oxidative stress, the imbalance of the antioxidant system, results in an accumulation of neurotoxic proteins in Alzheimer's disease (AD). The antioxidant system is composed of exogenous and endogenous antioxidants to maintain homeostasis. Superoxide dismutase (SOD) is an endogenous enzymatic antioxidant that converts superoxide ions to hydrogen peroxide in cells. SOD supplementation in mice prevented cognitive decline in stress-induced cells by reducing lipid peroxidation and maintaining neurogenesis in the hippocampus. Furthermore, SOD decreased expression of BACE1 while reducing plaque burden in the brain. Additionally, Astaxanthin (AST), a potent exogenous carotenoid, scavenges superoxide anion radicals. Mice treated with AST showed slower memory decline and decreased depositions of amyloid-beta (A β ) and tau protein. Currently, the neuroprotective potential of these supplements has only been examined separately in studies. However, a single antioxidant cannot sufficiently resist oxidative damage to the brain, therefore, a combinatory approach is proposed as a relevant therapy for ameliorating pathological changes in AD.
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Deshmukh, Devendra R., Oleg Mirochnitchenko, Vikram S. Ghole, Doreen Agnese, Pritesh C. Shah, Michael Reddell, Robert E. Brolin, and Masayori Inouye. "Intestinal ischemia and reperfusion injury in transgenic mice overexpressing copper-zinc superoxide dismutase." American Journal of Physiology-Cell Physiology 273, no. 4 (October 1, 1997): C1130—C1135. http://dx.doi.org/10.1152/ajpcell.1997.273.4.c1130.
Повний текст джерелаАнотація:
Superoxide dismutase (SOD) scavenges oxygen radicals that are implicated in the pathogenesis of intestinal ischemia-reperfusion injury. The effect of intestinal ischemia and reperfusion was investigated in transgenic mice overexpressing human Cu-Zn SOD. Ischemia was induced by occluding the superior mesenteric artery. Myeloperoxidase activity was determined as an index of neutrophil infiltration, and malondialdehyde levels were measured as an indicator of lipid peroxidation. Forty-five minutes of intestinal ischemia followed by 4 h of reperfusion caused an increase in intestinal levels of malondialdehyde in both nontransgenic and transgenic mice, but the concentration of malondialdehyde was significantly greater in nontransgenic mice. Intestinal ischemia-reperfusion also caused an increase in intestinal and pulmonary myeloperoxidase activity in nontransgenic and transgenic mice, but the transgenic mice had significantly lower levels of myeloperoxidase activity than nontransgenic mice. Transgenic mice had higher levels of intestinal SOD activity than nontransgenic mice. There were no significant differences in the catalase or glutathione peroxidase activities. In conclusion, our study demonstrates that the overexpression of SOD protects tissues from neutrophil infiltration and lipid peroxidation during intestinal ischemia-reperfusion.
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Suliman, Hagir B., Lisa K. Ryan, Lisa Bishop, and Rodney J. Folz. "Prevention of influenza-induced lung injury in mice overexpressing extracellular superoxide dismutase." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 1 (January 1, 2001): L69—L78. http://dx.doi.org/10.1152/ajplung.2001.280.1.l69.
Повний текст джерелаАнотація:
Reactive oxygen and nitrogen species such as superoxide and nitric oxide are released into the extracellular spaces by inflammatory and airway epithelial cells. These molecules may exacerbate lung injury after influenza virus pneumonia. We hypothesized that enhanced expression of extracellular superoxide dismutase (EC SOD) in mouse airways would attenuate the pathological effects of influenza pneumonia. We compared the pathogenic effects of a nonlethal primary infection with mouse-adapted Hong Kong influenza A/68 virus in transgenic (TG) EC SOD mice versus non-TG (wild-type) littermates. Compared with wild-type mice, EC SOD TG mice showed less lung injury and inflammation as measured by significant blunting of interferon-γ induction, reduced cell count and total protein in bronchoalveolar lavage fluid, reduced levels of lung nitrite/nitrate nitrotyrosine, and markedly reduced lung pathology. These results demonstrate that enhancing EC SOD in the conducting and distal airways of the lung minimizes influenza-induced lung injury by both ameliorating inflammation and attenuating oxidative stress.
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Tanaka, Ken-Ichiro, Tomoaki Ishihara, Arata Azuma, Shoji Kudoh, Masahito Ebina, Toshihiro Nukiwa, Yukihiko Sugiyama, et al. "Therapeutic effect of lecithinized superoxide dismutase on bleomycin-induced pulmonary fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 3 (March 2010): L348—L360. http://dx.doi.org/10.1152/ajplung.00289.2009.
Повний текст джерелаАнотація:
Idiopathic pulmonary fibrosis (IPF) is thought to involve inflammatory infiltration of leukocytes, lung injury induced by reactive oxygen species (ROS), in particular superoxide anion, and fibrosis (collagen deposition). No treatment has been shown to improve definitively the prognosis for IPF patients. Superoxide dismutase (SOD) catalyzes the dismutation of superoxide anion to hydrogen peroxide, which is subsequently detoxified by catalase. Lecithinized SOD (PC-SOD) has overcome clinical limitations of SOD, including low tissue affinity and low stability in plasma. In this study, we examined the effect of PC-SOD on bleomycin-induced pulmonary fibrosis. Severity of the bleomycin-induced fibrosis in mice was assessed by various methods, including determination of hydroxyproline levels in lung tissue. Intravenous administration of PC-SOD suppressed the bleomycin-induced increase in the number of leukocytes in bronchoalveolar lavage fluid. Bleomycin-induced collagen deposition and increased hydroxyproline levels in the lung were also suppressed in animals treated with PC-SOD, suggesting that PC-SOD suppresses bleomycin-induced pulmonary fibrosis. The dose-response profile of PC-SOD was bell-shaped, but concurrent administration of catalase restored the ameliorative effect at high doses of PC-SOD. Intratracheal administration or inhalation of PC-SOD also attenuated the bleomycin-induced inflammatory response and fibrosis. The bell-shaped dose-response profile of PC-SOD was not observed for these routes of administration. We consider that, compared with intravenous administration, inhalation of PC-SOD may be a more therapeutically beneficial route of administration due to the higher safety and quality of life of the patient treated with this drug.
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Sheldon, R. Ann, Christine Windsor, Byong Sop Lee, Olatz Arteaga Cabeza, and Donna M. Ferriero. "Erythropoietin Treatment Exacerbates Moderate Injury after Hypoxia-Ischemia in Neonatal Superoxide Dismutase Transgenic Mice." Developmental Neuroscience 39, no. 1-4 (2017): 228–37. http://dx.doi.org/10.1159/000472710.
Повний текст джерелаАнотація:
The neonatal brain is highly susceptible to oxidative stress as developing endogenous antioxidant mechanisms are overwhelmed. In the neonate, superoxide dismutase (SOD) overexpression worsens hypoxic-ischemic injury due to H2O2 accumulation in the brain. Erythropoietin (EPO) is upregulated in 2 phases after HI, early (4 h) and late (7 days), and exogenous EPO has been effective in reducing the injury, possibly through reducing oxidative stress. We hypothesized that exogenous EPO would limit injury from excess H2O2 seen in SOD1-overexpressing mice, and thus enhance recovery after HI. We first wanted to confirm our previous findings in postnatal day 7 (P7) SOD-tg (CD1) mice using a P9 model of the Vannucci procedure of HI with SOD-tg mice from a different background strain (C57Bl/6), and then determine the efficacy of EPO treatment in this strain and their wild-type (WT) littermates. Thus, mice overexpressing copper/zinc SOD1 were subjected to HI, modified for the P9 mouse, and recombinant EPO (5 U/g) or vehicle (saline) was administered intraperitoneally 3 times: at 0 h, 24 h, and 5 days. Injury was assessed 7 days after HI. In addition, protein expression for EPO and EPO receptor was assessed in the cortex and hippocampus 24 h after HI. With the moderate insult, the SOD-tg mice had greater injury than the WT overall, confirming our previous results, as did the hippocampus and striatum when analyzed separately, but not the cortex or thalamus. EPO treatment worsened injury in SOD-tg overall and in the WT and SOD-tg hippocampus and striatum. With the more severe insult, all groups had greater injury than with the moderate insult, but differences between SOD-tg and WT were no longer observed and EPO treatment had no effect. Increased protein expression of EPO was observed in the cortex of SOD-tg mice given recombinant human EPO compared to SOD-tg given vehicle. This study confirms our previous results showing greater injury with SOD overexpression in the neonatal brain after HI at P7 in a different strain. These results also suggest that EPO treatment cannot ameliorate the damage seen in situations where there is excess H2O2 accumulation, and it may exacerbate injury in settings of extreme oxidative stress.
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Manni, Michelle L., Michael W. Epperly, Wei Han, Timothy S. Blackwell, Steven R. Duncan, Jon D. Piganelli, and Tim D. Oury. "Leukocyte-derived extracellular superoxide dismutase does not contribute to airspace EC-SOD after interstitial pulmonary injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 302, no. 1 (January 1, 2012): L160—L166. http://dx.doi.org/10.1152/ajplung.00360.2010.
Повний текст джерелаАнотація:
The antioxidant enzyme extracellular superoxide dismutase (EC-SOD) is abundant in the lung and is known to limit inflammation and fibrosis following numerous pulmonary insults. Previous studies have reported a loss of full-length EC-SOD from the pulmonary parenchyma with accumulation of proteolyzed EC-SOD in the airspace after an interstitial lung injury. However, following airspace only inflammation, EC-SOD accumulates in the airspace without a loss from the interstitium, suggesting this antioxidant may be released from an extrapulmonary source. Because leukocytes are known to express EC-SOD and are prevalent in the bronchoalveolar lavage fluid (BALF) after injury, it was hypothesized that these cells may transport and release EC-SOD into airspaces. To test this hypothesis, C57BL/6 wild-type and EC-SOD knockout mice were irradiated and transplanted with bone marrow from either wild-type mice or EC-SOD knockout mice. Bone marrow chimeric mice were then intratracheally treated with asbestos and killed 3 and 7 days later. At both 3 and 7 days following asbestos injury, mice without pulmonary EC-SOD expression but with EC-SOD in infiltrating and resident leukocytes did not have detectable levels of EC-SOD in the airspaces. In addition, leukocyte-derived EC-SOD did not significantly lessen inflammation or early stage fibrosis that resulted from asbestos injury in the lungs. Although it is not influential in the asbestos-induced interstitial lung injury model, EC-SOD is still known to be present in leukocytes and may play an influential role in attenuating pneumonias and other inflammatory diseases.
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Watanabe, Kenji, Shuichi Shibuya, Yusuke Ozawa, Hidetoshi Nojiri, Naotaka Izuo, Koutaro Yokote, and Takahiko Shimizu. "Superoxide Dismutase 1 Loss Disturbs Intracellular Redox Signaling, Resulting in Global Age-Related Pathological Changes." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/140165.
Повний текст джерелаАнотація:
Aging is characterized by increased oxidative stress, chronic inflammation, and organ dysfunction, which occur in a progressive and irreversible manner. Superoxide dismutase (SOD) serves as a major antioxidant and neutralizes superoxide radicals throughout the body.In vivostudies have demonstrated that copper/zinc superoxide dismutase-deficient (Sod1−/−) mice show various aging-like pathologies, accompanied by augmentation of oxidative damage in organs. We found that antioxidant treatment significantly attenuated the age-related tissue changes and oxidative damage-associated p53 upregulation inSod1−/−mice. This review will focus on various age-related pathologies caused by the loss ofSod1and will discuss the molecular mechanisms underlying the pathogenesis inSod1−/−mice.
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Anis, Roomisa, Misbah-ul Qamar, Ayesha Shafqat, Ayesha Aftab, Zarafshan Bader, and Shumaela Kanwal. "Assessment of Degree of Association Between Markers of Oxidative Stress in Lead Poisoned Mice." Pakistan Journal of Medical and Health Sciences 15, no. 9 (September 30, 2021): 2952–54. http://dx.doi.org/10.53350/pjmhs211592952.
Повний текст джерелаАнотація:
Lead (Pb) is an abundant and one of the most lethal metals found in the earth’s crust. Its use by humans dates back to thousands of year. Even the low doses of lead are responsible for the production of reactive oxygen species which leads to oxidative load. This oxidative stress mitigates production of malondialdehyde (MDA) and down regulates antioxidant enzyme superoxide dismutase (SOD). Study Design: Quasi experimental Study. Place and duration of study: Department of Biochemistry, ANMCH, Islamabad, Pakistan in collaboration with NIH, Islamabad from November, 2018 to April, 2019. Methodology: A total of 40 BALB/c mice were divided into two groups of 20 mice each. Group was given normal standard diet. Group was given lead acetate in drinking water with normal diet without any supplementation. Levels of malondialdehyde were measured by using Thiobarbituric acid reactive substances (TBARS) and Superoxide Dismutase (SOD) was estimated by xanthine oxidase method at the end of study. Results: The results of our study showed increase in MDA and decrease in SOD in lead treated group when compared with the control group. Pearson correlation was applied to assess the degree of association between two parameters, it showed significant negative correlation with value of r = -0.96 and p-value of 0.001 Conclusion: It was concluded from our study that increase in MDA leads to decrease in SOD indicating strong negative correlation in lead poisoned mice. Key words: Lead poisoning, Malondialdehyde, Oxidative Stress, Superoxide Dismutase
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Auten, Richard L., Michael A. O'Reilly, Tim D. Oury, Eva Nozik-Grayck, and Mary H. Whorton. "Transgenic extracellular superoxide dismutase protects postnatal alveolar epithelial proliferation and development during hyperoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 1 (January 2006): L32—L40. http://dx.doi.org/10.1152/ajplung.00133.2005.
Повний текст джерелаАнотація:
Transgenic (TG) human (h) extracellular superoxide dismutase (EC-SOD) targeted to type II cells protects postnatal newborn mouse lung development against hyperoxia by unknown mechanisms. Because alveolar development depends on timely proliferation of type II epithelium and differentiation to type I epithelium, we measured proliferation in bronchiolar and alveolar (surfactant protein C-positive) epithelium in air and 95% O2-exposed wild-type (WT) and TG hEC-SOD newborn mice at postnatal days 3, 5, and 7 (P3-P7), traversing the transition from saccular to alveolar stages. We found that TG hEC-SOD ameliorated the 95% O2-impaired bromodeoxyuridine uptake in alveolar and bronchiolar epithelium at P3, but not at P5 and P7, when overall epithelial proliferation rates were lower in air-exposed WT mice. Mouse EC-, CuZn-, and Mn-SOD expression were unaffected by hyperoxia or genotype. TG mice had less DNA damage than 95% O2-exposed WT mice at P3, measured by TdT-mediated dUTP nick end labeling ( P < 0.05). Hyperoxia induced cell-cycle inhibitory protein p21 cip/waf mRNA at P3, WT > TG, P = 0.06. 95% O2 impaired apical expression of type I cell α protein (T1α) in WT but not in TG mice at P3 and increased T1α in WT and TG mice at P7. Reducing the 95% O2-induced impairment of epithelial proliferation at a critical window of lung development was associated with protection against DNA damage and preservation of apical T1α expression at P3.
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Yan, Changdong, An Huang, Zhiping Wu, Pawel M. Kaminski, Michael S. Wolin, Thomas H. Hintze, Gabor Kaley, and Dong Sun. "Increased superoxide leads to decreased flow-induced dilation in resistance arteries of Mn-SOD-deficient mice." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 5 (May 2005): H2225—H2231. http://dx.doi.org/10.1152/ajpheart.01036.2004.
Повний текст джерелаАнотація:
The role of mitochondrial manganese-superoxide dismutase (Mn-SOD) in the maintenance of vascular function has not yet been studied. Thus we examined flow- and agonist-induced dilations in isolated mesenteric arteries (∼90 μm in diameter) of Mn-SOD heterozygous (Mn-SOD+/−) and wild-type (WT) mice. Increases in flow elicited dilations in all vessels, but the magnitude of the dilation was significantly less in vessels of Mn-SOD+/− mice than in those of WT mice (64 vs. 74% of passive diameter). Nω-nitro-l-arginine methyl ester inhibited the dilation in vessels of WT mice but had no effect on vessels of Mn-SOD+/− mice. Tempol or tiron (superoxide scavengers) increased flow-induced dilation in vessels of Mn-SOD+/− mice. Acetylcholine- and sodium nitroprusside-induced, but not adenosine-induced, dilations were also decreased in arteries of Mn-SOD+/− mice. Superoxide levels in the arteries of Mn-SOD+/− mice were significantly increased. Western blot analysis confirmed a 50% reduction of Mn-SOD protein in the vessels of Mn-SOD+/− mice. A 41% reduction in endothelial nitric oxide synthase (eNOS) protein and a 37% reduction in eNOS activity were also found in the vessels of Mn-SOD+/− mice. Whereas there was no difference in eNOS protein in kidney homogenates of WT and Mn-SOD+/− mice, a significant reduction of nitric oxide synthase activity was found in Mn-SOD+/− mice, which could be restored by the administration of tiron. We conclude that an increased concentration of superoxide due to reduced activity of Mn-SOD, which inactivates nitric oxide and inhibits eNOS activity, contributes to the impaired vasodilator function of isolated mesenteric arteries of Mn-SOD+/− mice. These results suggest that Mn-SOD contributes significantly to the regulation of vascular function.
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Kataoka, Takahiro, Reo Etani, Norie Kanzaki, Yusuke Kobashi, Yuto Yunoki, Tsuyoshi Ishida, Akihiro Sakoda, Yuu Ishimori та Kiyonori Yamaoka. "Radon inhalation induces manganese-superoxide dismutase in mouse brain via nuclear factor-κB activation". Journal of Radiation Research 58, № 6 (4 вересня 2017): 887–93. http://dx.doi.org/10.1093/jrr/rrx048.
Повний текст джерелаАнотація:
Abstract Although radon inhalation increases superoxide dismutase (SOD) activities in mouse organs, the mechanisms and pathways have not yet been fully clarified. The aim of this study was to determine the details of SOD activation in mouse brain tissue following the inhalation of radon at concentrations of 500 or 2000 Bq/m3 for 24 h. After inhalation, brains were removed quickly for analysis. Radon inhalation increased the manganese (Mn)-SOD level and mitochondrial SOD activity. However, the differences were not significant. There were no changes in the Cu/Zn-SOD level or cytosolic SOD activity. Radon inhalation increased the brain nuclear factor (NF)-κB content, which regulates the induction of Mn-SOD, in the nuclear and cytosolic compartments. The level of inhibitor of nuclear factor κB kinase subunit β (IKK-β), which activates NF-κB, was slightly increased by radon inhalation. The expression of cytoplasmic ataxia-telangiectasia mutated kinase in mice inhaling radon at 500 Bq/m3 was 50% higher than in control mice. In addition, NF-κB–inducing kinase was slightly increased after inhaling radon at 2000 Bq/m3. These findings suggest that radon inhalation might induce Mn-SOD protein via NF-κB activation that occurs in response to DNA damage and oxidative stress.
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Petrache, Irina, Terry R. Medler, Amy T. Richter, Krzysztof Kamocki, Ugonma Chukwueke, Lijie Zhen, Yuan Gu, et al. "Superoxide dismutase protects against apoptosis and alveolar enlargement induced by ceramide." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 1 (July 2008): L44—L53. http://dx.doi.org/10.1152/ajplung.00448.2007.
Повний текст джерелаАнотація:
The molecular events leading to emphysema development include generation of oxidative stress and alveolar cell apoptosis. Oxidative stress upregulates ceramides, proapoptotic signaling sphingolipids that trigger further oxidative stress and alveolar space enlargement, as shown in an experimental model of emphysema due to VEGF blockade. As alveolar cell apoptosis and oxidative stress mutually interact to mediate alveolar destruction, we hypothesized that the oxidative stress generated by ceramide is required for its pathogenic effect on lung alveoli. To model the direct lung effects of ceramide, mice received ceramide intratracheally (Cer12:0 or Cer8:0; 1 mg/kg) or vehicle. Apoptosis was inhibited with a general caspase inhibitor. Ceramide augmentation shown to mimic levels found in human emphysema lungs increased oxidative stress, and decreased, independently of caspase activation, the lung superoxide dismutase activity at 48 h. In contrast to their wild-type littermates, transgenic mice overexpressing human Cu/Zn SOD were significantly protected from ceramide-induced superoxide production, apoptosis, and air space enlargement. Activation of lung acid sphingomyelinase in response to ceramide treatment was abolished in the Cu/Zn SOD transgenic mice. Since cigarette smoke-induced emphysema in mice is similarly ameliorated by the Cu/Zn SOD overexpression, we hypothesized that cigarette smoke may induce ceramides in the mouse lung. Utilizing tandem mass spectrometry, we documented increased lung ceramides in adult mice exposed to cigarette smoke for 4 wk. In conclusion, ceramide-induced superoxide accumulation in the lung may be a critical step in ceramide's proapoptotic effect in the lung. This work implicates excessive lung ceramides as amplifiers of lung injury through redox-dependent mechanisms.
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Nakatani-Okuda, Akemi, Haruyasu Ueda, Shin-ichiro Kashiwamura, Atsuo Sekiyama, Akira Kubota, Yukihisa Fujita, Susumu Adachi, Yoshiyuki Tsuji, Takakuni Tanizawa, and Haruki Okamura. "Protection against bleomycin-induced lung injury by IL-18 in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 2 (August 2005): L280—L287. http://dx.doi.org/10.1152/ajplung.00380.2004.
Повний текст джерелаАнотація:
The role of interleukin (IL)-18 in the protection from interstitial pneumonia and pulmonary fibrosis induced by bleomycin (BLM) was investigated by comparing the severity of BLM-induced lung injuries between wild-type and C57BL/6 mice with a targeted knockout mutation of the IL-18 gene (IL-18−/− mice). IL-18−/− mice showed much worse lung injuries than wild-type mice, as assessed by the survival rate, histological images, and leukocyte infiltration in the bronchoalveolar lavage fluid and myeloperoxidase activity. In wild-type mice, administration of IL-18 before BLM instillation resulted in suppression of lung injuries, increases in the hydroxyproline content, and decreases in the granulocyte-macrophage colony-stimulating factor content in the lung. Preadministration of IL-18 also resulted in prevention of the reduction of the lung IL-10 content caused by BLM-induced damage of alveolar epithelial. BLM instillation suppressed superoxide dismutase (SOD) activity in IL-18−/− mice to a greater extent than in wild-type mice. Pretreatment of IL-18 augmented Mn-containing superoxide dismutase (Mn-SOD) messenger RNA expression and SOD activity in the lung and prevented the reduction of SOD activity caused by BLM in both wild-type and IL-18−/− mice. These results suggest that IL-18 plays a protective role against BLM-induced lung injuries by upregulating a defensive molecule, Mn-SOD.
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Lu, Hua, Junhui Zhen, Tianfu Wu, Ai Peng, Ting Ye, Tao Wang, Xueqing Yu, Nosratola D. Vaziri, Chandra Mohan, and Xin J. Zhou. "Superoxide dismutase mimetic drug tempol aggravates anti-GBM antibody-induced glomerulonephritis in mice." American Journal of Physiology-Renal Physiology 299, no. 2 (August 2010): F445—F452. http://dx.doi.org/10.1152/ajprenal.00583.2009.
Повний текст джерелаАнотація:
Oxidative stress plays an important role in the pathogenesis of anti-glomerular basement membrane antibody-induced glomerulonephritis (anti-GBM-GN). Superoxide dismutase (SOD) is the first line of defense against oxidative stress by converting superoxide to hydrogen peroxide (H2O2). We investigated the effect of the SOD mimetic drug tempol on anti-GBM-GN in mice. 129/svJ mice were challenged with rabbit anti-mouse-GBM sera to induce GN and subsequently divided into tempol (200 mg·kg−1·day−1, orally) and vehicle-treated groups. Routine histology, SOD and catalase activities, malondialdehyde (MDA), H2O2, and immunohistochemical staining for neutrophils, lymphocytes, macrophages, p65-NF-κB, and osteopontin were performed. Mice with anti-GBM-GN had significantly reduced renal SOD and catalase activities and increased H2O2 and MDA levels. Unexpectedly, tempol administration exacerbated anti-GBM-GN as evidenced by intensification of proteinuria, the presence of severe crescentic GN with leukocyte influx, and accelerated mortality in the treated group. Tempol treatment raised SOD activity and H2O2 level in urine, upregulated p65-NF-κB and osteopontin in the kidney, but had no effect on renal catalase activity. Thus tempol aggravates anti-GBM-GN by increasing production of H2O2 which is a potent NF-κB activator and as such can intensify inflammation and renal injury. This supposition is supported by increases seen in p65-NF-κB, osteopontin, and leukocyte influx in the kidneys of the tempol-treated group.
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Fretland, Donald J., Deborah L. Widomski, Charles P. Anglin, Dennis Riley, Randy H. Weiss, and Timothy S. Gaginella. "Superoxide dismutase(SOD) protect against acetic acid-induced colitis in mice." Free Radical Biology and Medicine 9 (January 1990): 142. http://dx.doi.org/10.1016/0891-5849(90)90680-h.
Повний текст джерела
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Ghio, Andrew J., Hagir B. Suliman, Jacqueline D. Carter, Amir M. Abushamaa, and Rodney J. Folz. "Overexpression of extracellular superoxide dismutase decreases lung injury after exposure to oil fly ash." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 1 (July 1, 2002): L211—L218. http://dx.doi.org/10.1152/ajplung.00409.2001.
Повний текст джерелаАнотація:
The mechanism of tissue injury after exposure to air pollution particles is not known. The biological effect has been postulated to be mediated via an oxidative stress catalyzed by metals present in particulate matter (PM). We utilized a transgenic (Tg) mouse model that overexpresses extracellular superoxide dismutase (EC-SOD) to test the hypothesis that lung injury after exposure to PM results from an oxidative stress in the lower respiratory tract. Wild-type (Wt) and Tg mice were intratracheally instilled with either saline or 50 μg of residual oil fly ash (ROFA). Twenty-four hours later, specimens were obtained and included bronchoalveolar lavage (BAL) and lung for both homogenization and light histopathology. After ROFA exposure, EC-SOD Tg mice showed a significant reduction in BAL total cell counts (composed primarily of neutrophils) and BAL total protein compared with Wt. EC-SOD animals also demonstrated diminished concentrations of inflammatory mediators in BAL. There was no statistically significant difference in BAL lipid peroxidation; however, EC-SOD mice had lower concentrations of oxidized glutathione in the BAL. We conclude that enhanced EC-SOD expression decreased both lung inflammation and damage after exposure to ROFA. This supports a participation of oxidative stress in the inflammatory injury after PM exposure rather than reflecting a response to metals alone.
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Qian, Yu, Jing Zhang, Xianrong Zhou, Ruokun Yi, Jianfei Mu, Xingyao Long, Yanni Pan, Xin Zhao, and Weiwei Liu. "Lactobacillus plantarum CQPC11 Isolated from Sichuan Pickled Cabbages Antagonizes d-galactose-Induced Oxidation and Aging in Mice." Molecules 23, no. 11 (November 20, 2018): 3026. http://dx.doi.org/10.3390/molecules23113026.
Повний текст джерелаАнотація:
Chinese pickled cabbage is a traditional fermented food that contains abundant microbes produced during the process of fermentation. In this work, an in vivo animal study was conducted to investigate the effects of a newly isolated lactic acid bacterium (Lactobacillus plantarum CQPC11, LP-CQPC11) on d-galactose-induced oxidation and aging in mice. Analysis of the serum and tissue samples of these mice using molecular biology approaches showed that LP-CQPC11 suppressed the decrease in thymus, brain, heart, liver, spleen, and kidney indices caused by oxidation and aging. Furthermore, LP-CQPC11 increased the levels of SOD (superoxide dismutase), GSH-Px (glutathione peroxidase), and GSH (glutathione), whereas it reduced the levels of NO (nitric oxide) and MDA (malondialdehyde) in the serum, liver, and spleen of oxidation and aging mouse models. Pathological observation indicated that LP-CQPC11 alleviated the damage caused by oxidation and aging on the liver and spleen of mice. qPCR analysis indicated that LP-CQPC11 effectively upregulated the expression of nNOS (neuronal nitric oxide synthase), eNOS (endothelial nitric oxide synthase), Cu/Zn-SOD (cuprozinc-superoxide dismutase), Mn-SOD (manganese superoxide dismutase), CAT (catalase), HO-1 (heme oxygenase-1), Nrf2 (nuclear factor-erythroid 2 related factor 2), γ-GCS (γ-glutamylcysteine synthetase), and NQO1 (NAD(P)H dehydrogenase [quinone] 1), but downregulated the expression of iNOS (inducible nitric oxide synthase) in the mouse liver and spleen. Western blot analysis showed that LP-CQPC11 effectively upregulated SOD1 (Cu/Zn-SOD), SOD2 (Mn-SOD), CAT, GSH1 (c-glutamylcysteine synthetase), and GSH2 (glutathione synthetase) protein expression in mouse liver and spleen tissues. These findings suggest that LP-CQPC11 can effectively prevent d-galactose-induced oxidation and aging in mice, and the effect is even better than that of the commonly used Lactobacillus delbruechii subsp. bulgaricus (LDSB) and vitamin C in the industry. Thus, LP-CQPC11 may be potentially employed as a probiotic strain.
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Zelko, Igor N., and Rodney J. Folz. "Extracellular Superoxide Dismutase Functions as a Major Repressor of Hypoxia-Induced Erythropoietin Gene Expression." Endocrinology 146, no. 1 (January 1, 2005): 332–40. http://dx.doi.org/10.1210/en.2004-1007.
Повний текст джерелаАнотація:
Hypoxia and biological responses to hypoxia are commonly encountered in both normal and pathologic cellular processes. Here we report that extracellular superoxide dismutase (EC-SOD) plays a major role in regulating the magnitude of hypoxia-induced erythropoietin (Epo) gene expression, thus implicating superoxide as an intermediary signal transduction molecule critical to this process. We found that mice which have the EC-SOD gene inactivated show a marked more than 100-fold elevation in hypoxia-induced Epo gene expression, compared with wild-type controls, which was both dose and time dependent. These mice also showed a significant increase in serum Epo levels after 1 d hypoxia. Interestingly, despite elevated Epo levels, reciprocal changes in hematocrit and reticulocyte counts were not found, suggesting that this newly synthesized Epo lacks functional hematopoietic effects. When EC-SOD was overexpressed in Hep3B cells, we found a significant reduction in Epo gene induction by both CoCl2 (50 μm) and hypoxia (1% O2). Similar findings were noted with another hypoxia-inducible gene, carbonic anhydrase IX. We conclude that EC-SOD functions as a major repressor of hypoxia-induced Epo gene expression, which implicates superoxide as a signaling intermediate whose downstream effects, at least in part, may be mediated by HIF-1α.
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Liu, Bihui, Ji Li, Ruokun Yi, Jianfei Mu, Xianrong Zhou, and Xin Zhao. "Preventive Effect of Alkaloids from Lotus plumule on Acute Liver Injury in Mice." Foods 8, no. 1 (January 19, 2019): 36. http://dx.doi.org/10.3390/foods8010036.
Повний текст джерелаАнотація:
Lotus plumule is a traditional Chinese food that can be used as a beverage. In this study, three kinds of Lotus plumules from different regions of China were selected to observe the preventive effects of extracted alkaloids on CCl4-induced liver injuries. Animal experiments revealed that alkaloids extracted from Lotus plumules decreased the serum AST (aspartate aminotransferase), ALT (alanine aminotransferase), and TBIL (total bilirubin) levels, enhanced SOD (superoxide dismutase) activity, and reduced MDA (malondialdehyde) level in the liver tissues of mice with liver injury. H&E observation confirmed that alkaloids from Lotus plumules could alleviate CCl4-induced injuries of liver tissues and inhibit the inflammatory effect on hepatocytes. Further qPCR experiments also demonstrated that alkaloids from Lotus plumules upregulated the expression of IκB-α (inhibitor of NF-κB alpha), Cu/Zn-SOD (copper/zinc superoxide dismutase), Mn-SOD (manganese superoxide dismutase), and CAT (catalase) mRNA and downregulated TNF-α (tumor necrosis factor alpha) and NF-κB (nuclear factor kappa B) expression in the liver tissues of mice with liver injury. All three kinds of alkaloids from Lotus plumules could prevent CCl4-induced liver injuries by regulating the levels of oxidative stress and inflammation in mice, and the therapeutic effect was comparable to that of silymarin, the medicine commonly used in the treatment of liver diseases. In summary, alkaloids from Lotus plumules contain bioactive substances with hepatic protective efficacy and possess potential application value in the field of functional food.
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Ho, Dao H., Mariah L. Burch, Benjamin Musall, Jacqueline B. Musall, Kelly A. Hyndman, and Jennifer S. Pollock. "Early life stress in male mice induces superoxide production and endothelial dysfunction in adulthood." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 9 (May 1, 2016): H1267—H1274. http://dx.doi.org/10.1152/ajpheart.00016.2016.
Повний текст джерелаАнотація:
Early life stress (ELS) is a risk for cardiovascular disease in adulthood although very little mechanistic insight is available. Because oxidative stress and endothelial dysfunction are major contributors to cardiovascular risk, we hypothesized that ELS induces endothelial dysfunction in adult male mice via increased superoxide production. Studies employed a mouse model of ELS, maternal separation with early weaning (MSEW), in which litters were separated from the dam for 4 h/day [ postnatal days (PD) 2–5] and 8 h/day (PD6-16), and weaned at PD17. Control litters remained undisturbed until weaning at PD21. When compared with control mice, thoracic aortic rings from adult male MSEW mice displayed significant endothelial dysfunction that was reversed by the superoxide scavenger, polyethylene glycol-superoxide dismutase (PEG-SOD). PEG-SOD-inhibitable superoxide production by aortae from MSEW mice was significantly greater than observed in control aortae, although unaffected by nitric oxide synthase inhibition, suggesting that uncoupled nitric oxide synthase was not responsible for the accelerated superoxide production. Aortic SOD expression, plasma SOD activity, and total antioxidant activity were similar in MSEW and control mice, indicating unaltered antioxidant capacity in MSEW mice. Increased expression of the NADPH oxidase subunits, NOX2 and NOX4, was evident in the aortae of MSEW mice. Moreover, endothelial dysfunction and superoxide production in MSEW mice was reversed with the NADPH oxidase inhibitor, apocynin, indicating increased NADPH oxidase-dependent superoxide production and endothelial dysfunction. The finding that MSEW induces superoxide production and endothelial dysfunction in adult mice may provide a mechanistic link between ELS and adult cardiovascular disease risk.
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Liu, John Q., and Rodney J. Folz. "Extracellular superoxide enhances 5-HT-induced murine pulmonary artery vasoconstriction." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 1 (July 2004): L111—L118. http://dx.doi.org/10.1152/ajplung.00006.2004.
Повний текст джерелаАнотація:
Accumulating evidence suggests that changes in both 5-hydroxytryptamine (5-HT) receptor activity and in the levels of reactive oxygen species (ROS) play an important role in regulating pulmonary artery (PA) vascular responsiveness, particularly in the setting of pulmonary hypertension. Therefore, we hypothesized that increased levels of superoxide enhance 5-HT-induced PA constriction. With the use of a small-vessel bioassay, 5-HT (0.01–10 μM) induced a concentration-dependent vasoconstriction in isolated wild-type murine intrapulmonary arteries (100–150 μm diameter) that was enhanced by both removal of the endothelium and by treatment with either NG-nitro-l-arginine methyl ester (30 μM) or xanthine (10 μM) + xanthine oxidase (0.005 U/ml). PA isolated from extracellular superoxide dismutase (EC-SOD) knockout mice also showed enhanced constriction. On the other hand, PA constriction to 5-HT was attenuated by either the addition of GR-127935 (0.1 μM, a selective inhibitor of 5-HT1B/1Dreceptor) or copper/zinc-containing superoxide dismutase (Cu/Zn SOD, 150 U/ml) and in PA isolated from transgenic mice overexpressing human EC-SOD. With the use of both oxidative fluorescent confocal microscopy and lucigenin-enhanced chemiluminescence, superoxide levels were increased significantly after 5-HT-induced PA vasoconstriction. This increase in superoxide levels could be blocked by the exogenous addition of Cu/Zn SOD (150 U/ml) or by apocynin (30 μM, an inhibitor of NADPH oxidase) but was not affected by gp91phoxknockout mice. Overall, our results are consistent with 5-HT increasing vascular smooth muscle superoxide production via an NADPH oxidase pathway that is independent of gp91phox, which leads to increases in extracellular superoxide levels, which in turn enhances 5-HT-induced murine pulmonary vasoconstriction.
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Larsen, Gary L., Carl W. White, Katsuyuki Takeda, Joan E. Loader, Dee Dee H. Nguyen, Anthony Joetham, Yoram Groner, and Erwin W. Gelfand. "Mice that overexpress Cu/Zn superoxide dismutase are resistant to allergen-induced changes in airway control." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 2 (August 1, 2000): L350—L359. http://dx.doi.org/10.1152/ajplung.2000.279.2.l350.
Повний текст джерелаАнотація:
Within the respiratory epithelium of asthmatic patients, copper/zinc-containing superoxide dismutase (Cu/Zn SOD) is decreased. To address the hypothesis that lung Cu/Zn SOD protects against allergen-induced injury, wild-type and transgenic mice that overexpress human Cu/Zn SOD were either passively sensitized to ovalbumin (OVA) or actively sensitized by repeated airway exposure to OVA. Controls included nonsensitized wild-type and transgenic mice given intravenous saline or airway exposure to saline. After aerosol challenge to saline or OVA, segments of tracheal smooth muscle were obtained for in vitro analysis of neural control. In response to electrical field stimulation, wild-type sensitized mice challenged with OVA had significant increases in cholinergic reactivity. Conversely, sensitized transgenic mice challenged with OVA were resistant to changes in neural control. Stimulation of tracheal smooth muscle to elicit acetylcholine release showed that passively sensitized wild-type but not transgenic mice released more acetylcholine after OVA challenge. Function of the M2 muscarinic autoreceptor was preserved in transgenic mice. These results demonstrate that murine airways with elevated Cu/Zn SOD were resistant to allergen-induced changes in neural control.
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Oñate, Angel A., Sandra Céspedes, Alex Cabrera, Rodolfo Rivers, Andrés González, Carola Muñoz, Hugo Folch, and Edilia Andrews. "A DNA Vaccine Encoding Cu,Zn Superoxide Dismutase of Brucella abortus Induces Protective Immunity in BALB/c Mice." Infection and Immunity 71, no. 9 (September 2003): 4857–61. http://dx.doi.org/10.1128/iai.71.9.4857-4861.2003.
Повний текст джерелаАнотація:
ABSTRACT This study was conducted to evaluate the immunogenicity and protective efficacy of a DNA vaccine encoding Brucella abortus Cu,Zn superoxide dismutase (SOD). Intramuscular injection of plasmid DNA carrying the SOD gene (pcDNA-SOD) into BALB/c mice elicited both humoral and cellular immune responses. Animals injected with pcDNA-SOD developed SOD-specific antibodies which exhibited a dominance of immunoglobulin G2a (IgG2a) over IgG1. In addition, the DNA vaccine elicited a T-cell-proliferative response and also induced the production of gamma interferon, but not interleukin-10 (IL-10) or IL-4, upon restimulation with either recombinant SOD or crude Brucella protein, suggesting the induction of a typical T-helper-1-dominated immune response in mice. The pcDNA-SOD (but not the control vector) induced a strong, significant level of protection in BALB/c mice against challenge with B. abortus virulent strain 2308; the level of protection was similar to the one induced by B. abortus vaccine strain RB51. Altogether, these data suggest that pcDNA-SOD is a good candidate for use in future studies of vaccination against brucellosis.
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Hohl, Mathias, Manuel Mayr, Lisa Lang, Alexander G. Nickel, Javier Barallobre-Barreiro, Xiaoke Yin, Thimoteus Speer, et al. "Cathepsin A contributes to left ventricular remodeling by degrading extracellular superoxide dismutase in mice." Journal of Biological Chemistry 295, no. 36 (July 9, 2020): 12605–17. http://dx.doi.org/10.1074/jbc.ra120.013488.
Повний текст джерелаАнотація:
In the heart, the serine carboxypeptidase cathepsin A (CatA) is distributed between lysosomes and the extracellular matrix (ECM). CatA-mediated degradation of extracellular peptides may contribute to ECM remodeling and left ventricular (LV) dysfunction. Here, we aimed to evaluate the effects of CatA overexpression on LV remodeling. A proteomic analysis of the secretome of adult mouse cardiac fibroblasts upon digestion by CatA identified the extracellular antioxidant enzyme superoxide dismutase (EC-SOD) as a novel substrate of CatA, which decreased EC-SOD abundance 5-fold. In vitro, both cardiomyocytes and cardiac fibroblasts expressed and secreted CatA protein, and only cardiac fibroblasts expressed and secreted EC-SOD protein. Cardiomyocyte-specific CatA overexpression and increased CatA activity in the LV of transgenic mice (CatA-TG) reduced EC-SOD protein levels by 43%. Loss of EC-SOD–mediated antioxidative activity resulted in significant accumulation of superoxide radicals (WT, 4.54 μmol/mg tissue/min; CatA-TG, 8.62 μmol/mg tissue/min), increased inflammation, myocyte hypertrophy (WT, 19.8 μm; CatA-TG, 21.9 μm), cellular apoptosis, and elevated mRNA expression of hypertrophy-related and profibrotic marker genes, without affecting intracellular detoxifying proteins. In CatA-TG mice, LV interstitial fibrosis formation was enhanced by 19%, and the type I/type III collagen ratio was shifted toward higher abundance of collagen I fibers. Cardiac remodeling in CatA-TG was accompanied by an increased LV weight/body weight ratio and LV end diastolic volume (WT, 50.8 μl; CatA-TG, 61.9 μl). In conclusion, CatA-mediated EC-SOD reduction in the heart contributes to increased oxidative stress, myocyte hypertrophy, ECM remodeling, and inflammation, implicating CatA as a potential therapeutic target to prevent ventricular remodeling.
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Kofler, Julia, Patricia D. Hurn, and Richard J. Traystman. "SOD1 Overexpression and Female Sex Exhibit Region-Specific Neuroprotection after Global Cerebral Ischemia Due to Cardiac Arrest." Journal of Cerebral Blood Flow & Metabolism 25, no. 9 (April 20, 2005): 1130–37. http://dx.doi.org/10.1038/sj.jcbfm.9600119.
Повний текст джерелаАнотація:
Cardiac arrest is often associated with poor neurologic outcome since therapeutic options are limited. We tested the hypothesis that overexpression of CuZn superoxide dismutase (SOD+/–) is neuroprotective in a new murine model of cardiac arrest and cardiopulmonary resuscitation (CPR). Second, we investigated if female and male mice sustain similar injury and if sex-specific outcomes are altered by SOD overexpression. Neuronal injury was quantified 3 days after 8 mins of KCl-induced cardiac arrest by calculating the percentage of ischemic neurons for caudoputamen and hippocampal CA1 region. In rostral caudoputamen, less neuronal cell loss was found for SOD+/– mice (31%+22%) when compared with wild-type (WT) mice (47%+31%, P<0.05). Superoxide dismutase overexpression did not reduce injury in the caudal caudoputamen. No sex-linked protection was evident in either genotype in the caudoputamen. Female WT mice had less CA1 injury than male WT mice (26%+31% versus 54%+30%, P<0.05), whereas no sex difference was found in SOD+/– mice (female: 42%+29%; male: 37%+37%). Comparison of hippocampal injury between genotypes revealed no differences for either males or females. In conclusion, SOD1 overexpression and female sex were associated with significant neuroprotection in this murine cardiac arrest model. However, no additive neuroprotection was observed, and these beneficial effects were restricted to specific brain regions.
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Guo, Guozheng, Yan Yan-Sanders, Beverly D. Lyn-Cook, Tieli Wang, Daniel Tamae, Julie Ogi, Alexander Khaletskiy, et al. "Manganese Superoxide Dismutase-Mediated Gene Expression in Radiation-Induced Adaptive Responses." Molecular and Cellular Biology 23, no. 7 (April 1, 2003): 2362–78. http://dx.doi.org/10.1128/mcb.23.7.2362-2378.2003.
Повний текст джерелаАнотація:
ABSTRACT Antioxidant enzymes are critical in oxidative stress responses. Radioresistant variants isolated from MCF-7 human carcinoma cells following fractionated ionizing radiation (MCF+FIR cells) or overexpression of manganese superoxide dismutase (MCF+SOD cells) demonstrated dose-modifying factors at 10% isosurvival of 1.8 and 2.3, respectively. MCF+FIR and MCF-7 cells (exposed to single-dose radiation) demonstrated 5- to 10-fold increases in MnSOD activity, mRNA, and immunoreactive protein. Radioresistance in MCF+FIR and MCF+SOD cells was reduced following expression of antisense MnSOD. DNA microarray analysis and immunoblotting identified p21, Myc, 14-3-3 zeta, cyclin A, cyclin B1, and GADD153 as genes constitutively overexpressed (2- to 10-fold) in both MCF+FIR and MCF+SOD cells. Radiation-induced expression of these six genes was suppressed in fibroblasts from Sod2 knockout mice (−/−) as well as in MCF+FIR and MCF+SOD cells expressing antisense MnSOD. Inhibiting NF-κB transcriptional activity in MCF+FIR cells, by using mutant IκBα, inhibited radioresistance as well as reducing steady-state levels of MnSOD, 14-3-3 zeta, GADD153, cyclin A, and cyclin B1 mRNA. In contrast, mutant IκBα was unable to inhibit radioresistance or reduce 14-3-3 zeta, GADD153, cyclin A, and cyclin B1 mRNAs in MCF+SOD cells, where MnSOD overexpression was independent of NF-κB. These results support the hypothesis that NF-κB is capable of regulating the expression of MnSOD, which in turn is capable of increasing the expression of genes that participate in radiation-induced adaptive responses.
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Parra, Augusto, Matthew J. McGirt, Huaxin Sheng, Robert D. Pearlstein, Daniel T. Laskowitz, and David S. Warner. "Effects of Extracellular Superoxide Dismutase on Arterial Vascular Structural Changes After Acute Subarachnoid Hemorrhage in the Mouse." Stroke 32, suppl_1 (January 2001): 359. http://dx.doi.org/10.1161/str.32.suppl_1.359-d.
Повний текст джерелаАнотація:
P113 Background and Purpose: Subarachnoid hemorrhage (SAH) is a known cause of cerebral vasospasm. Vasopasm may result from loss of endothelial NO synthesis. There is also evidence that Hgb products released after SAH bind NO and deplete its extracellular bioavailability. Cu/Zn superoxide dismutase (SOD) overexpression has been shown to provide protection against vasospasm presumably by reducing available superoxide to react with and deplete NO thereby increasing NO concentration. This study characterized the effects of extracellular SOD (EC-SOD) on vasospasm comparing transgenic EC-SOD overexpressing mice to wild type (WT) counterparts. Methods: Mice underwent halothane anesthesia and endovascular perforation of the right proximal anterior cerebral artery (ACA) using a 5–0 monofilament. Sham mice underwent surgery but no vascular perforation. Temperature, blood gases, & blood pressure were maintained within normal ranges. Three days after recovery, brains were sectioned and Gomori’s trichromic stained. Vascular wall thickness was measured in triplicate sections from the proximal and distal segments of the ACA with the observer blinded to genotype. N=5 per group. Results: There was no difference in wall thickness between EC-SOD overexpressors and wild type shams in either ACA segment (Proximal: EC-SOD = 64±22μm, WT = 72±8μm, p=0.62; Distal: EC-SOD = 77±13μm, WT = 68±9μm, p=0.2). For both genotypes, SAH caused increased wall thickness which was greater in the EC-SOD vs. wild type SAH groups in the proximal (EC-SOD = 164±9μm, WT = 108±27μm, p=0.01) but not distal (EC-SOD =136±37μm, WT = 106±38μm, p=0.28) ACA segments. Conclusions: We were unable to demonstrate amelioration of vasospasm by the five-fold increase of brain EC-SOD known to occur in these mutants. In fact, in the proximal ACA, wall thickness was greater in the EC-SOD overexpressors subjected to SAH. Absence of a beneficial EC-SOD effect might be attributable to the post-SAH measurement interval when processes other than NO metabolism are likely to account for vasospasm. The reason for the pattern of an adverse effect of EC-SOD overexpression is unknown.
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Oñate, Angel A., Ramesh Vemulapalli, Edilia Andrews, Gerhardt G. Schurig, Stephen Boyle, and Hugo Folch. "Vaccination with Live Escherichia coli ExpressingBrucella abortus Cu/Zn Superoxide Dismutase Protects Mice against Virulent B. abortus." Infection and Immunity 67, no. 2 (February 1, 1999): 986–88. http://dx.doi.org/10.1128/iai.67.2.986-988.1999.
Повний текст джерелаАнотація:
ABSTRACT Vaccination of mice with Escherichia coli expressingBrucella Cu/Zn superoxide dismutase (SOD) [E. coli(pBSSOD)] induced a significant level of protection against virulent Brucella abortus challenge, although this level was not as high as the one reached with B. abortusvaccine strain RB51. In addition, vaccination with E. coli(pBSSOD) induced antibodies to Cu/Zn SOD and a strong proliferative response of splenocytes when stimulated in vitro with a thioredoxin-Cu/Zn SOD fusion protein.
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Mirochnitchenko, O., and M. Inouye. "Effect of overexpression of human Cu,Zn superoxide dismutase in transgenic mice on macrophage functions." Journal of Immunology 156, no. 4 (February 15, 1996): 1578–86. http://dx.doi.org/10.4049/jimmunol.156.4.1578.
Повний текст джерелаАнотація:
Abstract Properties of macrophages from transgenic mice with the human Cu,Zn superoxide dismutase (SOD) gene under the control of the mouse hydroxyl-methyl coenzyme A reductase (HMGCR) promoter were studied. In these mice, a twofold overproduction of Cu,Zn SOD in intraperitoneal macrophages resulted in the significant reduction of their microbicidal and fungicidal activity. Intracellular production and release of H2O2 in macrophages from transgenic mice activated by PMA was found to be significantly increased, whereas extracellular release of O2- was inhibited. When treated with LPS or LPS plus IFN-gamma, macrophages from transgenic mice were found to produce less nitric oxide (NO) than normal mice, suggesting that the nitrocompound metabolism in macrophages overproducing Cu,Zn SOD was also affected. Analysis of NF-kappa B DNA-binding activity and antiphosphotyrosine immunoblotting experiments suggest that impairment of macrophage functions may be attributed to the inhibition of signal transduction pathways as well as to changes in oxygen radical metabolism. The present data support the notion that antioxidant enzymes play important roles in the function of macrophages.
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Guo, Ling, Lei Xu, Tao Wu, Shulin Fu, Yinsheng Qiu, Chien-An Andy Hu, Xinglong Ren, Rongrong Liu, and Mengdie Ye. "Evaluation of recombinant protein superoxide dismutase of Haemophilus parasuis strain SH0165 as vaccine candidate in a mouse model." Canadian Journal of Microbiology 63, no. 4 (April 2017): 312–20. http://dx.doi.org/10.1139/cjm-2016-0671.
Повний текст джерелаАнотація:
Haemophilus parasuis can cause a severe membrane inflammation disorder. It has been documented that superoxide dismutase (SOD) is a potential target to treat systemic inflammatory diseases. Therefore, we constructed an experimental H. parasuis subunit vaccine SOD and determined the protective efficacy of SOD using a lethal dose challenge against H. parasuis serovar 4 strain MD0322 and serovar 5 strain SH0165 in a mouse model. The results demonstrated that SOD could induce a strong humoral immune response in mice and provide significant immunoprotection efficacy against a lethal dose of H. parasuis serovar 4 strain MD0322 or serovar 5 strain SH0165 challenge. IgG subtype analysis indicated SOD protein could trigger a bias toward a Th1-type immune response and induce the proliferation of splenocytes and secretion of IL-2 and IFN-γ of splenocytes. In addition, serum in mice from the SOD-immunized group could inhibit the growth of strain MD0322 and strain SH0165 in the whole-blood killing bacteria assay. This is the first report that immunization of mice with SOD protein could provide protective effect against a lethal dose of H. parasuis serovar 4 and serovar 5 challenge in mice, which may provide a novel approach against heterogeneous serovar infection of H. parasuis in future.
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Gonçalves, Álisson de Carvalho, Renata Campos Leão, Fábio Lera Orsatti, and Guilherme Vannucchi Portari. "Benfotiamine reduces oxidative damage in muscle of endurance-trained mouse." Acta Scientiarum. Health Sciences 41 (September 25, 2019): e46888. http://dx.doi.org/10.4025/actascihealthsci.v41i1.46888.
Повний текст джерелаАнотація:
High levels of reactive oxygen species can trigger an imbalance in redox status, which generates oxidative damage in macromolecules. The present study aimed to investigate the influence of oral supplementation with benfotiamine on oxidative stress and antioxidant activity in muscle of trained mice. Twenty-five male Balb/c mice were placed in groups. Sta-Sed: standard diet and sedentary (n = 6); Ben-Sed: benfotiamine supplemented and sedentary (n = 6); Sta-Tr: standard diet and trained (n = 6); and Ben-Tr: benfotiamine supplemented and trained (n = 7). Standard diet was AIN-93 growth and supplemented diet was AIN-93 with benfotiamine (500 mg kg-1). Trained mice were submitted to 6-weeks of endurance swimming training. The concentration of thiobarbituric acid reactive substances (TBARS), non-protein thiols, catalase (CAT) and superoxide dismutase activities (SOD) were analyzed in the gastrocnemius muscle. TBARS concentration was lower in the Ben-Tr group than in Ben-Sed and Sta-Tr groups. Thiol levels were higher in the Ben-Sed group than in the non-supplemented groups. CAT activity was more pronounced in both supplemented groups while SOD activity was higher in the Ben-Tr group than in the non-supplemented groups. The results show that benfotiamine supplementation is effective in enhancing antioxidant defenses and reducing oxidative damage in muscle of endurance-trained mouse.
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Liu, Bihui, Xingxing Feng, Jing Zhang, Yang Wei, and Xin Zhao. "Preventive Effect of Anji White Tea Flavonoids on Alcohol-Induced Gastric Injury through Their Antioxidant Effects in Kunming Mice." Biomolecules 9, no. 4 (April 4, 2019): 137. http://dx.doi.org/10.3390/biom9040137.
Повний текст джерелаАнотація:
Anji white tea (Camellia sinensis) is a traditional Chinese tea beverage, which is classified as green tea and contains an abundant amount of flavonoids. In this study, the preventive effect of Anji white tea flavonoids (AJWTFs) on ethanol/hydrochloric acid-induced gastric injury in mice was evaluated. The serum and gastric tissues of mice were analyzed using a biochemical kit and by quantitative polymerase chain reaction (qPCR). Observation of the appearance of the stomach indicated that AJWTFs could effectively reduce the area of gastric injury caused by ethanol/hydrochloric acid, and the inhibition rate of AJWTF on gastric injury increased with an increase in AJWTF concentration. The Anji white tea flavonoids could also reduce the volume and pH of gastric juice in mice with gastric injury. Biochemical results showed that AJWTFs could increase the superoxide dismutase (SOD) and glutathione (GSH) activities, as well as decrease the malondialdehyde (MDA) level, in the serum and liver of mice with gastric injury. Pathological observation confirmed that AJWTFs could inhibit the tissue damage caused by ethanol/hydrochloric acid in the stomach of mice. Further qPCR experiments also showed that AJWTFs could inhibit the decreases in neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), copper/zinc superoxide dismutase (Cu/Zn–SOD), manganese superoxide dismutase (Mn–SOD), catalase (CAT), and the increase in inducible nitric oxide synthase (iNOS) expression in the gastric tissue of mice caused by gastric injury. As observed, AJWTFs exerted a good preventive effect on alcohol-induced gastric injury in mice induced by ethanol/hydrochloric acid, and the effect is close to that of ranitidine. Anji white tea flavonoids present good antioxidant effect, which allows them to effectively prevent alcoholic gastric injury and be used as biologically active substances with a broad range of applications.
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Watanabe, Kenji, Shuichi Shibuya, Yusuke Ozawa, Toshihiko Toda, and Takahiko Shimizu. "Pathological Relationship between Intracellular Superoxide Metabolism and p53 Signaling in Mice." International Journal of Molecular Sciences 22, no. 7 (March 29, 2021): 3548. http://dx.doi.org/10.3390/ijms22073548.
Повний текст джерелаАнотація:
Intracellular superoxide dismutases (SODs) maintain tissue homeostasis via superoxide metabolism. We previously reported that intracellular reactive oxygen species (ROS), including superoxide accumulation caused by cytoplasmic SOD (SOD1) or mitochondrial SOD (SOD2) insufficiency, induced p53 activation in cells. SOD1 loss also induced several age-related pathological changes associated with increased oxidative molecules in mice. To evaluate the contribution of p53 activation for SOD1 knockout (KO) (Sod1−/−) mice, we generated SOD1 and p53 KO (double-knockout (DKO)) mice. DKO fibroblasts showed increased cell viability with decreased apoptosis compared with Sod1−/− fibroblasts. In vivo experiments revealed that p53 insufficiency was not a great contributor to aging-like tissue changes but accelerated tumorigenesis in Sod1−/− mice. Furthermore, p53 loss failed to improve dilated cardiomyopathy or the survival in heart-specific SOD2 conditional KO mice. These data indicated that p53 regulated ROS-mediated apoptotic cell death and tumorigenesis but not ROS-mediated tissue degeneration in SOD-deficient models.
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Liu, Tongji, Fang Tan, Xingyao Long, Yanni Pan, Jianfei Mu, Xianrong Zhou, Runkun Yi, and Xin Zhao. "Improvement Effect of Lotus Leaf Flavonoids on Carbon Tetrachloride-Induced Liver Injury in Mice." Biomedicines 8, no. 2 (February 24, 2020): 41. http://dx.doi.org/10.3390/biomedicines8020041.
Повний текст джерелаАнотація:
In this study, the effect of lotus leaf flavonoids (LLF) on carbon tetrachloride (CCl4)-induced liver injury in mice was studied. CCl4 was injected intraperitoneally to induce liver injury in Kunming mice. Mice were treated with LLF by gavage, and the mRNA expression levels in serum and liver were detected. Compared with the model group, LLF significantly reduced the liver index and serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), and total cholesterol (TC) levels in mice with CCl4-induced liver injury. Pathological observation showed that LLF effectively reduced morphological incompleteness and hepatocyte necrosis in CCl4-treated liver tissue. The result of quantitative polymerase chain reaction (qPCR) indicated that LLF significantly up-regulated the mRNA expression levels of copper/zinc superoxide dismutase (Cu/Zn-SOD), manganese superoxide dismutase (Mn-SOD), and catalase (CAT) and down- regulated the expression levels of tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB), and interleukin-1β (IL-1β) (p < 0.05). Thus, LLF is an active ingredient that ameliorates liver injury, and it has good application prospect.
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Robinson, Austin T., Ibra S. Fancher, Varadarajan Sudhahar, Jing Tan Bian, Marc D. Cook, Abeer M. Mahmoud, Mohamed M. Ali, et al. "Short-term regular aerobic exercise reduces oxidative stress produced by acute high intraluminal pressure in the adipose microvasculature." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 5 (May 1, 2017): H896—H906. http://dx.doi.org/10.1152/ajpheart.00684.2016.
Повний текст джерелаАнотація:
High blood pressure has been shown to elicit impaired dilation in the vasculature. The purpose of this investigation was to elucidate the mechanisms through which high pressure may elicit vascular dysfunction and determine the mechanisms through which regular aerobic exercise protects arteries against high pressure. Male C57BL/6J mice were subjected to 2 wk of voluntary running (~6 km/day) for comparison with sedentary controls. Hindlimb adipose resistance arteries were dissected from mice for measurements of flow-induced dilation (FID; with or without high intraluminal pressure exposure) or protein expression of NADPH oxidase II (NOX II) and superoxide dismutase (SOD). Microvascular endothelial cells were subjected to high physiological laminar shear stress (20 dyn/cm2) or static condition and treated with ANG II + pharmacological inhibitors. Cells were analyzed for the detection of ROS or collected for Western blot determination of NOX II and SOD. Resistance arteries from exercised mice demonstrated preserved FID after high pressure exposure, whereas FID was impaired in control mouse arteries. Inhibition of ANG II or NOX II restored impaired FID in control mouse arteries. High pressure increased superoxide levels in control mouse arteries but not in exercise mouse arteries, which exhibited greater ability to convert superoxide to H2O2. Arteries from exercised mice exhibited less NOX II protein expression, more SOD isoform expression, and less sensitivity to ANG II. Endothelial cells subjected to laminar shear stress exhibited less NOX II subunit expression. In conclusion, aerobic exercise prevents high pressure-induced vascular dysfunction through an improved redox environment in the adipose microvasculature. NEW & NOTEWORTHY We describe potential mechanisms contributing to aerobic exercise-conferred protection against high intravascular pressure. Subcutaneous adipose microvessels from exercise mice express less NADPH oxidase (NOX) II and more superoxide dismutase (SOD) and demonstrate less sensitivity to ANG II. In microvascular endothelial cells, shear stress reduced NOX II but did not influence SOD expression. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/exercise-averts-high-pressure-induced-vascular-dysfunction/ .