Journal articles: 'The oxidative model'

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Zhu, An, Fuli Zheng, Wenjing Zhang, Ludi Li, Yingzi Li, Hong Hu, Yajiao Wu, et al. "Oxidation and Antioxidation of Natural Products in the Model Organism Caenorhabditis elegans." Antioxidants 11, no. 4 (April 2, 2022): 705. http://dx.doi.org/10.3390/antiox11040705.

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Natural products are small molecules naturally produced by multiple sources such as plants, animals, fungi, bacteria and archaea. They exert both beneficial and detrimental effects by modulating biological targets and pathways involved in oxidative stress and antioxidant response. Natural products’ oxidative or antioxidative properties are usually investigated in preclinical experimental models, including virtual computing simulations, cell and tissue cultures, rodent and nonhuman primate animal models, and human studies. Due to the renewal of the concept of experimental animals, especially the popularization of alternative 3R methods for reduction, replacement and refinement, many assessment experiments have been carried out in new alternative models. The model organism Caenorhabditis elegans has been used for medical research since Sydney Brenner revealed its genetics in 1974 and has been introduced into pharmacology and toxicology in the past two decades. The data from C. elegans have been satisfactorily correlated with traditional experimental models. In this review, we summarize the advantages of C. elegans in assessing oxidative and antioxidative properties of natural products and introduce methods to construct an oxidative damage model in C. elegans. The biomarkers and signaling pathways involved in the oxidative stress of C. elegans are summarized, as well as the oxidation and antioxidation in target organs of the muscle, nervous, digestive and reproductive systems. This review provides an overview of the oxidative and antioxidative properties of natural products based on the model organism C. elegans.

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Kusuhara, S., M. Ito, T. Sato, W. Yokoi, Y. Yamamoto, K. Harada, H. Ikemura, and K. Miyazaki. "Intracellular GSH of Streptococcus thermophilus shows anti-oxidative activity against low-density lipoprotein oxidation in vitro and in a hyperlipidaemic hamster model." Beneficial Microbes 9, no. 1 (January 29, 2018): 143–52. http://dx.doi.org/10.3920/bm2017.0065.

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Streptococcus thermophilus YIT 2001 (ST-1), a lactic acid bacterial strain, was shown to have inhibitory effects on the oxidation of low-density lipoprotein (LDL) and the development of aortic fatty lesions in an animal model, and lower the serum levels of malondialdehyde-modified LDL, an oxidative modification product of LDL, in a clinical trial. This study aimed to identify the intracellular active component of ST-1 associated with anti-oxidative activity against LDL oxidation. High-performance liquid chromatography-electrospray ionisation mass spectrometry analysis after fractionation of the cellular extract by reversed-phase chromatography demonstrated that the active fraction contained reduced glutathione (GSH). GSH showed anti-oxidative activity in a dose-dependent manner, while this activity disappeared following thiol derivatisation. ST-1 had the strongest anti-oxidative activity against LDL oxidation and the highest level of intracellular GSH among five strains of S. thermophilus. In addition, the anti-oxidative activity of ST-1 after thiol derivatisation decreased by about half, which was similar to that of three other strains containing poor or no intracellular GSH or thiol components. Moreover, anti-oxidative activity against LDL oxidation was observed in hyperlipidaemic hamsters fed with high GSH ST-1 cells but not in those given low GSH cells. These findings suggest that intracellular GSH in ST-1 may provide beneficial effects via anti-oxidative activity against LDL oxidation and excess oxidative stress in the blood.

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Miricescu, Daniela, Iulia Stanescu, Paula Perlea, Bogdan Calenic, Radu Radulescu, Alexandra Totan, Bogdana Virgolici, Cristina Sabliov, and Maria Grea. "Oxidative Stress Following PLGA Nanoparticles Administration to an Animal Model." Materiale Plastice 54, no. 2 (June 30, 2017): 249–52. http://dx.doi.org/10.37358/mp.17.2.4826.

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In the recent years, engineered nanoparticles (NPs) such as PLGA or poly-lactic-co-glycolic acid, have raised a substantial interest due to their possible medical applications in vaccination, diagnostic imaging procedures, cancer therapy or sustained delivery of drugs. The main aim of the present work is to evaluate key oxidative stress parameters in several organs following NPs administration in an animal model. Our data shows that acute oral administration of PLGA NPs induces a change in the antioxidant status in both rat liver and spleen, but may not induce oxidative stress damage to cell structures such as lipid or protein oxidation.

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Muraya, Nanako, Daisuke Kadowaki, Shigeyuki Miyamura, Kenichiro Kitamura, Kohei Uchimura, Yuki Narita, Yohei Miyamoto, et al. "Benzbromarone Attenuates Oxidative Stress in Angiotensin II- and Salt-Induced Hypertensive Model Rats." Oxidative Medicine and Cellular Longevity 2018 (June 5, 2018): 1–8. http://dx.doi.org/10.1155/2018/7635274.

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Oxidative stress induced by hyperuricemia is closely associated with the renin-angiotensin system, as well as the onset and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). It is therefore important to reduce oxidative stress to treat hyperuricemia. We previously found that benzbromarone, a uricosuric agent, has a direct free radical scavenging effect in vitro. The antioxidant effects of benzbromarone were evaluated in vivo via oral administration of benzbromarone for 4 weeks to model rats with angiotensin II- and salt-induced hypertension. Benzbromarone did not alter plasma uric acid levels or blood pressure but significantly reduced the levels of advanced oxidation protein products, which are oxidative stress markers. Furthermore, dihydroethidium staining of the kidney revealed a reduction in oxidative stress after benzbromarone administration. These results suggest that benzbromarone has a direct antioxidant effect in vivo and great potential to prevent CVD and CKD.

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Zeynalov, Eldar, Joerg Friedrich, Manfred Wagner, and Gundula Hidde. "Effect of Br-Grafted Multi-Walled Carbon Nanotubes on the Model Oxidative Environment." Chemistry & Chemical Technology 9, no. 1 (March 15, 2015): 51–54. http://dx.doi.org/10.23939/chcht09.01.051.

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Chiu, Harold Henrison C., Susan D. Arco, Zhang Chun Ping, and Nelson R. Villarante. "Efficient Oxidative Desulfurization of Model Oil at Room Temperature with Ionic Liquid as Extraction Solvent." KIMIKA 24, no. 1 (January 21, 2013): 2–7. http://dx.doi.org/10.26534/kimika.v24i1.2-7.

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The oxidative desulfurization of model oil (hexane solution of thiophene) was carried out at room temperature in a two-step method involving: 1) the acetic acid catalyzed oxidation of thiophene with hydrogen peroxide and 2) the subsequent extraction of the oxidized products with three 1-alkyl-3-methylimidazolium bromide [RMIM]Br ionic liquids of varying alkyl substituent R chain length (R: C2, C4, C6) and with acetonitrile as control. For purposes of comparison, a non-oxidative extractive desulfurization of model oil with the above ionic liquid and with acetonitrile was also performed. The thiophene extraction efficiencies of the ionic liquids and that of the control in both the oxidative and non-oxidative procedures were determined by means of gas chromatography. The ionic liquid of the shortest alkyl substituent chain length (R: C2), [EMIM] Br exhibited the highest extraction efficiency in the oxidative desulfurization of the model oil; the extraction efficiency of [EMIM] Br was also observed to exceed that of acetonitrile. In general, the oxidative desulfurization with the above [RMIM]Br’s is apparently a more efficient method of thiophene removal from the model oil as compared to a non-oxidative procedure with the same extraction solvents. The extraction efficiency of [RMIM]Br’s was observed to decrease with the lengthening of the alkyl substituent chain. The same trend is observed in the non-oxidative extractive desulfurization of the model oil. Recyclability analysis of [EMIM]Br showed that [EMIM]Br can be recycled thrice with no significant decrease in extraction efficiency.

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Chimienti, Guglielmina, Antonella Orlando, Francesco Russo, Benedetta D’Attoma, Manuela Aragno, Eleonora Aimaretti, Angela Maria Serena Lezza, and Vito Pesce. "The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease." Genes 12, no. 9 (September 18, 2021): 1439. http://dx.doi.org/10.3390/genes12091439.

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Nonalcoholic fatty liver disease (NAFLD) is the leading liver chronic disease featuring hepatic steatosis. Mitochondrial β-oxidation participates in the derangement of lipid metabolism at the basis of NAFLD, and mitochondrial oxidative stress contributes to the onset of the disease. We evaluated the presence and effects of mitochondrial oxidative stress in the liver from rats fed a high-fat plus fructose (HF-F) diet inducing NAFLD. Supplementation with dehydroepiandrosterone (DHEA), a multitarget antioxidant, was tested for efficacy in delaying NAFLD. A marked mitochondrial oxidative stress was originated by all diets, as demonstrated by the decrease in Superoxide Dismutase 2 (SOD2) and Peroxiredoxin III (PrxIII) amounts. All diets induced a decrease in mitochondrial DNA content and an increase in its oxidative damage. The diets negatively affected mitochondrial biogenesis as shown by decreased peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α), mitochondrial transcription factor A (TFAM), and the COX-IV subunit from the cytochrome c oxidase complex. The reduced amounts of Beclin-1 and lipidated LC3 II form of the microtubule-associated protein 1 light chain 3 (LC3) unveiled the diet-related autophagy’s decrease. The DHEA supplementation did not prevent the diet-induced changes. These results demonstrate the relevance of mitochondrial oxidative stress and the sequential dysfunction of the organelles in an obesogenic diet animal model of NAFLD.

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Qin, Bei, Kuan Yang, and Ruijun Cao. "Synthesis and Antioxidative Activity of Piperine Derivatives Containing Phenolic Hydroxyl." Journal of Chemistry 2020 (July 21, 2020): 1–9. http://dx.doi.org/10.1155/2020/2786359.

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Piperine was used in this study in its raw form, and different steps, such as amide hydrolysis and amidation, were used to synthesize piperine derivatives containing a phenolic hydroxyl group. DPPH and ABTS free radical scavenging assays were used to assess piperine derivative antioxidant activities. We constructed an AAPH oxidative stress erythrocyte model to study the effect of piperine derivatives on the hemolysis rate of oxidatively damaged erythrocytes as well as the hemoglobin oxidation rate. This AAPH model was also used to determine piperine derivative effects on antioxidant enzyme activity and malondialdehyde (MDA) content. Results showed that spectroscopic methods could synthesize and identify piperine derivatives containing phenolic hydroxyl groups (H-1∼H-3). Moreover, DPPH and ABTS assay results showed that piperine derivative free radical clearance rates were higher compared with the parent compound. Additionally, piperine derivatives (H-1∼H-3) were found to provide protection to AAPH oxidatively damaged erythrocytes in their ability to inhibit AAPH-induced erythrocyte lysis, while hemoglobin oxidation was higher compared with the parent compound. Piperine derivatives may protect intracellular glutathione peroxidase (GSH-Px) antioxidant enzyme system activities, safeguarding against oxidative damage. This study synthesized novel piperine derivatives for use as potential antioxidant agent candidates.

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Timoshnikov, Viktor A., Lilia A. Kichigina, Olga Yu Selyutina, Nikolay E. Polyakov, and George J. Kontoghiorghes. "Antioxidant Activity of Deferasirox and Its Metal Complexes in Model Systems of Oxidative Damage: Comparison with Deferiprone." Molecules 26, no. 16 (August 20, 2021): 5064. http://dx.doi.org/10.3390/molecules26165064.

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Deferasirox is an orally active, lipophilic iron chelating drug used on thousands of patients worldwide for the treatment of transfusional iron overload. The essential transition metals iron and copper are the primary catalysts of reactive oxygen species and oxidative damage in biological systems. The redox effects of deferasirox and its metal complexes with iron, copper and other metals are of pharmacological, toxicological, biological and physiological importance. Several molecular model systems of oxidative damage caused by iron and copper catalysis including the oxidation of ascorbic acid, the peroxidation of linoleic acid micelles and the oxidation of dihydropyridine have been investigated in the presence of deferasirox using UV-visible and NMR spectroscopy. Deferasirox has shown antioxidant activity in all three model systems, causing substantial reduction in the rate of oxidation and oxidative damage. Deferasirox showed the greatest antioxidant activity in the oxidation of ascorbic acid with the participation of iron ions and reduced the reaction rate by about a 100 times. Overall, deferasirox appears to have lower affinity for copper in comparison to iron. Comparative studies of the antioxidant activity of deferasirox and the hydrophilic oral iron chelating drug deferiprone in the peroxidation of linoleic acid micelles showed lower efficiency of deferasirox in comparison to deferiprone.

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Wongnen, Chantira, Naiya Ruzzama, Manat Chaijan, Ling-Zhi Cheong, and Worawan Panpipat. "Glochidion wallichianum Leaf Extract as a Natural Antioxidant in Sausage Model System." Foods 11, no. 11 (May 25, 2022): 1547. http://dx.doi.org/10.3390/foods11111547.

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This study highlighted the role of an 80% ethanolic Mon-Pu (Glochidion wallichianum) leaf extract (MPE), a novel natural antioxidative ingredient, in controlling the oxidative stability and physicochemical properties of a cooked sausage model system (SMS). MPE had a total extractable phenolic content of 16 mg/100 g, with DPPH● scavenging activity, ABTS●+ scavenging activity, and ferric reducing antioxidant power of 2.3, 1.9, and 1.2 mmole Trolox equivalents (TE)/g, respectively. The effects of different concentrations of MPE (0.01–10%, w/w) formulated into SMS on lipid oxidation, protein oxidation, and discoloration were compared to synthetic butylated hydroxyl toluene (BHT; 0.003%, w/w) and a control (without antioxidant). The peroxide value (PV), thiobarbituric acid reactive substances (TBARS), and protein carbonyl contents of SMS tended to increase with increasing MPE concentration (p < 0.05), indicating that high MPE excipient has a pro-oxidative effect. The lowest lipid oxidation (PV and TBARS) and protein carbonyl contents were observed when 0.01% MPE was used to treat SMS (p < 0.05), which was comparable or even greater than BHT-treated SMS. High concentrations (1–10%) of MPE incorporation led to increases in the discoloration of SMS (p < 0.05) with a negligible change in pH of SMS. The water exudate was reduced when MPE was incorporated into SMS compared to control (p < 0.05). Furthermore, MPE at 0.01% significantly reduced lipid oxidation in cooked EMS during refrigerated storage. According to the findings, a low amount of MPE, particularly at 0.01%, in a formulation could potentially maintain the oxidative stability and physicochemical qualities of cooked SMS that are comparable to or better than synthetic BHT.

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Pochiraju, K. V., and G. P. Tandon. "Modeling Thermo-Oxidative Layer Growth in High-Temperature Resins." Journal of Engineering Materials and Technology 128, no. 1 (August 1, 2005): 107–16. http://dx.doi.org/10.1115/1.2128427.

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This paper describes modeling of degradation behavior of high-temperature polymers under thermo-oxidative aging conditions. Thermo-oxidative aging is simulated with a diffusion-reaction model in which temperature, oxygen concentration, and weight-loss effects are considered. A parametric reaction model based on a mechanistic view of the reaction is used for simulating reaction-rate dependence on the oxygen availability in the polymer. Macroscopic weight-loss measurements are used to determine the reaction and polymer consumption parameters. The diffusion-reaction partial differential equation system is solved using Runge-Kutta methods. Simulations illustrating oxidative layer growth in a high-temperature PMR-15 polyimide resin system under isothermal conditions are presented and correlated with experimental observations of oxidation layer growth. Finally, parametric studies are conducted to examine the sensitivity of material parameters in predicting oxidation development.

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Singh, Abhishek Kumar, Sandeep Singh, Geetika Garg, and Syed Ibrahim Rizvi. "Rapamycin alleviates oxidative stress-induced damage in rat erythrocytes." Biochemistry and Cell Biology 94, no. 5 (October 2016): 471–79. http://dx.doi.org/10.1139/bcb-2016-0048.

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An imbalanced cellular redox system promotes the production of reactive oxygen species (ROS) that may lead to oxidative stress-mediated cell death. Erythrocytes are the best-studied model of antioxidant defense mechanism. The present study was undertaken to investigate the effect of the immunosuppressant drug rapamycin, an inducer of autophagy, on redox balance of erythrocytes and blood plasma of oxidatively challenged rats. Male Wistar rats were oxidatively challenged with HgCl2 (5 mg/kg body mass (b.m.)). A significant (p < 0.05) induction in ROS production, plasma membrane redox system (PMRS), intracellular Ca2+ influx, lipid peroxidation (LPO), osmotic fragility, plasma protein carbonyl (PCO) content, and plasma advanced oxidation protein products (AOPP) and simultaneously significant reduction in glutathione (GSH) level and ferric reducing ability of plasma (FRAP) were observed in rats exposed to HgCl2. Furthermore, rapamycin (0.5 mg/kg b.m.) provided significant protection against HgCl2-induced alterations in rat erythrocytes and plasma by reducing ROS production, PMRS activity, intracellular Ca2+ influx, LPO, osmotic fragility, PCO content, and AOPP and also restored the level of antioxidant GSH and FRAP. Our observations provide evidence that rapamycin improves redox status and attenuates oxidative stress in oxidatively challenged rats. Our data also demonstrate that rapamycin is a comparatively safe immunosuppressant drug.

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Dong, Wen Li, Xue Gong, Jing Dong, Ling Jin, and Yu Xiang Wei. "Oxidation Kinetics of Hazelnut Shelf-Life Prediction Model." Applied Mechanics and Materials 200 (October 2012): 466–69. http://dx.doi.org/10.4028/www.scientific.net/amm.200.466.

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The changing patterns of filbert peroxide value through the determination of different storage temperature conditions,research the dynamics characteristics of oxidative rancidity of filbert. By regression analysis base on the storage time and the logarithm of peroxide value,it concluded the grease oxidation reaction first-order kinetic equation of filbert.Using Arrhenius equation and Q10 model for 5 ~ 35 °C temperature within the shelf life of any temperature prediction model.

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Talal Nawaf, Amer. "Optimal Kinetic Parameters of Trickle bed Reactor for Oxidation of 2-Proplymercaptan in Naphtha." DJES 12, no. 2 (June 1, 2019): 83–100. http://dx.doi.org/10.24237/djes.2019.12209.

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The best kinetic of the reaction are estimated based on experimental data obtained from the literature using parameter estimation technique. The best mathematical model for oxidative 2-proplymercaption via oxygen is taking into account the apparent intrinsic kinetics considering internal diffusion and TBR hydrodynamic effect on the reaction process mainly , catalyst wetting efficiency, catalyst effectiveness factor, Thiele model and the effective diffusivity. The optimal operating condition for oxidative process is carried out utilizing. The optimization technique based upon the minimization of the sum squared error between experimental and predicted composition of naphtha oxidative process to determine the best parameters of kinetics models. The predicted product compositions for oxidation process found to be a good agreement with the experimental data for wide range of operating conditions (2.5-10 hr-1, 75-300 ppm and 293-353K) with minimum error 5% among all results

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Zizola, Cynthia, Peter J. Kennel, Hirokazu Akashi, Ruiping Ji, Estibaliz Castillero, Isaac George, Shunichi Homma, and P. Christian Schulze. "Activation of PPARδ signaling improves skeletal muscle oxidative metabolism and endurance function in an animal model of ischemic left ventricular dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 308, no. 9 (May 1, 2015): H1078—H1085. http://dx.doi.org/10.1152/ajpheart.00679.2014.

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Exercise intolerance in heart failure has been linked to impaired skeletal muscle oxidative capacity. Oxidative metabolism and exercise capacity are regulated by PPARδ signaling. We hypothesized that PPARδ stimulation reverts skeletal muscle oxidative dysfunction. Myocardial infarction (MI) was induced in C57BL/6 mice and the development of ventricular dysfunction was monitored over 8 wk. Mice were randomized to the PPARδ agonist GW501516 (5 mg/kg body wt per day for 4 wk) or placebo 8 wk post-MI. Muscle function was assessed through running tests and grip strength measurements. In muscle, we analyzed muscle fiber cross-sectional area and fiber types, metabolic gene expression, fatty acid (FA) oxidation and ATP content. Signaling pathways were studied in C2C12 myotubes. FA oxidation and ATP levels decreased in muscle from MI mice compared with sham- operated mice. GW501516 administration increased oleic acid oxidation levels in skeletal muscle of the treated MI group compared with placebo treatment. This was accompanied by transcriptional changes including increased CPT1 expression. Further, the PPARδ-agonist improved running endurance compared with placebo. Cell culture experiments revealed protective effects of GW501516 against the cytokine-induced decrease of FA oxidation and changes in metabolic gene expression. Skeletal muscle dysfunction in HF is associated with impaired PPARδ signaling and treatment with the PPARδ agonist GW501516 corrects oxidative capacity and FA metabolism and improves exercise capacity in mice with LV dysfunction. Pharmacological activation of PPARδ signaling could be an attractive therapeutic intervention to counteract the progressive skeletal muscle dysfunction in HF.

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Kobiela, Jarek, Jacek Krajewski, Beata Kalińska-Błach, and Tomasz Stefaniak. "Selectivity of oxidative stress targeting in estrogen-induced experimental nephrocarcinogenesis." Acta Biochimica Polonica 49, no. 1 (March 31, 2002): 51–58. http://dx.doi.org/10.18388/abp.2002_3820.

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Specificity of targeting of the oxidative stress towards lipid and protein fractions in a model of estrogen-induced Syrian hamster nephrocarcinogenesis was evaluated. The amount of proteins modified by oxidative stress was significantly elevated as early as one month after the initial implantation of estradiol to the experimental versus the control group, while the stress did not affect lipids. Subcellular localization of the oxidative stress target was determined by the analysis of protein oxidation in subcellular fractions of kidney cells. The endoplasmic reticulum membranes were the fraction most affected by the oxidative stress.

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Staňková, Pavla, Otto Kučera, Eva Peterová, Halka Lotková, Tumisang Edward Maseko, Kateřina Nožičková, and Zuzana Červinková. "Adaptation of Mitochondrial Substrate Flux in a Mouse Model of Nonalcoholic Fatty Liver Disease." International Journal of Molecular Sciences 21, no. 3 (February 7, 2020): 1101. http://dx.doi.org/10.3390/ijms21031101.

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Maladaptation of mitochondrial oxidative flux seems to be a considerable feature of nonalcoholic fatty liver disease (NAFLD). The aim of this work was to induce NAFLD in mice fed a Western-style diet (WD) and to evaluate liver mitochondrial functions. Experiments were performed on male C57BL/6J mice fed with a control diet or a WD for 24 weeks. Histological changes in liver and adipose tissue as well as hepatic expression of fibrotic and inflammatory genes and proteins were evaluated. The mitochondrial respiration was assessed by high-resolution respirometry. Oxidative stress was evaluated by measuring lipoperoxidation, glutathione, and reactive oxygen species level. Feeding mice a WD induced adipose tissue inflammation and massive liver steatosis accompanied by mild inflammation and fibrosis. We found decreased succinate-activated mitochondrial respiration and decreased succinate dehydrogenase (SDH) activity in the mice fed a WD. The oxidative flux with other substrates was not affected. We observed increased ketogenic capacity, but no impact on the capacity for fatty acid oxidation. We did not confirm the presence of oxidative stress. Mitochondria in this stage of the disease are adapted to increased substrate flux. However, inhibition of SDH can lead to the accumulation of succinate, an important signaling molecule associated with inflammation, fibrosis, and carcinogenesis.

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Stocker, Roland, and John F. Keaney. "Role of Oxidative Modifications in Atherosclerosis." Physiological Reviews 84, no. 4 (October 2004): 1381–478. http://dx.doi.org/10.1152/physrev.00047.2003.

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This review focuses on the role of oxidative processes in atherosclerosis and its resultant cardiovascular events. There is now a consensus that atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein oxidation in the vascular wall. The oxidative modification hypothesis of atherosclerosis predicts that low-density lipoprotein (LDL) oxidation is an early event in atherosclerosis and that oxidized LDL contributes to atherogenesis. In support of this hypothesis, oxidized LDL can support foam cell formation in vitro, the lipid in human lesions is substantially oxidized, there is evidence for the presence of oxidized LDL in vivo, oxidized LDL has a number of potentially proatherogenic activities, and several structurally unrelated antioxidants inhibit atherosclerosis in animals. An emerging consensus also underscores the importance in vascular disease of oxidative events in addition to LDL oxidation. These include the production of reactive oxygen and nitrogen species by vascular cells, as well as oxidative modifications contributing to important clinical manifestations of coronary artery disease such as endothelial dysfunction and plaque disruption. Despite these abundant data however, fundamental problems remain with implicating oxidative modification as a (requisite) pathophysiologically important cause for atherosclerosis. These include the poor performance of antioxidant strategies in limiting either atherosclerosis or cardiovascular events from atherosclerosis, and observations in animals that suggest dissociation between atherosclerosis and lipoprotein oxidation. Indeed, it remains to be established that oxidative events are a cause rather than an injurious response to atherogenesis. In this context, inflammation needs to be considered as a primary process of atherosclerosis, and oxidative stress as a secondary event. To address this issue, we have proposed an “oxidative response to inflammation” model as a means of reconciling the response-to-injury and oxidative modification hypotheses of atherosclerosis.

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Faber, Samantha C., Nicole A. McNabb, Pablo Ariel, Emily R. Aungst, and Shaun D. McCullough. "Exposure Effects Beyond the Epithelial Barrier: Transepithelial Induction of Oxidative Stress by Diesel Exhaust Particulates in Lung Fibroblasts in an Organotypic Human Airway Model." Toxicological Sciences 177, no. 1 (June 11, 2020): 140–55. http://dx.doi.org/10.1093/toxsci/kfaa085.

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Abstract In vitro bronchial epithelial monoculture models have been pivotal in defining the adverse effects of inhaled toxicant exposures; however, they are only representative of one cellular compartment and may not accurately reflect the effects of exposures on other cell types. Lung fibroblasts exist immediately beneath the bronchial epithelial barrier and play a central role in lung structure and function, as well as disease development and progression. We tested the hypothesis that in vitro exposure of a human bronchial epithelial cell barrier to the model oxidant diesel exhaust particulates caused transepithelial oxidative stress in the underlying lung fibroblasts using a human bronchial epithelial cell and lung fibroblast coculture model. We observed that diesel exhaust particulates caused transepithelial oxidative stress in underlying lung fibroblasts as indicated by intracellular accumulation of the reactive oxygen species hydrogen peroxide, oxidation of the cellular antioxidant glutathione, activation of NRF2, and induction of oxidative stress-responsive genes. Further, targeted antioxidant treatment of lung fibroblasts partially mitigated the oxidative stress response gene expression in adjacent human bronchial epithelial cells during diesel exhaust particulate exposure. This indicates that exposure-induced oxidative stress in the airway extends beyond the bronchial epithelial barrier and that lung fibroblasts are both a target and a mediator of the adverse effects of inhaled chemical exposures despite being separated from the inhaled material by an epithelial barrier. These findings illustrate the value of coculture models and suggest that transepithelial exposure effects should be considered in inhalation toxicology research and testing.

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Cavarra, Eleonora, Monica Lucattelli, Federica Gambelli, Barbara Bartalesi, Silvia Fineschi, Andras Szarka, Fabiola Giannerini, Piero A. Martorana, and Giuseppe Lungarella. "Human SLPI inactivation after cigarette smoke exposure in a new in vivo model of pulmonary oxidative stress." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 2 (August 1, 2001): L412—L417. http://dx.doi.org/10.1152/ajplung.2001.281.2.l412.

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The role of oxidative stress in inactivating antiproteases is the object of debate. To address this question, we developed an in vivo model of pulmonary oxidative stress induced by cigarette smoke (CS) in mice. The major mouse trypsin inhibitor contrapsin is not sensitive to oxidation, and the mouse secretory leukoprotease inhibitor (SLPI) does not inhibit trypsin. Instead, human recombinant (hr) SLPI inhibits trypsin and is sensitive to oxidation. Thus we determined the effect of CS in vivo on hrSLPI antiproteolytic function in the airways of mice. CS caused a significant decrease in total antioxidant capacity in bronchoalveolar lavage fluid (BALF) and significant changes in oxidized glutathione, ascorbic acid, protein thiols, and 8-epi-PGF2α. Intratracheal hrSLPI significantly increased BALF antitryptic activity. CS induced a 50% drop in the inhibitory activity of hrSLPI. Pretreatment with N-acetylcysteine prevented the CS-induced loss of hrSLPI activity, the decrease in antioxidant defenses, and the elevation of 8-epi-PGF-2α. Thus an inactivation of hrSLPI was demonstrated in this model. This is a novel model for studying in vivo the effects of CS oxidative stress on human protease inhibitors with antitrypsin activity.

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Il'yasova, Dora, Ivan Spasojevic, Frances Wang, Adviye A. Tolun, Karel Base, Sarah P. Young, P. Kelly Marcom, et al. "Urinary Biomarkers of Oxidative Status in a Clinical Model of Oxidative Assault." Cancer Epidemiology Biomarkers & Prevention 19, no. 6 (May 25, 2010): 1506–10. http://dx.doi.org/10.1158/1055-9965.epi-10-0211.

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Claros, Silvia, Antonio Gil, Mauro Martinelli, Nadia Valverde, Estrella Lara, Federica Boraldi, Jose Pavia, Elisa Martín-Montañez, and María Garcia-Fernandez. "Impact of Glucocorticoid on a Cellular Model of Parkinson’s Disease: Oxidative Stress and Mitochondrial Function." Brain Sciences 11, no. 8 (August 22, 2021): 1106. http://dx.doi.org/10.3390/brainsci11081106.

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Stress seems to contribute to the neuropathology of Parkinson’s disease (PD), possibly by dysregulation of the hypothalamic–pituitary–adrenal axis. Oxidative distress and mitochondrial dysfunction are key factors involved in the pathophysiology of PD and neuronal glucocorticoid-induced toxicity. Animal PD models have been generated to study the effects of hormonal stress, but no in vitro model has yet been developed. Our aim was to examine the impact of corticosterone (CORT) administration on a dopaminergic neuronal cell model of PD induced by the neurotoxin MPP+, as a new combined PD model based on the marker of endocrine response to stress, CORT, and oxidative-mitochondrial damage. We determined the impact of CORT, MPP+ and their co-incubation on reactive oxygen species production (O2−•), oxidative stress cellular markers (advanced-oxidation protein products and total antioxidant status), mitochondrial function (mitochondrial membrane potential and mitochondrial oxygen consumption rate) and neurodegeneration (Fluoro-Jade staining). Accordingly, the administration of MPP+ or CORT individually led to cell damage compared to controls (p < 0.05), as determined by several methods, whereas their co-incubation produced strong cell damage (p < 0.05). The combined model described here could be appropriate for investigating neuropathological hallmarks and for evaluating potential new therapeutic tools for PD patients suffering mild to moderate emotional stress.

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Tian, Yajie, Yue Yao, Yanhui Zhi, Lijun Yan, and Shuxiang Lu. "Combined Extraction–Oxidation System for Oxidative Desulfurization (ODS) of a Model Fuel." Energy & Fuels 29, no. 2 (January 26, 2015): 618–25. http://dx.doi.org/10.1021/ef502396b.

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Huh, Jung-Do, and Raymond E. Robertson. "Modeling of Oxidative Aging Behavior of Asphalts from Short-Term, High-Temperature Data as a Step toward Prediction of Pavement Aging." Transportation Research Record: Journal of the Transportation Research Board 1535, no. 1 (January 1996): 91–97. http://dx.doi.org/10.1177/0361198196153500112.

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The oxidative aging data collected during the Strategic Highway Research Program have been analyzed in terms of kinetics of viscosity change with time and temperature. Changes in viscosity have been used as the measure of the progress of aging. The objective is to model viscosity increases accurately enough to be able to predict aging (in terms of viscosity changes) at pavement temperatures from short-term test data acquired at high temperature. This involved constituting a mathematical model, based on oxidative reactions, and a nonlinear regression of the data to test predictability of the proposed model. Clearly, there is a point beyond which viscosity change becomes independent of time, but no data were collected to that extent. Separately, it has been shown that oxidation of aliphatic sulfide to sulfoxide and oxidation of benzylic carbon to carbonyl are the principal chemical reactions that contribute to an increase in viscosity. The data fit the proposed equation sufficiently well to allow calculation of rate constants of viscosity increases for both reactions, and, hence, allow development of an Arrhenius temperature relationship. Finally, it is hoped that the proposed equation will provide reasonable estimates of rates of oxidative aging of asphalts at pavement temperatures from short-term, high-temperature oxidative aging data measured in a laboratory.

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Mokhnache, Kamel, Ahlem Karbab, Soraya Madoui, Hanane Khither, El-Khamsa Soltani, and Noureddine Charef. "Evaluation of isoniazid-oxidative reactions in mice model." Journal of Drug Delivery and Therapeutics 9, no. 6 (November 15, 2019): 36–37. http://dx.doi.org/10.22270/jddt.v9i6.3654.

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In this study the anti-tubercular drug; isoniazid (INH) was investigated for their adverse effect; the oxidative stress. This effect was evaluated by using mice model, at the dose of 151 mg/kg. We found that oxidative stress induced by INH is associated with lipid peroxidation expressed by the increase in the level of MDA from 76.9 ± 1.74 to 79.61 ± 2.67 nmol/g tissue. The oxidative stress of INH is accompanied by a decrease in reduced GSH level (from 79.9 ± 12 μmol / mg to 68.48 ± 4.28 μmol / mg compared to of the control group). After treatment with INH at 151 mg/kg, a decrease in CAT activities occurred compared to control (2.53 ± 0.39 U/mg Pr vs 5.07 ± 0.73 U/mg Pr). Keywords: isoniazid, oxidative stress, MDA, GSH, CAT

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26

Aliyev, A. M., Z. A. Shabanova, M. K. Aliyeva, and G. A. Alizadeh. "THE KINETIC MODEL OF THE REACTION OF OXIDATIVE DEHYDROGENATION OF CYCLOHEXANOL OVER MODIFIED ZEOLITE CATALYST." Chemical Problems 15, no. 3 (2017): 341–45. http://dx.doi.org/10.32737/2221-8688-2017-3-341-345.

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de la Torre-Ruiz, Maria, Nuria Pujol, and Venkatraghavan Sundaran. "Coping With Oxidative Stress. The Yeast Model." Current Drug Targets 16, no. 1 (January 19, 2015): 2–12. http://dx.doi.org/10.2174/1389450115666141020160105.

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Ercal, Nuran, Nukhet Aykin-Burns, Hande Gurer-Orhan, and J. David McDonald. "Oxidative stress in a phenylketonuria animal model." Free Radical Biology and Medicine 32, no. 9 (May 2002): 906–11. http://dx.doi.org/10.1016/s0891-5849(02)00781-5.

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Korzeniewski, Bernard, and Wojciech Froncisz. "An extended dynamic model of oxidative phosphorylation." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1060, no. 2 (October 1991): 210–23. http://dx.doi.org/10.1016/s0005-2728(09)91009-x.

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McDaniel, Candace F. "Diabetes: A model of oxidative accelerated aging." AGE 22, no. 4 (October 1999): 145–48. http://dx.doi.org/10.1007/s11357-999-0016-1.

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Bistolfi, M., G. Fornasari, M. Molinari, S. Palmery, M. Dente, and E. Ranzi. "Kinetic model for methane oxidative coupling reactors." Chemical Engineering Science 47, no. 9-11 (June 1992): 2647–52. http://dx.doi.org/10.1016/0009-2509(92)87107-2.

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32

Coballase-Urrutia, E., L. Navarro, J. L. Ortiz, L. Verdugo-Díaz, J. M. Gallardo, Maria Eugenia Hernández, and F. Estrada-Rojo. "Static Magnetic Fields Modulate the Response of Different Oxidative Stress Markers in a Restraint Stress Model Animal." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/3960408.

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Stress is a state of vulnerable homeostasis that alters the physiological and behavioral responses. Stress induces oxidative damage in several organs including the brain, liver, kidney, stomach, and heart. Preliminary findings suggested that the magnetic stimulation could accelerate the healing processes and has been an effective complementary therapy in different pathologies. However, the mechanism of action of static magnetic fields (SMFs) is not well understood. In this study, we demonstrated the effects of static magnetic fields (0.8 mT) in a restraint stressed animal model, focusing on changes in different markers of oxidative damage. A significant increase in the plasma levels of nitric oxide (NO), malondialdehyde (MDA), and advanced oxidation protein products (AOPP), and a decrease in superoxide dismutase (SOD), glutathione (GSH), and glycation end products (AGEs) were observed in restraint stress model. Exposure to SMFs over 5 days (30, 60, and 240 min/day) caused a decrease in the NO, MDA, AGEs, and AOPP levels; in contrast, the SOD and GSH levels increased. The response to SMFs was time-dependent. Thus, we proposed that exposure to weak-intensity SMFs could offer a complementary therapy by attenuating oxidative stress. Our results provided a new perspective in health studies, particularly in the context of oxidative stress.

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Petersen, J. Claine, and P. Michael Harnsberger. "Asphalt Aging: Dual Oxidation Mechanism and Its Interrelationships with Asphalt Composition and Oxidative Age Hardening." Transportation Research Record: Journal of the Transportation Research Board 1638, no. 1 (January 1998): 47–55. http://dx.doi.org/10.3141/1638-06.

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The kinetic data and chemistry of asphalt oxidative age hardening suggested a sequential, dual mechanism for asphalt oxidation. The dual mechanism rationalizes conflicts between earlier mechanistic investigations and explains the hyperbolic-like, time-versus-property plots characteristic of asphalt oxidative aging. The oxidation kinetics provide further confirmation of the asphalt microstructural model. It is proposed that the rapid initial oxidation rate of asphalt results from reaction of oxygen with limited amounts of highly reactive hydrocarbons. Final oxidation products of this initial reaction are sulfoxides and, most likely, ring aromatization. During this initial reaction, a slower oxidation reaction of asphalt benzylic carbons is initiated; final products are ketones and sulfoxides. The ratio of ketones to sulfoxides formed and the rate of age hardening were found to be dependent on temperature and oxygen pressure. Low-temperature oxidative aging, as occurs in pavements, was found significantly more sensitive to variations in temperature and asphalt composition than 100°C pressure vessel aging.

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Silva, Maísa, Joyce Ferreira da Costa Guerra, Ana Flávia Santos Sampaio, Wanderson Geraldo de Lima, Marcelo Eustáquio Silva, and Maria Lucia Pedrosa. "Iron Dextran Increases Hepatic Oxidative Stress and Alters Expression of Genes Related to Lipid Metabolism Contributing to Hyperlipidaemia in Murine Model." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/272617.

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The objective of this study was to investigate the effects of iron dextran on lipid metabolism and to determine the involvement of oxidative stress. Fischer rats were divided into two groups: the standard group (S), which was fed the AIN-93M diet, and the standard plus iron group (SI), which was fed the same diet but also received iron dextran injections. Serum cholesterol and triacylglycerol levels were higher in the SI group than in the S group. Iron dextran was associated with decreased mRNA levels ofpparα, and its downstream genecpt1a, which is involved in lipid oxidation. Iron dextran also increased mRNA levels ofapoB-100,MTP, andL-FABPindicating alterations in lipid secretion. Carbonyl protein and TBARS were consistently higher in the liver of the iron-treated rats. Moreover, a significant positive correlation was found between oxidative stress products,lfabpexpression, and iron stores. In addition, a negative correlation was found betweenpparαexpression, TBARS, carbonyl protein, and iron stores. In conclusion, our results suggest that the increase observed in the transport of lipids in the bloodstream and the decreased fatty acid oxidation in rats, which was promoted by iron dextran, might be attributed to increased oxidative stress.

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Yu, Fengli, Huibao Tang, Chunyu Liu, Congxia Xie, and Shitao Yu. "Oxidative Desulfurization of Model Diesel with O2Catalyzed by Oxidative-thermoregulated Bifunctional Ionic Liquids." Acta Chimica Sinica 72, no. 11 (2014): 1152. http://dx.doi.org/10.6023/a14080570.

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Arnould, Hélène, Vincent Baudouin, Anne Baudry, Luiz W. Ribeiro, Hector Ardila-Osorio, Mathéa Pietri, Cédric Caradeuc, et al. "Loss of prion protein control of glucose metabolism promotes neurodegeneration in model of prion diseases." PLOS Pathogens 17, no. 10 (October 5, 2021): e1009991. http://dx.doi.org/10.1371/journal.ppat.1009991.

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Corruption of cellular prion protein (PrPC) function(s) at the plasma membrane of neurons is at the root of prion diseases, such as Creutzfeldt-Jakob disease and its variant in humans, and Bovine Spongiform Encephalopathies, better known as mad cow disease, in cattle. The roles exerted by PrPC, however, remain poorly elucidated. With the perspective to grasp the molecular pathways of neurodegeneration occurring in prion diseases, and to identify therapeutic targets, achieving a better understanding of PrPC roles is a priority. Based on global approaches that compare the proteome and metabolome of the PrPC expressing 1C11 neuronal stem cell line to those of PrPnull-1C11 cells stably repressed for PrPC expression, we here unravel that PrPC contributes to the regulation of the energetic metabolism by orienting cells towards mitochondrial oxidative degradation of glucose. Through its coupling to cAMP/protein kinase A signaling, PrPC tones down the expression of the pyruvate dehydrogenase kinase 4 (PDK4). Such an event favors the transfer of pyruvate into mitochondria and its conversion into acetyl-CoA by the pyruvate dehydrogenase complex and, thereby, limits fatty acids β-oxidation and subsequent onset of oxidative stress conditions. The corruption of PrPC metabolic role by pathogenic prions PrPSc causes in the mouse hippocampus an imbalance between glucose oxidative degradation and fatty acids β-oxidation in a PDK4-dependent manner. The inhibition of PDK4 extends the survival of prion-infected mice, supporting that PrPSc-induced deregulation of PDK4 activity and subsequent metabolic derangements contribute to prion diseases. Our study posits PDK4 as a potential therapeutic target to fight against prion diseases.

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Wu, Qiang, Huaqiao Tang, and Hongbin Wang. "The Anti-Oxidation and Mechanism of Essential Oil of Paederia scandens in the NAFLD Model of Chicken." Animals 9, no. 10 (October 22, 2019): 850. http://dx.doi.org/10.3390/ani9100850.

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The aim of the study is to determine the underlying pathogenic mechanisms of oxidative stress and detect the anti-oxidative target of essential oil of Paederia scandens in non-alcoholic fatty liver disease (NAFLD). Chicken NAFLD was modeled by feeding with a high-capacity diet and Paederia scandens essential oil was used to treat the disease. The levels of hepatic reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and the differential proteins and network of protein–protein interactions were investigated in model and drug-treated groups. The results showed that essential oil of Paederia scandens down regulated the hepatic ROS and MDA level significantly (p < 0.05 and 0.01, respectively). The heat shock cognate 71 kDa protein (HSP7C) was down regulated significantly, which was in the center of the network and interacted with 22 other proteins. The results showed that oxidative stress played an important role in the pathogenesis of chicken NAFLD. The essential oil of Paederia scandens showed good anti-oxidation activity by down regulating the HSP7C protein, which can be used as a potential therapeutic target in chicken NAFLD.

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Jones, AR, and LA Chantrill. "Oxidative metabolic activity of boar spermatozoa: a system for assessing anti-glycolytic activity of potential inhibitors in vitro." Reproduction, Fertility and Development 1, no. 4 (1989): 357. http://dx.doi.org/10.1071/rd9890357.

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The oxidative metabolic capability of mature boar spermatozoa has been determined in vitro. The high rate of oxidation of fructose, glucose, glycerol, glycerol-3-phosphate and lactate to CO2 and the optimization of incubation conditions indicates that these cells could constitute a model system for investigating the anti-glycolytic activity of potential male anti-fertility agents. The effects of several chemical agents on the oxidative metabolism of boar spermatozoa are reported.

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Jaramillo, Isabel C., Chethan K. Gaddam, Randy L. Vander Wal, and JoAnn S. Lighty. "Effect of nanostructure, oxidative pressure and extent of oxidation on model carbon reactivity." Combustion and Flame 162, no. 5 (May 2015): 1848–56. http://dx.doi.org/10.1016/j.combustflame.2014.12.006.

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40

Akopyan, Argam, Polina Polikarpova, Anna Vutolkina, Kirill Cherednichenko, Valentine Stytsenko, and Aleksandr Glotov. "Natural clay nanotube supported Mo and W catalysts for exhaustive oxidative desulfurization of model fuels." Pure and Applied Chemistry 93, no. 2 (February 1, 2021): 231–41. http://dx.doi.org/10.1515/pac-2020-0901.

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Abstract Oxidative desulfurization is a promising way to produce, under mild conditions, clean ecological fuels with ultra-low sulfur content. Herein, we present for the first time heterogeneous catalysts based on natural aluminosilicate nanotubes (halloysite) loaded with transition metal oxides for oxidative sulfur removal using hydrogen peroxide as environmentally safe oxidant. The halloysite nanotubes (HNTs) provide acid sites for C–S bond scission, while the Mo and W oxides act as hydrogen peroxide activators. The structure and acidity of both the clay support and catalysts were investigated by low-temperature nitrogen adsorption/desorption, Fourier-transform infrared spectroscopy, X-ray fluorescence analysis, and transmission electron microscopy techniques. These clay-based catalysts revealed the high activity in the oxidation of various classes of sulfur-containing compounds (sulfides, heteroatomic sulfur compounds) under mild reaction conditions. The conversion of various substrates decreases in the following trend: MeSPh > Bn2S > DBT > 4-MeDBT > BT, which deals with substrate electron density and steric hindrance. The influence of the temperature, oxidant to sulfur molar ratio, and reaction time on catalytic behavior was evaluated for Mo- and W-containing systems with various metal content. The complete oxidation of the most intractable dibenzothiophene to the corresponding sulfone was achieved at 80 °C and H2O2:S = 6:1 (molar) for 2 h both for Mo- and W-containing systems. These transition metal oxides HNTs supported catalysts are stable for 10 cycles of dibenzothiophene oxidation, which makes them promising systems for clean fuel production.

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Ravandeh, Mehdi, Giulia Coliva, Heike Kahlert, Amir Azinfar, Christiane A. Helm, Maria Fedorova, and Kristian Wende. "Protective Role of Sphingomyelin in Eye Lens Cell Membrane Model against Oxidative Stress." Biomolecules 11, no. 2 (February 13, 2021): 276. http://dx.doi.org/10.3390/biom11020276.

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In the eye lens cell membrane, the lipid composition changes during the aging process: the proportion of sphingomyelins (SM) increases, that of phosphatidylcholines decreases. To investigate the protective role of the SMs in the lens cell membrane against oxidative damage, analytical techniques such as electrochemistry, high-resolution mass spectrometry (HR-MS), and atomic force microscopy (AFM) were applied. Supported lipid bilayers (SLB) were prepared to mimic the lens cell membrane with different fractions of PLPC/SM (PLPC: 1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphocholine). The SLBs were treated with cold physical plasma. A protective effect of 30% and 44% in the presence of 25%, and 75% SM in the bilayer was observed, respectively. PLPC and SM oxidation products were determined via HR-MS for SLBs after plasma treatment. The yield of fragments gradually decreased as the SM ratio increased. Topographic images obtained by AFM of PLPC-bilayers showed SLB degradation and pore formation after plasma treatment, no degradation was observed in PLPC/SM bilayers. The results of all techniques confirm the protective role of SM in the membrane against oxidative damage and support the idea that the SM content in lens cell membrane is increased during aging in the absence of effective antioxidant systems to protect the eye from oxidative damage and to prolong lens transparency.

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Culic, Carina, Alina Elena Parvu, Sandu Florin Alb, Camelia Alb, and Angela Pop. "EFFECT OF CIMETIDINE ON NITRO-OXIDATIVE STRESS IN A RAT MODEL OF PERIODONTITIS." Medicine and Pharmacy Reports 87, no. 3 (August 5, 2014): 177–81. http://dx.doi.org/10.15386/cjmed-273.

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Background and aims. Periodontitis is a chronic inflammation that involves nitro-oxidative stress with damaging periodontal structural effects. We aimed to evaluate the consequences of low-dose cimetidine on nitro-oxidative stress in periodontitis. Methods. A rat model of ligature-induced periodontitis was used. After two weeks, the periodontitis groups were treated with cimetidine, aminoguanidine, N-nitro-L-arginine methyl ester and trolox for one week. On day 21, blood was drawn and the serum analyzed for measurement of total nitrites and nitrates, total oxidative status, total antioxidant response, and oxidative stress index. Results. Cimetidine had an inhibitory effect on the synthesis of nitric oxide (p=0.001), total oxidative status (p=0.01) and oxidative stress index (p=0.01). Total antioxidant reactivity was increased by cimetidine (p=0.01). The effects of cimetidine were almost like those of aminoguanidine, NG-nitro-L-arginine methyl ester, and trolox. Conclusions. Low-dose cimetidine can be used as adjunctive host modulatory therapy in chronic periodontitis because it reduces nitro-oxidative stress.

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Witkiewicz-Kucharczyk, Aleksandra, Wojciech Goch, Jacek Olędzki, Andrea Hartwig, and Wojciech Bal. "The Reactions of H2O2 and GSNO with the Zinc Finger Motif of XPA. Not A Regulatory Mechanism, But No Synergy with Cadmium Toxicity." Molecules 25, no. 18 (September 12, 2020): 4177. http://dx.doi.org/10.3390/molecules25184177.

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Tetrathiolate zinc fingers are potential targets of oxidative assault under cellular stress conditions. We used the synthetic 37-residue peptide representing the tetrathiolate zinc finger domain of the DNA repair protein XPA, acetyl-DYVICEECGKEFMSYLMNHFDLPTCDNCRDADDKHK-amide (XPAzf) as a working model to study the reaction of its Zn(II) complex (ZnXPAzf) with hydrogen peroxide and S-nitrosoglutathione (GSNO), as oxidative and nitrosative stress agents, respectively. We also used the Cd(II) substituted XPAzf (CdXPAzf) to assess the situation of cadmium assault, which is accompanied by oxidative stress. Using electrospray mass spectrometry (ESI-MS), HPLC, and UV-vis and circular dichroism spectroscopies we demonstrated that even very low levels of H2O2 and GSNO invariably cause irreversible thiol oxidation and concomitant Zn(II) release from ZnXPAzf. In contrast, CdXPAzf was more resistant to oxidation, demonstrating the absence of synergy between cadmium and oxidative stresses. Our results indicate that GSNO cannot act as a reversible modifier of XPA, and rather has a deleterious effect on DNA repair.

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Devaraj, Sridevi, Shaina V. Hirany, Raymond F. Burk, and Ishwarlal Jialal. "Divergence between LDL Oxidative Susceptibility and Urinary F2-Isoprostanes as Measures of Oxidative Stress in Type 2 Diabetes." Clinical Chemistry 47, no. 11 (November 1, 2001): 1974–79. http://dx.doi.org/10.1093/clinchem/47.11.1974.

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Abstract Background: Oxidative stress is pivotal in atherogenesis. Although the most widely used indirect assay to quantify oxidative stress is LDL oxidative susceptibility, direct assays such as urinary F2-isoprostanes have shown great promise. Methods: We evaluated the utility of both a direct measure of oxidative stress (urinary F2-isoprostanes) and an indirect measure of copper-catalyzed, LDL oxidation in a model of increased oxidative stress (diabetes). We also evaluated an enzyme immunoassay (EIA) method for urinary F2-isoprostanes with a gas chromatography–mass spectrometry method. Results: Excellent intraassay and interassay CVs of <4% were obtained with our EIA method. A good correlation was obtained between the two methods (r = 0.80; n = 68) of F2-isoprostane measurement. An excellent correlation for F2-isoprostane concentrations was obtained between a timed collection vs 24-h urine (r = 0.96; n = 46). Baseline F2-isoprostane concentrations by EIA were significantly higher in both type 2 diabetics with and without macrovascular complications compared with controls (P <0.001). Supplementation with α-tocopherol led to a significant reduction in F2-isoprostane concentrations in all diabetic patients compared with baseline values (2.51 ± 1.76 compared with 1.69 ± 1.32 ng/mg creatinine; P <0.001). There were no significant differences in LDL oxidation in both diabetic groups compared with controls. α-Tocopherol supplementation led to significant increases in the lag phase of oxidation as measured by 3 indices in all groups. Conclusions: The measurement of urinary F2-isoprostanes provides a direct measure of in vivo lipid peroxidation and oxidative stress and appears to be superior to an indirect measure, e.g., LDL oxidative susceptibility, in type 2 diabetes.

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Chen, Yueying, Aiguo Xue, Haomin Jiang, Yujuan Cheng, Yuan Ren, Yanzhi Sun, and Yongmei Chen. "A two-phase reaction system for selective oxidative degradation of lignin model compounds." BioResources 15, no. 3 (July 8, 2020): 6526–38. http://dx.doi.org/10.15376/biores.15.3.6526-6538.

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Lignin depolymerization through an oxidation method could provide value-added products, but it is challenging in terms of recovering catalysts or separating products in time to avoid over-oxidation. In this study, a process of selectively oxidative degradation of lignin model compounds was operated in a two-phase reaction system. Lignin model compounds of 4-benzyloxyphenol (PBP) or guaiacylglycerol-β-guaiacyl ether (GGE) in a bottom phase of 1-butyl-3-methylimidazole chloride ([BMIM]Cl) ionic liquid were selectively oxidized by H2O2 in the presence of a solid acid (SO42-/Fe2O3-ZrO2), and the degradation products immediately diffused into the upper organic solvent phase (butyl acetate). In this kind of reaction system, the yield of the products was improved due to the prolonged life of ∙OH in ionic liquid, and the product selectivity was maintained due to the timely product separation, and the ionic liquid and the catalyst were easily recycled.

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Gonçalves, Ana C., Radhia Aitfella Lahlou, Gilberto Alves, Cristina Garcia-Viguera, Diego A. Moreno, and Luís R. Silva. "Potential Activity of Abrantes Pollen Extract: Biochemical and Cellular Model Studies." Foods 10, no. 11 (November 15, 2021): 2804. http://dx.doi.org/10.3390/foods10112804.

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The aim of this study was to determine the grain composition and (poly)phenolic profile of pollen from Abrantes (Portugal), as well as its antioxidative and antidiabetic properties, and abilities to protect human erythrocytes against induced hemoglobin oxidation, lipid peroxidation, and hemolysis. The phytochemical profile of the Abrantes’ bee pollen revealed twenty phenolic compounds, identified by high-performance liquid chromatography with electrospray ionization mass spectrometry coupled with photodiode array detection. Among them, quercetin derivatives were the most abundant. Concerning the biological potential, the pollen extract showed notable capacity for 2,2-diphenyl-1-picrylhydrazyl, nitric oxide, and superoxide radicals, as well as for inhibition of α-glucosidase action, and protection of human erythrocytes against oxidative damage. Non-cytotoxic effects regarding the NHDF normal cell line, human adenocarcinoma Caco-2, and human liver HepG2 cells were observed. The results obtained contributed to further research on modes of action related to oxidative damage and metabolic health problems, to generate deeper knowledge of potential health-promoting effects to develop novel pharmaceutical drugs, nutraceuticals, and dietary supplements.

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Majka, Tomasz M., Gabriela Berkowicz-Płatek, and Witold Żukowski. "Modeling of the Kinetics of Polyoxymethylene Decomposition under Oxidative and Non-Oxidative Conditions." Materials 14, no. 9 (April 28, 2021): 2281. http://dx.doi.org/10.3390/ma14092281.

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Research on the thermal and thermo-oxidative degradation of polyacetals allows for the development of effective methods of utilization of the waste of these polymers towards the recovery of monomers. For this purpose, in addition to qualitative analysis, it is necessary to understand the mechanisms of chemical reactions accompanying the decomposition process under the influence of temperature. Therefore, in this article, with the experimental results from the thermal analysis of the POM homopolymer of three various stages of life—POM-P—unprocessed sample; POM-R—recycled sample, and POM-O—sample waste—we took steps to determine the basic kinetic parameters using two well-known and commonly used kinetic models: Friedman and Ozawa-Flynn-Wall (OFW). Knowing the values of the course of changes in apparent activation energy as a function of partial mass loss, theoretical curves were fitted to the experimental data. The applied calculation models turned out to be consistent in terms of the nature of the curve changes and similar in terms of Ea in the entire range of mass loss. Both kinetic models showed a very similar course of the Ea curves. The samples that decompose under oxidative conditions obtained the best fit for the reaction of nth order with autocatalysis by product B model and the samples that decompose under inert conditions for the n-dimensional nucleation according to the Avrami–Erofeev model.

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Kobiela, Jarek, Tomasz Stefaniak, Jacek Krajewski, Beata Kalinska-Blach, Dorota Zurawa-Janicka, Andrzej Lachinski, Daniel Gackowski, et al. "Dynamics of estrogen-induced oxidative stress." Acta Biochimica Polonica 54, no. 2 (May 15, 2007): 289–95. http://dx.doi.org/10.18388/abp.2007_3249.

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The objective of this study was to assess the dynamics of oxidative damage to cellular macromolecules such as proteins, lipids and DNA under conditions of oxidative stress triggering early stages of estrogen-dependent carcinogenesis. A rodent model of carcinogenesis was used. Syrian hamsters were sacrificed after 1, 3, 5 h and one month from the initial implantation of estradiol. Matching control groups were used. Kidneys as target organs for estradiol-mediated oxidative stress were excised and homogenized for biochemical assays. Subcellular fractions were isolated. Carbonyl groups (as a marker of protein oxidation) and lipid hydroxyperoxides were assessed. DNA was isolated and 8-oxodGuo was assessed. Electron paramagnetic resonance spectroscopy was used to confirm the results for lipid peroxidation. Exposition to estradiol in the rodent model leads to damage of macromolecules of the cell, including proteins and DNA, but not lipids. Proteins appear to be the primary target of the damage but are closely followed by DNA. It has previously been speculated that protein peroxides can increase DNA modifications. This time sequence was observed in our study. Nevertheless, the direct relation between protein and DNA damage still remains unsolved.

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Berto, B. M., R. K. A. Garcia, G. D. Fernandes, D. Barrera-Arellano, and G. G. Pereira. "Linseed oil: Characterization and study of its oxidative degradation." Grasas y Aceites 71, no. 1 (January 14, 2020): 337. http://dx.doi.org/10.3989/gya.1059182.

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This paper proposes to characterize and monitor the degradation of linseed oil under two oxidation conditions using some traditional oxidative and quality parameters. The experimental section of this study was divided into 2 stages. In the first one, three commercial linseed oil samples (OL1, OL2, and OL3) were characterized according to oxidative stability (90 °C) and fatty acid composition. In the second stage, the OL1 sample, selected due to its availability, was subjected to the following oxidation procedures: storage at room temperature conditions with exposure to light and air (temperature ranging from 7 to 35 °C) for 140 days and accelerated oxidation at 100 °C for 7h. Samples were collected at different time intervals and analyzed for oxidative stability (90 °C), peroxide value, and acid value. The results showed that all the samples presented a similar fatty acid profile and that the OL3 sample showed a higher induction period (p < 0.05). Regarding the oxidative degradation, the induction period of the OL1 sample reduced from 9.7 to 5.7 and 9.7 to 6.3 during 140 days of storage under room temperature and 7 h of accelerated oxidation, respectively. The end of induction period of the OL1 sample is expected to occur within 229 days according to an exponential mathematical model fitted to the induction period values at different temperatures. In addition, the OL1 sample met the limits proposed by Codex and Brazilian regulations for peroxide and acid values during the oxidation time intervals.

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Li, Yunlei, Yanjie Zhang, Panfeng Wu, Caiting Feng, and Ganglin Xue. "Catalytic Oxidative/Extractive Desulfurization of Model Oil using Transition Metal Substituted Phosphomolybdates-Based Ionic Liquids." Catalysts 8, no. 12 (December 8, 2018): 639. http://dx.doi.org/10.3390/catal8120639.

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Abstract:

Polyoxometalates based ionic liquids (POM-ILs) exhibit a high catalytic activity in oxidative desulfurization. In this paper, four new POM-IL hybrids based on transition metal mono-substituted Keggin-type phosphomolybdates, [Bmim]5[PMo11M(H2O)O39] (Bmim = 1-butyl 3-methyl imidazolium; M = Co2+, Ni2+, Zn2+, and Mn2+), have been synthesized and used as catalysts for the oxidation/extractive desulfurization of model oil, in which ILs are used as the extraction solvent and H2O2 as an oxidant under very mild conditions. The factors that affected the desulfurization efficiency were studied and the optimal reaction conditions were obtained. The results showed that the [Bmim]5[PMo11Co(H2O)O39] catalyst demonstrated the best catalytic activity, with sulfur-removal of 99.8%, 85%, and 63% for dibenzothiophene (DBT), 4,6-dimethyldibenzothiophene (4,6-DMDBT), and benzothiophene (BT), respectively, in the case of extraction combining with a oxidative desulfurization system under optimal reaction conditions (5 mL model oil (S content 500 ppm), n(catalyst) = 4 μmol, n(H2O2)/n(Substrate) = 5, T = 50 °C for 60 min with [Omim]BF4 (1 mL) as the extractant). The catalyst can be recycled at least 8 times, and still has stability and high catalytic activity for consecutive desulfurization. Probable reaction mechanisms have been proposed for catalytic oxidative/extractive desulfurization.

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Journal articles on the topic 'The oxidative model'

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