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Journal articles on the topic 'Psychoneuroimmunology; stress; the oxidative model'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Antoni, Michael H. "Stress Management and Psychoneuroimmunology in HIV Infection." CNS Spectrums 8, no. 1 (January 2003): 40–51. http://dx.doi.org/10.1017/s1092852900023440.

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AbstractDoes stress management affect psychological and immune functioning in persons with human immunodeficiency virus infections? Stress-management techniques, such as relaxation training and imagery, cognitive restructuring, coping-skills training, and interpersonal-skills training, may reduce anxiety, depression, and social isolation in HIV-infected persons by lowering physical tension and increasing a sense of control and self-efficacy. A psychoneuroimmunologic model is proposed wherein these psychological changes are hypothesized to be accompanied by an improved ability to regulate neuroendocrine functioning, which in turn may be associated with a partial normalization of immune system functions such as lymphocyte proliferation and cytotoxicity, providing more efficient surveillance of latent viruses that may contribute directly to increased HIV replication and generate opportunistic infections or cancer if left unchecked. Such a normalization of stress-associated immune system decrements are hypothesized to forestall or minimize increases in viral load and expression of clinical symptoms. This model is useful for testing the factors contributing to the health effects of stress-management interventions in HIV-infected persons. In this context, one general research strategy for testing the effects of stress-management interventions is to target them toward the more prevalent psychosocial challenges that HIV-infected people face at various points in the disease process; enroll an HIV-infected population (eg, HIV-positive homosexual and bisexual men) into a randomized trial; and monitor changes in cognitive, affective, behavioral, and social factors in parallel with hormonal, immunologic, viral, and clinical changes over the course of time. This article will review the major psychoneuroimmunologic findings that have emerged using this paradigm and suggest future research directions and clinical applications.

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2

Koenig, Harold G. "Religion and Medicine III: Developing a Theoretical Model." International Journal of Psychiatry in Medicine 31, no. 2 (June 2001): 199–216. http://dx.doi.org/10.2190/2ybg-nl9t-ek7y-f6a3.

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In this third of a four-article series on religion and medicine, I describe a theoretical model to illustrate the complex pathways by which religion may influence physical health. Genetic factors, childhood training, psychological and social influences, health behaviors, and healthcare practices are discussed as part of this model. Considerable space is given to recent advances in psychoneuroimmunology and to stress-induced cardiovascular changes that demonstrate physiological pathways by which cognitive, emotional, and behavioral processes may influence susceptibility to disease and disease course. I also discuss research illustrating the important role that social support plays in moderating the physiological effects of stress and improving health outcomes. If religious beliefs and practices improve coping, reduce stress, prevent or facilitate the resolution of depression, improve social support, promote healthy behaviors, and prevent alcohol and drug abuse, then a plausible mechanism exists by which physical health may be affected.

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3

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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4

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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5

Panayi, Adriana C., Yori Endo, Mehran Karvar, Prerana Sensharma, Valentin Haug, Siqi Fu, Bobin Mi, Yang An, and Dennis P. Orgill. "Low mortality oxidative stress murine chronic wound model." BMJ Open Diabetes Research & Care 8, no. 1 (September 2020): e001221. http://dx.doi.org/10.1136/bmjdrc-2020-001221.

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IntroductionInvestigators have struggled to produce a reliable chronic wound model. Recent progress with antioxidant enzyme inhibitors shows promise, but mortality rates are high. We modified the dosage and administration of an antioxidant enzyme inhibitor regimen to reduce mortality while inducing a chronic wound environment.Research design and methodsTo chemically induce a chronic wound environment, we applied modified doses of catalase (3-amino-1,2,4-triazole; intraperitoneal 0.5 g/kg) and glutathione peroxidase (mercaptosuccinic acid; topical 300 mg/kg) inhibitors to the dorsal wounds of 11-week-old db/db mice. A cohort of these mice was treated with a collagen-glycosaminoglycan scaffold. Both groups were compared with Diabetic control mice.ResultsThis study successfully induced a chronic wound in 11-week-old db/db mice, with no animal deaths. The antioxidant enzyme treated groups showed delayed wound contraction and significantly higher levels of inflammatory tissue, collagen deposition, cellular proliferation and leukocyte infiltration than the Diabetic control group. Angiogenesis was significantly higher in the antioxidant enzyme treated groups, but the vessels were immature and friable. Scaffold engraftment was poor but appeared to promote blood vessel maturation.ConclusionsOverall, the two in vivo groups treated with the antioxidant enzyme inhibitors appeared to be arrested in the inflammatory stage of wound healing, while the Diabetic control group progressed to the maturation phase and ultimately remodeling. This model may be instrumental for the development of new wound therapeutics.

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Adams, James D., Lori K. Klaidman, Carl P. LeBel, and Ifeoma N. Odunze. "Oxidative stress in the brain: A new model." Free Radical Biology and Medicine 9 (January 1990): 92. http://dx.doi.org/10.1016/0891-5849(90)90499-9.

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7

Breitenbach, Michael. "Oxidative stress and neurodegeneration: the yeast model system." Frontiers in Bioscience 18, no. 3 (2013): 1174. http://dx.doi.org/10.2741/4171.

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8

Tomás‐Zapico, Cristina, Beatriz Caballero, Verónica Sierra, Ignacio Vega‐Naredo, Óscar Álvarez‐García, Delio Tolivia, María Josefa Rodríguez‐Colunga, and Ana Coto‐Montes. "Survival mechanisms in a physiological oxidative stress model." FASEB Journal 19, no. 14 (September 26, 2005): 2066–68. http://dx.doi.org/10.1096/fj.04-3595fje.

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9

Oliveira, Renato B., Lázaro Alessandro Soares Nunes, Rodrigo Perroni Ferraresso, René Brenzikofer, Denise Vaz Macedo, and Rodrigo Hohl. "Oxidative Stress of an Endurance Overtraining Animal Model." Medicine & Science in Sports & Exercise 42 (May 2010): 786–87. http://dx.doi.org/10.1249/01.mss.0000386281.00666.6d.

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10

Fumoto, Toshio, Shouhei Kinoshita, Takao Sasaki, Norihito Shimamura, and Hiroki Ohkuma. "Oxidative Stress Mediates Vascular Tortuosity." Antioxidants 10, no. 6 (June 7, 2021): 926. http://dx.doi.org/10.3390/antiox10060926.

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Vascular tortuosity is associated with various disorders and is being increasingly detected through advances in imaging techniques. The underlying mechanisms for vascular tortuosity, however, remain unclear. Here, we tested the hypothesis that oxidative stress mediates the generation of tortuous vessels. We used the bilateral common carotid artery (CCA) ligation model to induce vascular tortuosity. Both young and adult rats showed basilar artery tortuous morphological changes one month after bilateral CCA ligation. These tortuous changes were permanent but more pronounced in the adult rats. Microarray and real-time PCR analysis revealed that these tortuous changes were accompanied by the induction of oxidative stress-related genes. Moreover, the indicated model in rabbits showed that tortuous morphological changes to the basilar artery were suppressed by antioxidant treatment. These results are highly suggestive of the significance of oxidative stress in the development of vascular tortuosity. Although further studies will be needed to elucidate the possible mechanisms by which oxidative stress enhances vascular tortuosity, our study also points toward possible prophylaxis and treatment for vascular tortuosity.

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11

Gelfand, Steven L., Maximo Vento, Juan Sastre, W. David Lust, Mark A. Smith, George Perry, Michele Walsh, and Richard Martin. "A New Model of Oxidative Stress in Rat Pups." Neonatology 94, no. 4 (2008): 293–99. http://dx.doi.org/10.1159/000151649.

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12

Beauséjour, A., K. Bibeau, J. C. Lavoie, J. St-Louis, and M. Brochu. "Placental Oxidative Stress in a Rat Model of Preeclampsia." Placenta 28, no. 1 (January 2007): 52–58. http://dx.doi.org/10.1016/j.placenta.2005.12.003.

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13

Feng, Rentian, Wei He, and Hirotomo Ochi. "A new murine oxidative stress model associated with senescence." Mechanisms of Ageing and Development 122, no. 6 (May 2001): 547–59. http://dx.doi.org/10.1016/s0047-6374(01)00232-9.

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14

Bates, Kristyn A., Ralph N. Martins, and Alan R. Harvey. "Oxidative stress in a rat model of chronic gliosis." Neurobiology of Aging 28, no. 7 (July 2007): 995–1008. http://dx.doi.org/10.1016/j.neurobiolaging.2006.05.003.

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15

Tafazoli, Shahrzad, and Peter J. O’Brien. "Amodiaquine-induced oxidative stress in a hepatocyte inflammation model." Toxicology 256, no. 1-2 (February 2009): 101–9. http://dx.doi.org/10.1016/j.tox.2008.11.006.

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16

Sorg, Olivier. "Oxidative stress: a theoretical model or a biological reality?" Comptes Rendus Biologies 327, no. 7 (July 2004): 649–62. http://dx.doi.org/10.1016/j.crvi.2004.05.007.

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17

Acer, Semra, Gökhan Pekel, Vural Küçükatay, Aysun Karabulut, Ramazan Yağcı, Ebru Nevin Çetin, Şahika Pınar Akyer, and Barbaros Şahin. "Oxidative stress of crystalline lens in rat menopausal model." Arquivos Brasileiros de Oftalmologia 79, no. 4 (2016): 222–25. http://dx.doi.org/10.5935/0004-2749.20160064.

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18

SEDEEK, M. "Increased oxidative stress in a rat model of preeclampsia." American Journal of Hypertension 17, no. 5 (May 2004): S142. http://dx.doi.org/10.1016/j.amjhyper.2004.03.376.

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19

Brown, Jacob L., Marcus M. Lawrence, Bumsoo Ahn, Parker Kneis, Katarzyna M. Piekarz, Rizwan Qaisar, Rojina Ranjit, et al. "Cancer cachexia in a mouse model of oxidative stress." Journal of Cachexia, Sarcopenia and Muscle 11, no. 6 (September 12, 2020): 1688–704. http://dx.doi.org/10.1002/jcsm.12615.

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20

Wang, Da-Hong, Noriyoshi Masuoka, and Shohei Kira. "Animal model for oxidative stress research—Catalase mutant mice." Environmental Health and Preventive Medicine 8, no. 2 (May 2003): 37–40. http://dx.doi.org/10.1007/bf02897924.

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21

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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22

Balmus, Ioana-Miruna, Radu Lefter, Alin Ciobica, Sabina Cojocaru, Samson Guenne, Daniel Timofte, Carol Stanciu, Anca Trifan, and Luminita Hritcu. "Preliminary Biochemical Description of Brain Oxidative Stress Status in Irritable Bowel Syndrome Contention-Stress Rat Model." Medicina 55, no. 12 (December 6, 2019): 776. http://dx.doi.org/10.3390/medicina55120776.

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Background and objectives: Oxidative stress and inflammation have been implicated in the etiology of irritable bowel syndrome (IBS), a common gastrointestinal functional disease. This study aimed to further characterize the contention-stress rat model by exploring a possible correlation between oxidative stress markers measured in brain tissues with behavioral components of the aforementioned model. Thus, it is hereby proposed a possible IBS animal model relevant to pharmacological and complementary medicine studies. Materials and Methods: Wild-type male Wistar rats (n = 5/group) were chronically exposed to 6-hour/day contention, consisting of isolating the animals in small, vital space-granting plastic devices, for seven consecutive days. Following contention exposure, temporal lobes were extracted and subjected to biochemical analyses to assess oxidative stress-status parameters. Results: Our results show increased brain oxidative stress in contention-stress rat model: decreased superoxide dismutase and glutathione peroxidase activities and increased malondialdehyde production in the IBS group, as compared to the control group. Furthermore, the biochemical ratios which are used to evaluate the effectiveness of an antioxidant system on oxidative stress could be described in this model. Conclusions: The correlations between the behavioral patterns and biochemical oxidative stress features could suggest that this may be a complex model, which can successfully mimic IBS symptomatology further providing evidence of a strong connection between the digestive system, enteric nervous system, and the central nervous system.

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23

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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24

Colaianna, Marilena, Stefania Schiavone, Margherita Zotti, Paolo Tucci, Maria Grazia Morgese, Liselotte Bäckdahl, Rikard Holmdahl, Karl-Heinz Krause, Vincenzo Cuomo, and Luigia Trabace. "Neuroendocrine Profile in a Rat Model of Psychosocial Stress: Relation to Oxidative Stress." Antioxidants & Redox Signaling 18, no. 12 (April 20, 2013): 1385–99. http://dx.doi.org/10.1089/ars.2012.4569.

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25

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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Rodrigues, Graziella, Andrea Janz Moreira, Silvia Bona, Elizângela Schemitt, Cláudio Augusto Marroni, Fábio Cangeri Di Naso, Alexandre Simões Dias, Thienne Rocha Pires, Jaqueline Nascimento Picada, and Norma Possa Marroni. "Simvastatin Reduces Hepatic Oxidative Stress and Endoplasmic Reticulum Stress in Nonalcoholic Steatohepatitis Experimental Model." Oxidative Medicine and Cellular Longevity 2019 (June 18, 2019): 1–10. http://dx.doi.org/10.1155/2019/3201873.

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Objective. In this study, we evaluated the efficacy of simvastatin in the treatment of nonalcoholic steatohepatitis induced by methionine and choline-deficient diet in mice and its possible effect on factors involved in the pathogenesis of the disease including oxidative stress and endoplasmic reticulum stress. Method. Male C57BL6 mice were fed either a normal diet (control) or a methionine and choline-deficient diet for four weeks and then treated orally with simvastatin (4 mg/kg once a day) for two final weeks. At the end of the experimental period, liver integrity, biochemical analysis, hepatic lipids, histology, DNA damage, biomarkers of oxidative stress, and endoplasmic reticulum stress were assessed. Results. Simvastatin treatment was able to significantly reduce hepatic damage enzymes and hepatic lipids and lower the degree of hepatocellular ballooning, without showing genotoxic effects. Simvastatin caused significant decreases in lipid peroxidation, with some changes in antioxidant enzymes superoxide dismutase and glutathione peroxidase. Simvastatin activates antioxidant enzymes via Nrf2 and inhibits endoplasmic reticulum stress in the liver. Conclusions. In summary, the results provide evidence that in mice with experimental nonalcoholic steatohepatitis induced by a methionine and choline-deficient diet, the reduction of liver damage by simvastatin is associated with attenuated oxidative and endoplasmic reticulum stress.

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27

Bărbînţă Pătraşcu, Marcela Elisabeta, Nicoleta Maria Badea, Laura Ţugulea, and Aurelia Meghea. "Photo-Oxidative Stress on Model Membranes – Studies by Optical Methods." Key Engineering Materials 415 (September 2009): 29–32. http://dx.doi.org/10.4028/www.scientific.net/kem.415.29.

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Photophysical studies on oxidative stress induced by illumination with ultraviolet (UV) light from artificial light sources, were performed on small unilamellar liposomes (SUVs) as models of biomembranes. Different liposoluble antioxidants were incorporated in the liposome bilayer during the lipid film preparation. The quercetin containing bilayers exhibited a high tolerance to photooxidative stress. The light-driven reactive oxygen species (ROS) effects on liposomal membranes were monitored by optical methods: UV-VIS absorption, fluorescence and chemiluminescence (CL), exploiting the spectral properties of chlorophyll a (Chla) embedded into some liposome bilayers (Chla/lipid molar ratio = 1/100). The interaction between Chla and the other liposome components resulted in changes in their absorption and emission fluorescence properties.

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28

Ścibior, Agnieszka, and Joanna Kurus. "Vanadium and Oxidative Stress Markers - In Vivo Model: A Review." Current Medicinal Chemistry 26, no. 29 (October 26, 2019): 5456–500. http://dx.doi.org/10.2174/0929867326666190108112255.

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:This review article is an attempt to summarize the current state of knowledge of the impact of Vanadium (V) on Oxidative Stress (OS) markers in vivo. It shows the results of our studies and studies conducted by other researchers on the influence of different V compounds on the level of selected Reactive Oxygen Species (ROS)/Free Radicals (FRs), markers of Lipid peroxidation (LPO), as well as enzymatic and non-enzymatic antioxidants. It also presents the impact of ROS/peroxides on the activity of antioxidant enzymes modulated by V and illustrates the mechanisms of the inactivation thereof caused by this metal and reactive oxygen metabolites. It also focuses on the mechanisms of interaction of V with some nonenzymatic compounds of the antioxidative system. Furthermore, we review the routes of generation of oxygen-derived FRs and non-radical oxygen derivatives (in which V is involved) as well as the consequences of FR-mediated LPO (induced by this metal) together with the negative/ positive effects of LPO products. A brief description of the localization and function of some antioxidant enzymes and low-molecular-weight antioxidants, which are able to form complexes with V and play a crucial role in the metabolism of this element, is presented as well. The report also shows the OS historical background and OS markers (determined in animals under V treatment) on a timeline, collects data on interactions of V with one of the elements with antioxidant potential, and highlights the necessity and desirability of conducting studies of mutual interactions between V and antioxidant elements.

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Zabot, Gilmara Pandolfo, Gustavo Franco Carvalhal, Norma Possa Marroni, Francielli Licks, Renata Minuzzo Hartmann, Vinícius Duval da Silva, and Henrique Sarubbi Fillmann. "Glutamine prevents oxidative stress in a model of portal hypertension." World Journal of Gastroenterology 23, no. 25 (2017): 4529. http://dx.doi.org/10.3748/wjg.v23.i25.4529.

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30

Dobrian, Anca D., Michael J. Davies, Suzanne D. Schriver, Thomas J. Lauterio, and Russell L. Prewitt. "Oxidative Stress in a Rat Model of Obesity-Induced Hypertension." Hypertension 36, suppl_1 (October 2000): 685–86. http://dx.doi.org/10.1161/hyp.36.suppl_1.685-e.

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45 The mechanisms underlying the development of hypertension in obesity are not yet fully understood. We recently reported the development of hypertension in a rat model of diet-induced obesity (Dobrian AD et al Hypertension 2000;35: in press). When Sprague-Dawley rats (n=60) are fed a moderately high fat diet(32kcal% fat) for 10-16 weeks, about half of them develop obesity (obesity-prone (OP) and mild hypertension (153±3.4 mmHg systolic pressure), whereas the other half (obesity-resistant, OR) maintains body weight equivalent to low fat control (C) and are normotensive. We examined the potential role of oxidative stress in the development of hypertension in this model. Lipid peroxides measured as thiobarbituric acid reactive substances (TBARS) are showing a significant increase in the LDL fraction of OP rats (2.8±0.32 nmol MDA/mg protein) compared to OR and C (0.9±0.3 nmol MDA/mg protein). Also, aortic and kidney TBARS showed a significant 3- and 5- fold increase in OP rats after 16 weeks of diet (3.3±0.44 aorta and 6.7±0.52 nmol MDA/mg protein kidney) vs OR. In addition, superoxide generation by aortic rings, measured by lucigenin (25μM) luminescence showed a 2-fold increase in the OP group (4325.6±174 RLU/15 min/mg DNA X10 5 ) compared to both OR and C. Plasma renin activity was 2-fold increased in OP vs both OR and control groups.The urine nitrate/nitrite measured by LDH colorimetric method showed a 1.8-fold decrease in OP rats (2.4±0.17 μmoles) compared to OR. A similar 1.6-fold decrease was found for plasma nitrate/nitrite in OP rats vs OR and C. However, eNOS expression assessed by semiquantitative RT-PCR showed a strong increase in the OP rats vs OR and controls in both kidney cortex(eNOS/β-actin ratio of 0.78±0.21 in OP vs 0.32±0.16 in OR)and medulla(0.86±0.18 in OP vs 0.36±0.14 in OR), suggesting a possible shift toward superoxide vs NO production by the eNOS enzyme.Also, eNOS expression was increased ∼4.8-fold in the thoracic aorta of OP compared to OR rats. Collectively, data show a decreased NO production in OP animals, due in part to the increased oxidative stress, possibly generated by the activation of renin-angiotensin system and increased eNOS expression.

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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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32

Formanowicz, Dorota, Adam Kozak, and Piotr Formanowicz. "A Petri net based model of oxidative stress in atherosclerosis." Foundations of Computing and Decision Sciences 37, no. 2 (October 1, 2012): 59–78. http://dx.doi.org/10.2478/v10209-011-0005-x.

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Abstract. In this paper a Petri net based model of the process of oxidative stress in atherosclerosis is presented and analyzed. Model expressed in the language of Petri net theory have, on one hand, an intuitive graphical representation, and on the other hand their formal properties can be analyzed using rigorous mathematical methods. Moreover, the behavior of a net can be simulated what supports the process of model development and an interpretation of the results of the analysis. Both the analysis and the simulation can be supported by many freely available software tools. In the case of biological systems an analysis the t-invariants is especially important since they correspond to some elementary biological subprocesses. In this paper the results of such an analysis are presented. In particular, minimal t-invariants, MCT-sets and t-clusters are calculated, their biological meaning is determined and some biological conclusions are drawn.

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TATLI, Özgür, Yunus Karaca, Ahmet Alver, Ahmet Menteşe, Esin Yuluğ, Mücahit Günaydın, Aynur Şahin, Umut Eryiğit, Samad Shams Vahdadi, and Ali Aygün. "EXAMINATION OF OXIDATIVE STRESS PARAMETERS IN EXPERIMENTAL MESENTERIC ISCHEMIA MODEL." Kırıkkale Üniversitesi Tıp Fakültesi Dergisi 19, no. 1 (April 24, 2017): 21. http://dx.doi.org/10.24938/kutfd.292279.

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34

Tálosi, Gyula, Ilona Németh, and Sándor Pintér. "OXIDATIVE STRESS IN A NEW MODEL OF HELLP SYNDROME. † 1473." Pediatric Research 39 (April 1996): 248. http://dx.doi.org/10.1203/00006450-199604001-01496.

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35

Hassan, Zeinab K., Mai A. Elobeid, Promy Virk, Sawsan A. Omer, Maha ElAmin, Maha H. Daghestani, and Ebtisam M. AlOlayan. "Bisphenol A Induces Hepatotoxicity through Oxidative Stress in Rat Model." Oxidative Medicine and Cellular Longevity 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/194829.

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Reactive oxygen species (ROS) are cytotoxic agents that lead to significant oxidative damage. Bisphenol A (BPA) is a contaminant with increasing exposure to it and exerts both toxic and estrogenic effects on mammalian cells. Due to limited information concerning the effect of BPA on liver, this study investigates whether BPA causes hepatotoxicity by induction of oxidative stress in liver. Rats were divided into five groups: The first four groups, BPA (0.1, 1, 10, 50 mg/kg/day) were administrated orally to rats for four weeks. The fifth group was taken water with vehicle. The final body weights in the 0.1 mg group showed a significant decrease compared to control group. Significant decreased levels of reduced glutathione, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and catalase activity were found in the 50 mg BPA group compared to control groups. High dose of BPA (50 mg/kg) significantly increased the biochemical levels of ALT, ALP and total bilirubin. BPA effect on the activity of antioxidant genes was confirmed by real time PCR in which the expression levels of these genes in liver tissue were significantly decrease compared to control. Data from this study demonstrate that BPA generate ROS and reduce the antioxidant gene expression that causes hepatotoxicity.

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Orhan, Cemal, Fatih Akdemir, Mehmet Tuzcu, Nurhan Sahin, Ismet Yilmaz, Jayant Deshpande, Vijaya Juturu, and Kazim Sahin. "Mesozeaxanthin Protects Retina from Oxidative Stress in a Rat Model." Journal of Ocular Pharmacology and Therapeutics 32, no. 9 (November 2016): 631–37. http://dx.doi.org/10.1089/jop.2015.0154.

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Charniot, Jean-Christophe, Dominique Bonnefont-Rousselot, Jean-Paul Albertini, Khaled Zerhouni, Sylvie Dever, Isabelle Richard, Patrick Nataf, et al. "Oxidative stress implication in a newex-vivocardiac concordant xenotransplantation model." Free Radical Research 41, no. 8 (January 2007): 911–18. http://dx.doi.org/10.1080/10715760701429775.

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Dobrian, Anca D., Michael J. Davies, Suzanne D. Schriver, Thomas J. Lauterio, and Russell L. Prewitt. "Oxidative Stress in a Rat Model of Obesity-Induced Hypertension." Hypertension 37, no. 2 (February 2001): 554–60. http://dx.doi.org/10.1161/01.hyp.37.2.554.

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Velena, Astrida, Neven Zarkovic, Koraljka Gall Troselj, Egils Bisenieks, Aivars Krauze, Janis Poikans, and Gunars Duburs. "1,4-Dihydropyridine Derivatives: Dihydronicotinamide Analogues—Model Compounds Targeting Oxidative Stress." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–35. http://dx.doi.org/10.1155/2016/1892412.

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Many 1,4-dihydropyridines (DHPs) possess redox properties. In this review DHPs are surveyed as protectors against oxidative stress (OS) and related disorders, considering the DHPs as specific group of potential antioxidants with bioprotective capacities. They have several peculiarities related to antioxidant activity (AOA). Several commercially available calcium antagonist, 1,4-DHP drugs, their metabolites, and calcium agonists were shown to express AOA. Synthesis, hydrogen donor properties, AOA, and methods and approaches used to reveal biological activities of various groups of 1,4-DHPs are presented. Examples of DHPs antioxidant activities and protective effects of DHPs against OS induced damage in low density lipoproteins (LDL), mitochondria, microsomes, isolated cells, and cell cultures are highlighted. Comparison of the AOA of different DHPs and other antioxidants is also given. According to the data presented, the DHPs might be considered as bellwether among synthetic compounds targeting OS and potential pharmacological model compounds targeting oxidative stress important for medicinal chemistry.

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Ichiseki, Toru, Tadami Matsumoto, Mitsuru Nishino, Ayumi Kaneuji, and Shogo Katsuda. "Oxidative stress and vascular permeability in steroid-induced osteonecrosis model." Journal of Orthopaedic Science 9, no. 5 (September 2004): 509–15. http://dx.doi.org/10.1007/s00776-004-0816-1.

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Vaculin, Simon, Miloslav Franek, and Martin Vejrazka. "Role of oxidative stress in animal model of visceral pain." Neuroscience Letters 477, no. 2 (June 2010): 82–85. http://dx.doi.org/10.1016/j.neulet.2010.04.037.

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Counterman, A. E., T. G. D'Onofrio, A. M. Andrews, and P. S. Weiss. "A physical model of axonal damage due to oxidative stress." Proceedings of the National Academy of Sciences 103, no. 14 (March 28, 2006): 5262–66. http://dx.doi.org/10.1073/pnas.0504134103.

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Ilhan, Atilla, M. Arif Aladag, Abdulkadir Kocer, Ayhan Boluk, Ahmet Gurel, and Ferah Armutcu. "Erdosteine ameliorates PTZ-induced oxidative stress in mice seizure model." Brain Research Bulletin 65, no. 6 (May 2005): 495–99. http://dx.doi.org/10.1016/j.brainresbull.2005.02.027.

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Li, Bojiang, Qiannan Weng, Zequn Liu, Ming Shen, Jiaqing Zhang, Wangjun Wu, and Honglin Liu. "Selection of antioxidants against ovarian oxidative stress in mouse model." Journal of Biochemical and Molecular Toxicology 31, no. 12 (December 2017): e21997. http://dx.doi.org/10.1002/jbt.21997.

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Bao, Aihua, and Xin Zhou. "Oxidative Stress Impairs Glucocorticoids Sensitivity of Allergic Asthma Animal Model." Chest 149, no. 4 (April 2016): A32. http://dx.doi.org/10.1016/j.chest.2016.02.034.

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Danchuk, S. D., J. Denson, Y. Hong, and J. B. Puschett. "Evidence of Oxidative Stress in a Rat Model of Preeclampsia." Journal of Investigative Medicine 54, no. 2_suppl (March 2006): 346. http://dx.doi.org/10.1177/108155890605402s19.

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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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Galligan, James J., Rebecca L. Smathers, Colin T. Shearn, Kristofer S. Fritz, Donald S. Backos, Hua Jiang, Christopher C. Franklin, David J. Orlicky, Kenneth N. MacLean, and Dennis R. Petersen. "Oxidative Stress and the ER Stress Response in a Murine Model for Early-Stage Alcoholic Liver Disease." Journal of Toxicology 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/207594.

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Alcoholic liver disease (ALD) is a primary cause of morbidity and mortality in the United States and constitutes a significant socioeconomic burden. Previous work has implicated oxidative stress and endoplasmic reticulum (ER) stress in the etiology of ALD; however, the complex and interrelated nature of these cellular responses presently confounds our understanding of ethanol-induced hepatopathy. In this paper, we assessed the pathological contribution of oxidative stress and ER stress in a time-course mouse model of early-stage ALD. Ethanol-treated mice exhibited significant hepatic panlobular steatosis and elevated plasma ALT values compared to isocaloric controls. Oxidative stress was observed in the ethanol-treated animals through a significant increase in hepatic TBARS and immunohistochemical staining of 4-HNE-modified proteins. Hepatic glutathione (GSH) levels were significantly decreased as a consequence of decreased CBS activity, increased GSH utilization, and increased protein glutathionylation. At the same time, immunoblot analysis of the PERK, IRE1α, ATF6, and SREBP pathways reveals no significant role for these UPR pathways in the etiology of hepatic steatosis associated with early-stage ALD. Collectively, our results indicate a primary pathogenic role for oxidative stress in the early initiating stages of ALD that precedes the involvement of the ER stress response.

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Nemeikaitė-Čėnienė, Aušra, Eglė Sergedienė, Henrikas Nivinskas, and Narimantas Čėnas. "Cytotoxicity of Natural Hydroxyanthraquinones: Role of Oxidative Stress." Zeitschrift für Naturforschung C 57, no. 9-10 (October 1, 2002): 822–27. http://dx.doi.org/10.1515/znc-2002-9-1012.

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In order to assess the role of oxidative stress in the cytotoxicity of natural hydroxyanthraquinones, we compared rhein, emodin, danthron, chrysophanol, and carminic acid, and a series of model quinones with available values of single-electron reduction midpoint potential at pH 7.0 (E17), with respect to their reactivity in the single-electron enzymatic reduction, and their mammalian cell toxicity. The toxicity of model uinones to the bovine leukemia virus-transformed lamb kidney fibroblasts (line FLK), and HL-60, a human promyelocytic leukemia cell line, increased with an increase in their E17. A close parallelism was found between the reactivity of hydroxyanthraquinones and model quinones with single-electron transferring flavoenzymes ferredoxin: NADP+ reductase and NADPH: cytochrome P-450 reductase, and their cytotoxicity. This points to the importance of oxidative stress in the toxicity of hydroxyanthraquinones in these cell lines, which was further evidenced by the protective effects of desferrioxamine and the antioxidant N,N′-diphenyl-p-phenylene diamine, by the potentiating effects of 1,3-bis-(2-chloroethyl)-1-nitrosourea, and an increase in lipid peroxidation.

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Oktaviasari, Dianti Ias. "Pengaruh Pemberian Jus Buncis (Phaseolus Vulgaris Linn) terhadap Kadar Malondialdehide Tikus Model Stres Psikologis." Jurnal Ilmiah Kedokteran Wijaya Kusuma 7, no. 2 (September 30, 2018): 141. http://dx.doi.org/10.30742/jikw.v7i2.435.

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Psychological stress is often suffered by people with body rhythm disorders, one of whom is a person with sleep disorders upside down. Psychological stress can trigger oxidative stress. Oxidative stress can be overcome by increasing antioxidants, beans as antioxidants are considered to reduce oxodative stress. The objective of the study was to examine the effect of green bean juice on the levels of Malondialdehyde (MDA) in male white wistar strains exposed to psychological stress. The design used in this research is Randomized Post Test Only Group Design. There were 5 groups tested, 2 normal and stress control groups, and 3 treatment groups. Exposure to psychological stress with reverse sleep guard pattern, so that the condition of experimental animals experiencing oxidative stress, then given bean juice with a dose of 4.5 gr / 1 ml in the treatment group. The results showed MDA levels dropped in the first hour and remained down until the 24th hour after the provision of bean juice. The effect of antioxidant flavonoids on beans decreases the amount of free radicals by scavenging mechanisms in free radicals and increases levels of endogenous antioxidants and increases insulin levels. The role of arginine in beans acts as a precursor of the formation of Nitric Oxide (NO) as vasodilator of blood vessels so as to decrease oxidative stress. A single dose of bean juice in experimental animals has been shown to overcome oxidative stress due to exposure to psychological stress since the first hour of green bean juice and its antioxidant activity persisted until the 24th hour.

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