scholarly journals The magic mountain or death in Venice: chronic hypoxia may alleviate oxidative stress in the kidney

2007 ◽  
Vol 582 (1) ◽  
pp. 1-1 ◽  
Author(s):  
Pontus B. Persson
Keyword(s):  
Oxidative Stress ◽  
Chronic Hypoxia ◽  
Death In Venice

Effects of Chronic Ghrelin Treatment on Hypoxia-Induced Brain Oxidative Stress and Inflammation in a Rat Normobaric Chronic Hypoxia Model

2017 ◽  
Vol 18 (2) ◽  
pp. 145-151 ◽  
Author(s):  
Hasan Omrani ◽  
Mohammad Reza Alipour ◽  
Fereshteh Farajdokht ◽  
Hadi Ebrahimi ◽  
Mehran Mesgari Abbasi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Hypoxia ◽  
Brain Oxidative Stress

Chronic hypoxia aggravates renal injury via suppression of Cu/Zn-SOD: a proteomic analysis

2008 ◽  
Vol 294 (1) ◽  
pp. F62-F72 ◽  
Author(s):  
Daisuke Son ◽  
Ichiro Kojima ◽  
Reiko Inagi ◽  
Makiko Matsumoto ◽  
Toshiro Fujita ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Proteomic Analysis ◽  
Chronic Hypoxia ◽  
Kidney Diseases ◽  
Pcr Analysis ◽  
Tubulointerstitial Injury ◽  
Tnf Α

Accumulating evidence suggests a pathogenic role of chronic hypoxia in various kidney diseases. Chronic hypoxia in the kidney was induced by unilateral renal artery stenosis, followed 7 days later by observation of tubulointerstitial injury. Proteomic analysis of the hypoxic kidney found various altered proteins. Increased proteins included lipocortin-5, calgizzarin, ezrin, and transferrin, whereas the decreased proteins were α2u-globulin PGCL1, eukaryotic translation elongation factor 1α2, and Cu/Zn superoxide dismutase (SOD1). Among these proteins, we focused on Cu/Zn-SOD, a crucial antioxidant. Western blot analysis and real-time quantitative PCR analysis confirmed the downregulation of Cu/Zn-SOD in the chronic hypoxic kidney. Furthermore, our laser capture microdissection system showed that the expression of Cu/Zn-SOD was predominant in the tubulointerstitium and was decreased by chronic hypoxia. The tubulointerstitial injury estimated by histology and immunohistochemical markers was ameliorated by tempol, a SOD mimetic. This amelioration was associated with a decrease in levels of the oxidative stress markers 4-hydroxyl-2-nonenal and nitrotyrosine. Our in vitro studies utilizing cultured tubular cells revealed a role of TNF-α in downregulation of Cu/Zn-SOD. Since the administration of anti-TNF-α antibody ameliorated Cu/Zn-SOD suppression, TNF-α seems to be one of the suppressants of Cu/Zn-SOD. In conclusion, our proteomic analysis revealed a decrease in Cu/Zn-SOD, at least partly by TNF-α, in the chronic hypoxic kidney. This study, for the first time, uncovered maladaptive suppression of Cu/Zn-SOD as a mediator of a vicious cycle of oxidative stress and subsequent renal injury induced by chronic hypoxia.

Chronic hypoxia and glutathione-dependent detoxication in rat small intestine

1996 ◽  
Vol 270 (4) ◽  
pp. G725-G729 ◽  
Author(s):  
T. S. LeGrand ◽  
T. Y. Aw
Keyword(s):  
Oxidative Stress ◽  
Chronic Hypoxia ◽  
Thiobarbituric Acid ◽  
Redox System ◽  
Thiobarbituric Acid Reactive Substance ◽  
Sprague Dawley ◽  
Distal Intestine ◽  
Key Enzyme ◽  
Cysteine Synthetase ◽  
Glucose 6 Phosphate Dehydrogenase

It has previously been found that chronic O2 deficiency decreases activity of the enzymes of the glutathione (GSH) redox system in the liver. To study the effects of O2 deficiency on intestinal detoxication capacity, pair-fed (16 g food/day) Sprague-Dawley rats were exposed to air (20.9% O2; n = 4) or 10% O2 (n = 4) for 10 days. Animals were killed, and intestinal mucosal homogenate (20% wt/vol) was obtained and assayed for activities of glucose-6-phosphate dehydrogenase (G6PD), GSH peroxidase (GSHPx), GSH disulfide reductase (GSSGRd), and gamma-glutamyl cysteine synthetase (gamma-GCS). Hypoxia decreases activities of GSHPx, GSSGRd, and gamma-GCS by approximately 50%, which suggests compromised detoxication. A proximal-to-distal reduction in enzymatic capacity indicates impairment of detoxication may be more pronounced in the distal intestine. G6PD, a key enzyme in NADPH production, remains unchanged. Urinary malondialdehyde was also monitored. Hypoxic rats exhibited a threefold increase in thiobarbituric acid-reactive substance, consistent with a generalized oxidative stress in these animals. Taken together, the results indicate that chronic hypoxia promotes tissue oxidative stress and impairs the ability of the enterocyte to metabolize ingested oxidants.

scholarly journals Melatonin Reduces Oxidative Stress in the Right Ventricle of Newborn Sheep Gestated under Chronic Hypoxia

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1658
Author(s):  
Alejandro Gonzaléz-Candia ◽  
Pamela V. Arias ◽  
Simón A. Aguilar ◽  
Esteban G. Figueroa ◽  
Roberto V. Reyes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Right Ventricle ◽  
Manganese Superoxide Dismutase ◽  
Cardiac Tissue ◽  
Chronic Hypoxia ◽  
Experimental Period ◽  
Health Concern ◽  
Right Ventricle Dysfunction ◽  
Beneficial Effects ◽  
Pulmonary Arterial

Pulmonary arterial hypertension of newborns (PAHN) constitutes a critical condition involving both severe cardiac remodeling and right ventricle dysfunction. One main cause of this condition is perinatal hypoxia and oxidative stress. Thus, it is a public health concern for populations living above 2500 m and in cases of intrauterine chronic hypoxia in lowlands. Still, pulmonary and cardiac impairments in PAHN lack effective treatments. Previously we have shown the beneficial effects of neonatal melatonin treatment on pulmonary circulation. However, the cardiac effects of this treatment are unknown. In this study, we assessed whether melatonin improves cardiac function and modulates right ventricle (RV) oxidative stress. Ten lambs were gestated, born, and raised at 3600 m. Lambs were divided in two groups. One received daily vehicle as control, and another received daily melatonin (1 mg·kg−1·d−1) for 21 days. Daily cardiovascular measurements were recorded and, at 29 days old, cardiac tissue was collected. Melatonin decreased pulmonary arterial pressure at the end of the experimental period. In addition, melatonin enhanced manganese superoxide dismutase and catalase (CAT) expression, while increasing CAT activity in RV. This was associated with a decrease in superoxide anion generation at the mitochondria and NADPH oxidases in RV. Finally, these effects were associated with a marked decrease of oxidative stress markers in RV. These findings support the cardioprotective effects of an oral administration of melatonin in newborns that suffer from developmental chronic hypoxia.

scholarly journals Chronic Hypoxia Impairs Cytochrome Oxidase Activity Via Oxidative Stress in Selected Fetal Guinea Pig Organs

2012 ◽  
Vol 20 (3) ◽  
pp. 299-307 ◽  
Author(s):  
Yazan M. Al-Hasan ◽  
LaShauna C. Evans ◽  
Gerard A. Pinkas ◽  
Erinne R. Dabkowski ◽  
William C. Stanley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Guinea Pig ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Chronic Hypoxia ◽  
Cytochrome Oxidase Activity
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