Topic
Oxidative stress
About: Oxidative stress is a research topic. Over the lifetime, 86513 publications have been published within this topic receiving 3845790 citations. The topic is also known as: oxydative stress.
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TL;DR: Redox mechanisms involved in ischemic preconditioning, one of the most effective ways of protecting the heart against IR injury, are reviewed, and several of these protective pathways converge on the inhibition of mPTP opening during reperfusion.
460 citations
TL;DR: Observations suggest that ROS act as intracellular messengers and integral glucose signaling molecules in diabetic kidney.
Abstract: Diabetic nephropathy is characterized by excessive deposition of extracellular matrix (ECM) in the kidney. TGF-beta1 has been identified as the key mediator of ECM accumulation in diabetic kidney. High glucose induces TGF-beta1 in glomerular mesangial and tubular epithelial cells and in diabetic kidney. Antioxidants inhibit high glucose-induced TGF-beta1 and ECM expression in glomerular mesangial and tubular epithelial cells and ameliorate features of diabetic nephropathy, suggesting that oxidative stress plays an important role in diabetic renal injury. High glucose induces intracellular reactive oxygen species (ROS) in mesangial and tubular epithelial cells. High glucose-induced ROS in mesangial cells can be effectively blocked by inhibition of protein kinase C (PKC), NADPH oxidase, and mitochondrial electron transfer chain complex I, suggesting that PKC, NADPH oxidase, and mitochondrial metabolism all play a role in high glucose-induced ROS generation. Advanced glycation end products, TGF-beta1, and angiotensin II can also induce ROS generation and may amplify high glucose-activated signaling in diabetic kidney. Both high glucose and ROS activate signal transduction cascade (PKC, mitogen-activated protein kinases, and janus kinase/signal transducers and activators of transcription) and transcription factors (nuclear factor-kappaB, activated protein-1, and specificity protein 1) and upregulate TGF-beta1 and ECM genes and proteins. These observations suggest that ROS act as intracellular messengers and integral glucose signaling molecules in diabetic kidney. Future studies elucidating various other target molecules activated by ROS in renal cells cultured under high glucose or in diabetic kidney will allow a better understanding of the final cellular responses to high glucose.
459 citations
TL;DR: It is suggested that prolonged low-grade oxidative stress impairs insulin-stimulated GLUT4 translocation, potentially by interfering with compartment-specific activation of PI 3-kinase.
Abstract: Prolonged exposure of 3T3-L1 adipocytes to micromolar concentrations of H2O2 results in an impaired response to the acute metabolic effects of insulin. In this study, we further characterized the mechanisms by which oxidative stress impairs insulin stimulation of glucose transport activity. Although insulin induced a 2.5-fold increase in plasma membrane GLUT4 content and a 50% reduction in its abundance in the low-density microsomal (LDM) fraction in control cells, oxidation completely prevented these responses. The net effect of insulin on 2-deoxyglucose uptake activity was reduced in oxidized cells and could be attributed to GLUT1 translocation. Insulin stimulation of insulin receptor substrate (IRS) 1 tyrosine phosphorylation and the association of IRS-1 with phosphatidylinositol (PI) 3-kinase were not impaired by oxidative stress. However, a 1.9-fold increase in the LDM content of the p85 subunit of PI 3-kinase after insulin stimulation was observed in control, but not in oxidized, cells. Moreover, although insulin induced an increase in IRS-1-associated PI 3-kinase activity in the LDM in control cells, this effect was prevented by oxidation. These findings suggest that prolonged low-grade oxidative stress impairs insulin-stimulated GLUT4 translocation, potentially by interfering with compartment-specific activation of PI 3-kinase.
458 citations
TL;DR: While the induction of oxidative stress in spermatozoa is causally involved in the aetiology of male infertility, the prospects of using such a strategy for male contraception is fraught with potential problems, should the suppression of fertility be incomplete and DNA-damaged spermatozosa gain access to the oocyte.
458 citations
TL;DR: Moderate exercise, started at young age in mice, increased life span, decreased oxidative stress, and prevented the decline of cytochrome oxidase activity and behavioral performance at middle age but not at old age.
Abstract: Moderate exercise in a treadmill (10, 15, and 20 cm/s, for 5 min each, weekly) from 28 to 78 wk of age extended male and female mice life span by 19 and 9% accompanied by 36 and 13% and 13 and 9% increased performance in behavioral assays (tightrope and T-maze tests) at 52 wk of age. Moderate exercise significantly decreased the aging-associated development of oxidative stress by preventing 1) the increase in protein carbonyls and thiobarbituric acid-reactive substances contents of submitochondrial membranes; 2) the decrease in antioxidant enzyme activities (Mn- and Cu,Zn-superoxide dismutase and catalase); and 3) the decrease in mitochondrial NADH-cytochrome-c reductase and cytochrome oxidase activities observed at 52 wk of mice age in brain, heart, liver, and kidney. These effects were no longer significant at 78 wk of age in mice. Moderate exercise, started at young age in mice, increased life span, decreased oxidative stress, and prevented the decline of cytochrome oxidase activity and behavioral performance at middle age but not at old age.
458 citations