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: A number of studies have shown that there is no single "magic bullet" to combat oxidative stress, but instead a combination therapy, targeting oxidative stress in the various subcellular compartments, may prove to be more effective in COPD.
555 citations
TL;DR: A critical role is demonstrated for AKT-mediated induction of Runx2 in oxidative stress-induced VSMC calcification, which promotes a phenotypic switch of VSMC from contractile to osteogenic phenotype.
553 citations
TL;DR: The results are the first to show a significant decline in intracellular NAD+ levels and NAD∶NADH ratio in all organs by middle age compared to young rats, and suggest that adequate NAD+ concentrations may be an important longevity assurance factor.
Abstract: The cofactor nicotinamide adenine dinucleotide (NAD+) has emerged as a key regulator of metabolism, stress resistance and longevity. Apart from its role as an important redox carrier, NAD+ also serves as the sole substrate for NAD-dependent enzymes, including poly(ADP-ribose) polymerase (PARP), an important DNA nick sensor, and NAD-dependent histone deacetylases, Sirtuins which play an important role in a wide variety of processes, including senescence, apoptosis, differentiation, and aging. We examined the effect of aging on intracellular NAD+ metabolism in the whole heart, lung, liver and kidney of female wistar rats. Our results are the first to show a significant decline in intracellular NAD+ levels and NAD∶NADH ratio in all organs by middle age (i.e.12 months) compared to young (i.e. 3 month old) rats. These changes in [NAD(H)] occurred in parallel with an increase in lipid peroxidation and protein carbonyls (o- and m- tyrosine) formation and decline in total antioxidant capacity in these organs. An age dependent increase in DNA damage (phosphorylated H2AX) was also observed in these same organs. Decreased Sirt1 activity and increased acetylated p53 were observed in organ tissues in parallel with the drop in NAD+ and moderate over-expression of Sirt1 protein. Reduced mitochondrial activity of complex I–IV was also observed in aging animals, impacting both redox status and ATP production. The strong positive correlation observed between DNA damage associated NAD+ depletion and Sirt1 activity suggests that adequate NAD+ concentrations may be an important longevity assurance factor.
553 citations
TL;DR: A review of functional assays of oxidative stress status in humans including the strengths and limitations of various assays available for use in epidemiologic research on the following antioxidant nutrients: beta-carotene and other carotenoids, vitamin E, vitamin C and selenium.
Abstract: Oxidation of lipid, nucleic acids or protein has been suggested to be involved in the etiology of several chronic diseases including cancer, cardiovascular disease, cataract, age-related macular degeneration and aging in general. A large body of research has investigated the potential role of antioxidant nutrients in the prevention of these and other chronic diseases. This review concentrates on the following antioxidant nutrients: beta-carotene and other carotenoids, vitamin E, vitamin C and selenium. The first part of the review emphasizes the utility of biological markers of exposure for these nutrients and the relationship to dietary intake data. The second part considers functional assays of oxidative stress status in humans including the strengths and limitations of various assays available for use in epidemiologic research. A wide variety of functional assays both in vivo and ex vivo, are covered, including various measures of lipid oxidation (thiobarbituric acid reactive substances, exhaled pentane/ethane, low-density lipoprotein resistance to oxidation, isoprostanes), DNA oxidation (oxidized DNA bases such as 8-OHdG, autoantibodies to oxidized DNA, modified Comet assay) and protein oxidation (protein carbonyls). Studies that have examined the effects of antioxidant nutrients on these functional markers are included for illustrative purposes. The review concludes with a discussion of methodologic issues and challenges for studies involving biomarkers of exposure to antioxidant nutrients and of oxidative stress status.
553 citations
TL;DR: Novel antioxidants have shown great potential in mediating disease phenotypes and could be an area of interest for further research, as well as a highlight on the antioxidant-based therapies for alleviating disease severity.
Abstract: Increasing numbers of individuals, particularly the elderly, suffer from neurodegenerative disorders. These diseases are normally characterized by progressive loss of neuron cells and compromised motor or cognitive function. Previous studies have proposed that the overproduction of reactive oxygen species (ROS) may have complex roles in promoting the disease development. Research has shown that neuron cells are particularly vulnerable to oxidative damage due to their high polyunsaturated fatty acid content in membranes, high oxygen consumption, and weak antioxidant defense. However, the exact molecular pathogenesis of neurodegeneration related to the disturbance of redox balance remains unclear. Novel antioxidants have shown great potential in mediating disease phenotypes and could be an area of interest for further research. In this review, we provide an updated discussion on the roles of ROS in the pathological mechanisms of Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and spinocerebellar ataxia, as well as a highlight on the antioxidant-based therapies for alleviating disease severity.
552 citations