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.

Protein Nitration in Parkinson's Disease

Abstract: Oxidative stress has been proposed as a pathogenetic mechanism in Parkinson's disease (PD). One mechanism of oxidative cellular injury is the nitration of protein tyrosine residues, mediated by peroxynitrite, a reaction product of nitric oxide and superoxide radicals. We demonstrate here the presence of nitrotyrosine immunoreactivity in Lewy bodies within melanized neurons and in amorphous deposits associated with intact and degenerating neurons. The core of the Lewy body was frequently intensely immunolabeled, while the rim was lightly labeled or unlabeled. This likely reflects the fact that tyrosine residues of neurofilament proteins are primarily localized to Lewy body cores, and suggests that nitrotyrosine is present in neurofilament protein itself. Although these observations are as yet unable to provide a definitive link between oxidative stress and neuronal dysfunction, they demonstrate that oxidative stress has occurred within the vulnerable neurons of PD, leaving a permanent marker of oxidative modification of neuronal proteins within the target cells of neurodegeneration. In addition, these observations provide a potential link between excitotoxicity and oxidative stress within the vulnerable neurons of PD and represent a pathogenetic mechanism in common with the 2 other major age-related neurodegenerative diseases, Alzheimer disease and amyotrophic lateral sclerosis.

Manganese superoxide dismutase can reduce cellular damage mediated by oxygen radicals in transgenic plants.

Abstract: In plants, environmental adversity often leads to the formation of highly reactive oxygen radicals. Since resistance to such conditions may be correlated with the activity of enzymes involved in oxygen detoxification, we have generated transgenic tobacco plants which express elevated levels of manganese superoxide dismutase (MnSOD) within their chloroplasts or mitochondria. Leaf discs of these plants have been analyzed in conditions in which oxidative stress was generated preferentially within one or the other organelle. It was found that high level overproduction of MnSOD in the corresponding subcellular location could significantly reduce the amount of cellular damage which would normally occur. In contrast, small increases in MnSOD activity were deleterious under some conditions. A generally applicable model correlating the consequences of SOD with the magnitude of its expression is presented.

Plant Response and Tolerance to Abiotic Oxidative Stress: Antioxidant Defense Is a Key Factor

Abstract: In a persistently changing environment, plants are constantly challenged by various abiotic stresses such as salinity, drought, temperature extremes, heavy metal toxicity, high-light intensity, nutrient deficiency, UV-B radiation, ozone, etc. which cause substantial losses in the yield and quality of a crop. A key sign of such stresses at the molecular level is the accelerated production of reactive oxygen species (ROS) such as singlet oxygen (1O2), superoxide (O2•−), hydrogen peroxide (H2O2) and hydroxyl radicals (OH•). ROS are extremely reactive in nature because they can interact with a number of cellular molecules and metabolites, thereby leading to irreparable metabolic dysfunction and death. Plants have well-developed enzymatic and non-enzymatic scavenging pathways or detoxification systems to counter the deleterious effects of ROS that include the enzymes superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), glutathione reductase (GR), glutathione S-transferase (GST), glutathione peroxidase (GPX) and peroxidases (POX) as well as non-enzymatic compounds such as ascorbate (AsA), glutathione (GSH), carotenoids and tocopherols. In plant cells, specific ROS-producing and scavenging systems are found in different organelles and the ROS-scavenging pathways from different cellular compartments are coordinated. Recent studies in plants have shown that relatively low levels of ROS act as signaling molecules that induce abiotic stress tolerance by regulating the expression of defense genes. Additionally, numerous results have shown that plants with higher levels of antioxidants, whether constitutive or induced, showed greater resistance to different types of environmental stresses. In this chapter we attempt to summarize recent researches on the mechanisms and possible regulatory roles of ROS in abiotic stress tolerance. Further, we discuss the progress made during the last few decades in improving the oxidative stress tolerance of plants through genetic engineering by different components of ROS detoxification systems in plants.

Maturation-Dependent Vulnerability of Oligodendrocytes to Oxidative Stress-Induced Death Caused by Glutathione Depletion

Abstract: Death of oligodendrocyte (OL) precursors can be triggered in vitro by cystine deprivation, a form of oxidative stress that involves depletion of intracellular glutathione. We report here that OLs demonstrate maturation-dependent differences in survival when subjected to free radical-mediated injury induced by glutathione depletion. Using immunopanning to isolate rat preoligodendrocytes (preOLs), we generated highly enriched populations of preOLs and mature OLs under chemically defined conditions. Cystine deprivation caused a similar decrease in glutathione levels in OLs at both stages. However, preOLs were completely killed by cystine deprivation, whereas mature OLs remained viable. Although the glutathione-depleting agents buthionine sulfoximine and diethylmaleate were more potent in depleting glutathione in mature OLs, both agents were significantly more toxic to preOLs. Glutathione depletion markedly increased intracellular free radical generation in preOLs, but not in mature OLs, as indicated by oxidation of the redox-sensitive probe dihydrorhodamine 123. The antioxidants alpha-tocopherol, idebenone, and glutathione monoethylester prevented the oxidation of dihydrorhodamine in cystine-depleted preOLs and markedly protected against cell death. When the intracellular glutathione level was not manipulated, preOLs were also more vulnerable than mature OLs to exogenous free radical toxicity generated by a xanthine-xanthine oxidase system. Ultrastructural features of free radical-mediated injury in glutathione-depleted preOLs included nuclear condensation, margination of chromatin, and mitochondrial swelling. These observations indicate that preOLs are significantly more sensitive to the toxic effects of glutathione depletion and that oligodendroglial maturation is associated with decreased susceptibility to oxidative stress.

Amyloid‐β Deposition in Alzheimer Transgenic Mice Is Associated with Oxidative Stress

Abstract: Increased awareness for a role of oxidative stress in the pathogenesis of Alzheimer's disease has highlighted the issue of whether oxidative damage is a fundamental step in the pathogenesis or instead results from disease-associated pathology. In vitro experiments support both possibilities: Oxidative stress increases amyloid-beta production, and, conversely, amyloid-beta increases oxidative damage. To address the relationship between amyloid-beta and oxidative stress in vivo, we examined, using an array of oxidative markers, transgenic mice that overexpress amyloid-beta precursor protein and, as in Alzheimer's disease, develop characteristic amyloid-beta deposits within the brain parenchyma. Transgenic animals show the same type of oxidative damage that is found in Alzheimer's disease, and it is important that this damage directly correlates with the presence of amyloid-beta deposits. The significance of these studies is twofold. First, they provide evidence that amyloid-beta and oxidative damage are inextricably linked in vivo. Second, they support the use of transgenic animals for the development of antioxidant therapeutic strategies.