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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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Journal ArticleDOI
TL;DR: It is found that silver-ion-mediated ROS-generation affected bactericidal activity and silver ions strongly enhanced paraquat-induced oxidative stress, indicating close correlation and synergism between the conventional and ROS-mediated silver toxicity.

501 citations

Journal ArticleDOI
01 Apr 1999-Diabetes
TL;DR: The results indicate that the pancreatic beta-cells of GK rats are oxidatively stressed, and that chronic hyperglycemia might be responsible for the oxidative stress observed in the pancreato-cells.
Abstract: Reactive oxygen species are involved in a diversity of biological phenomena such as inflammation, carcinogenesis, aging, and atherosclerosis. We and other investigators have shown that the level of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker for oxidative stress, is increased in either the urine or the mononuclear cells of the blood of type 2 diabetic patients. However, the association between type 2 diabetes and oxidative stress in the pancreatic beta-cells has not been previously described. We measured the levels of 8-OHdG and 4-hydroxy-2-nonenal (HNE)-modified proteins in the pancreatic beta-cells of GK rats, a model of nonobese type 2 diabetes. Quantitative immunohistochemical analyses with specific antibodies revealed higher levels of 8-OHdG and HNE-modified proteins in the pancreatic beta-cells of GK rats than in the control Wistar rats, with the levels increasing proportionally with age and fibrosis of the pancreatic islets. We further investigated whether the levels of 8-OHdG and HNE-modified proteins would be modified in the pancreatic beta-cells of GK rats fed with 30% sucrose solution or 50 ppm of voglibose (alpha-glucosidase inhibitor). In the GK rats, the levels of 8-OHdG and HNE-modified proteins, as well as islet fibrosis, were increased by sucrose treatment but reduced by voglibose treatment. These results indicate that the pancreatic beta-cells of GK rats are oxidatively stressed, and that chronic hyperglycemia might be responsible for the oxidative stress observed in the pancreatic beta-cells.

501 citations

Journal ArticleDOI
TL;DR: Targeting the complex oxidative stress signaling pathways would offer a valuable perspective for exploration of potential therapeutic strategies in the treatment of this devastating disease.

501 citations

Journal ArticleDOI
08 Oct 1999-Science
TL;DR: A manganese(II) complex with a bis(cyclohexylpyridine)-substituted macrocyclic ligand was designed to be a functional mimic of the superoxide dismutase (SOD) enzymes that normally remove these radicals.
Abstract: Many human diseases are associated with the overproduction of oxygen free radicals that inflict cell damage. A manganese(II) complex with a bis(cyclohexylpyridine)-substituted macrocyclic ligand (M40403) was designed to be a functional mimic of the superoxide dismutase (SOD) enzymes that normally remove these radicals. M40403 had high catalytic SOD activity and was chemically and biologically stable in vivo. Injection of M40403 into rat models of inflammation and ischemia-reperfusion injury protected the animals against tissue damage. Such mimics may result in better clinical therapies for diseases mediated by superoxide radicals.

500 citations

Journal ArticleDOI
TL;DR: The Nrf2 cytoprotective adaptive response has evolved to be a powerful protective strategy for organisms against exposure to environmental toxicants and may provide insight into differential disease susceptibilities across populations and responses to therapies designed to alleviate these conditions.
Abstract: Human exposures to environmental toxicants have been associated with development of a number of diseases. Animal experiments have identified a number of cytoprotective enzymes under the transcriptional control of NF-E2-related factor 2 (Nrf2) including electrophile conjugation and antioxidative enzymes and enzymes responsible for the production of antioxidants, reducing equivalents and cofactors. The up-regulation of these enzymes represents an adaptive response which occurs in the face of exposure to electrophilic or oxidative compounds thereby leading to enhanced metabolism of these molecules or their reactive metabolites. This adaptive response is regulated by an interaction between Keap1 and Nrf2 in which the exposure to reactive molecules is sensed either directly by Keap1 or indirectly by cellular signaling cascades resulting in activation of Nrf2 transcriptional regulation. The Nrf2-mediated adaptive response has been shown to attenuate toxicity and carcinogenesis during electrophile or oxidative stress as well as inflammation in rodent models. The cytoprotective attributes of the Nrf2 signaling pathway have been targeted for chemoprevention as administration of Nrf2-inducing agents has been shown to result in decreased carcinogenesis in animal models and altered carcinogen metabolism in humans. On the other hand, polymorphisms in the Nrf2 signaling pathway can lead to differential susceptibility to disease while mutations in the Nrf2 signaling pathway have been shown to an effective mechanism for cancer cells to evade chemotherapy. Overall, the Nrf2 cytoprotective adaptive response has evolved to be a powerful protective strategy for organisms against exposure to environmental toxicants and may provide insight into differential disease susceptibilities across populations and responses to therapies designed to alleviate these conditions.

499 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20242
20238,839
202217,614
20216,457
20206,203
20195,669