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Protection from renal ischemia-reperfusion injury by the 2-methylaminochroman U83836E

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TLDR
There is a protective effect of U83836E in ischemia-reperfusion injury, in that tissue damage due to oxidative stress is reduced, thus ameliorating renal function impairment.
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This article is published in Kidney International.The article was published on 1998-09-01 and is currently open access. It has received 27 citations till now. The article focuses on the topics: Kidney & Kidney disease.

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Journal ArticleDOI

Reactive oxygen species and acute renal failure

TL;DR: Evidence indicating that the inordinate or aberrant generation of reactive oxygen species (ROS) may contribute to the initiation and maintenance of ATN is reviewed, and the possibility that ROS may participate in the recovery phase of ATn is raised.
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Mitochondria-Targeted Peptide Accelerates ATP Recovery and Reduces Ischemic Kidney Injury

TL;DR: Treatment with SS-31 protected mitochondrial structure and respiration during early reperfusion, accelerated recovery of ATP, reduced apoptosis and necrosis of tubular cells, and abrogated tubular dysfunction, suggesting that it may protect against ischemic renal injury.
Journal ArticleDOI

Resveratrol, a polyphenol found in wine, reduces ischemia reperfusion injury in rat kidneys.

TL;DR: The results suggest that resveratrol reduced the renal ischemia reperfusion injury through a nitric oxide-dependent mechanism.
Journal ArticleDOI

Oxidative stress and reactive nitrogen species generation during renal ischemia.

TL;DR: The data clearly demonstrate that oxidative stress and RNS generation occur in the kidney during ischemia, and indicates that reactive nitrogen species (RNS) formation during I-R injury is driven by oxidant stress.
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Oxidative stress and kidney dysfunction due to ischemia/reperfusion in rat: Attenuation by dehydroepiandrosterone

TL;DR: Rats supplemented with DHEA and subjected to I/R had reduced pro-oxidant state, oxidative damage, and improved renal functionality, indicating an attenuation of oxidative injury and dysfunctions mediated by I-R.
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