Ca2+-Independent Permeabilization of the Inner Mitochondrial Membrane by Peroxynitrite Is Mediated by Membrane Protein Thiol Cross-Linking and Lipid Peroxidation

Gadelha, Fernanda Ramos; Thomson, Leonor; Fagian, Márcia M.; Costa, Alexandre Dias Tavares; Radí, Rafael; Vercesi, Anı́bal E.

doi:10.1006/abbi.1997.0259

Cited by 123 publications

(74 citation statements)

References 48 publications

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“…Damage of mitochondrial membrane due to lipid peroxidation and protein cross linking 15 caused an increased in the inner membrane permeability leading to transmembrane collapse and cessation of ATP production. One among several methods commonly used in the evaluation of the inner mitochondrial membrane permeability is the swelling study.…”

Section: Discussionmentioning

confidence: 99%

The prevention of curcumin against rat liver mitochondrial swelling induced by tert-butylhydroperoxide

Susilowati¹,

Suyatna²,

Setiawati³

2006

Med J Indones

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Section: Discussionmentioning

confidence: 99%

The prevention of curcumin against rat liver mitochondrial swelling induced by tert-butylhydroperoxide

Susilowati¹,

Suyatna²,

Setiawati³

2006

Med J Indones

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“…Peroxynitrite can inhibit complex I, complex II, cytochrome oxidase, the ATP synthase, aconitase, Mn-SOD, creatine kinase, and probably many other proteins (2,10,28). Peroxynitrite is a strong oxidant and can also cause DNA damage, induce lipid peroxidation, and increase mitochondrial proton (and other ion) permeability (probably by lipid peroxidation or thiol cross-linking) (29).…”

Section: No Actions On Mitochondriamentioning

confidence: 99%

“…Cytochrome c is normally bound to cardiolipin on the inner mitochondrial membrane, but peroxidation causes the release of cytochrome c (74). Addition of peroxynitrite to isolated mitochondria causes lipid peroxidation and thiol cross-linking associated with increased proton and ion permeability, depolarisation and rapid swelling, which in the absence of calcium are not mediated by MPT (29). It has also been reported that addition of calcium to isolated mitochondria stimulates mtNOS, causing peroxynitrite production and (cyclosporin-insensitive) cytochrome c release associated with peroxidation of mitochondrial lipids (9).…”

Section: No-induced Cell Deathmentioning

confidence: 99%

Nitric Oxide, Mitochondria, and Cell Death

Brown¹,

Borutaitė²

2001

IUBMB Life

159

104

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“…Specifically, it has been shown that chemical inhibitors of the inducible nitric oxide synthase (iNOS), antisense oligonucleotides targeting mRNA encoding the enzyme or iNOS gene knockout, all result in the alleviation of renal tubular injury and improved structural and functional outcome (27,36). Cytotoxicity of NO and its metabolite peroxynitrite has been suggested to play a role in mitochondrial membrane lipid peroxidation (16) and in the inhibition of DNA synthesis (25).…”

mentioning

confidence: 99%

Oxidative and nitrosative stress in acute renal ischemia

Noiri

Nakao²,

Uchida

et al. 2001

American Journal of Physiology-Renal Physiology

275

253

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First Published July 12, 2001; 10.1152/ajprenal.0071.2001.—Generation of reactive oxygen species and nitric oxide in hypoxia-reperfusion injury may form a cytotoxic metabolite, peroxynitrite, which is capable of causing lipid peroxidation and DNA damage. This study was designed to examine the contribution of oxidative and nitrosative stress to the renal damage in ischemic acute renal failure (iARF). iARF was initiated in rats by 45-min renal artery clamping. This resulted in lipid peroxidation, DNA damage, and nitrotyrosine modification confirmed both by Western and immunohistochemical analyses. Three groups of animals were randomly treated with an inhibitor of inducible nitric oxide synthase (NOS),l- N 6-(1-iminoethyl)lysine (l-Nil), cell-permeable lecithinized superoxide dismutase (SOD), or both. Each treatment resulted in amelioration of renal dysfunction, as well as reduced nitrotyrosine formation, lipid peroxidation, and DNA damage, thus suggesting that peroxynitrite rather than superoxide anion is responsible for lipid peroxidation and DNA damage. Therefore, in a separate series of experiments, a scavenger of peroxynitrite, ebselen, was administered before the reperfusion period. This treatment resulted in a comparable degree of amelioration of iARF. In conclusion, the present study provides the first attempt to elucidate the role of peroxynitrite in initiation of the cascade of lipid peroxidation and DNA damage to ischemic kidneys. The results demonstrate that l-Nil , lecithinized SOD, and ebselen treatments improve renal function due to their suppression of peroxynitrite production or its scavenging, consequently preventing lipid peroxidation and oxidative DNA damage.

show abstract

Ca2+-Independent Permeabilization of the Inner Mitochondrial Membrane by Peroxynitrite Is Mediated by Membrane Protein Thiol Cross-Linking and Lipid Peroxidation

Cited by 123 publications

References 48 publications

The prevention of curcumin against rat liver mitochondrial swelling induced by tert-butylhydroperoxide

The prevention of curcumin against rat liver mitochondrial swelling induced by tert-butylhydroperoxide

Nitric Oxide, Mitochondria, and Cell Death

Oxidative and nitrosative stress in acute renal ischemia

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