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J. Biol. Chem., Vol. 280, Issue 40, 33864-33872, October 7, 2005

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Oxidative Stress Is Responsible for Mitochondrial Permeability Transition Induction by Salicylate in Liver Mitochondria^*

From the Dipartimento di Chimica Biologica, Universitá di Padova, Istituto di Neuroscienze del C.N.R., Unitá per lo studio delle Biomembrane, Viale G. Colombo 3, 35121 Padova, Italy

The interaction of salicylate with the respiratory chain of liver mitochondria generates hydrogen peroxide and, most probably, other reactive oxygen species, which in turn oxidize thiol groups and glutathione. This oxidative stress, confirmed by the prevention of action by antioxidant agents, leads to the induction of the mitochondrial permeability transition in the presence of Ca²⁺. This phenomenon induces further increase of oxidative damage resulting in impairment of oxidative phosphorylation and -oxidation, cardinal features of Reye's syndrome in the liver. Mitochondrial permeability transition induction also induces the release of cytochrome c and apoptotic inducing factor from mitochondria, suggesting that salicylate also behaves as a pro-apoptotic agent. The reactive group of salicylate for inducing oxidative stress is the hydroxyl group which, by interacting with a Fe-S cluster of mitochondrial Complex I, the so-called N-2(Fe-S) center, produces reactive oxygen species.

Received for publication, March 3, 2005 , and in revised form, July 28, 2005.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dipartimento di Chimica Biologica, Universitá di Padova, Viale G. Colombo 3, 35121 Padova, Italy. Tel.: 39-0498276134; Fax: 39-0498276133; E-mail: antonio.toninello{at}unipd.it1.

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