Artigo Produção Nacional Revisado por pares

[25] Thiol enzymes protecting mitochondria against oxidative damage

2002; Academic Press; Linguagem: Inglês

10.1016/s0076-6879(02)48644-2

ISSN

1557-7988

Autores

L.E.S. Netto, Alicia J. Kowaltowski, Roger F. Castilho, Anı́bal E. Vercesi,

Tópico(s)

Mitochondrial Function and Pathology

Resumo

Mitochondria constantly generate reactive oxygen species (ROS), which can damage their lipids, proteins, DNA, and RNA. The respiratory chain, responsible for a constant generation of ROS within the cell, is located mostly within the inner mitochondrial membrane. Much of the oxidative damage affecting mitochondrial membrane proteins involves thiol oxidation. Thiol oxidation can result in mitochondrial impairment secondary to respiratory chain inhibition or to opening of a nonselective pore in the inner membrane, known as mitochondrial permeability transition pore. These forms of mitochondrial impairment, if widespread, can significantly affect cellular energy balance and result in cell death. Because mitochondrial membrane proteins are major targets of ROS, these organelles contain antioxidant thiol enzymes, which are capable of preventing or reversing oxidative damage. This chapter reviews the techniques used to determine the protective effects of thiol enzymes on mitochondria. Two distinct systems are used: (1) treatment of isolated mammalian mitochondria with exogenous thiol enzymes and (2) evaluation of mitochondria within S. cerevisae spheroblasts, manipulated to remove naturally occurring thiol enzymes.

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