Mechanism of citrinin-induced dysfunction of mitochondria.

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http://www3.interscience.wiley.com/cgi-bin/abstract/8662/ABSTRACT

Cell Biochemistry and Function

Volume 15, Issue 3 , Pages 203 - 209

Published Online: 4 Dec 1998

Copyright © 1997 Wiley & Sons, Ltd.

Research Article

Mechanism of citrinin-induced dysfunction of mitochondria. V. Effect

on the homeostasis of the reactive oxygen species

M. R. Ribeiro, Generoso M. Chagas, Annibal P. Campello *, Ma.

Lúcia W. Kluppel

Departamento de Bioquímica da Universidade Federal do Paraná

Curitiba, Paraná, Brazil

*Correspondence to Annibal P. Campello, Departamento de Bioquímica,

UFPR. C.P. 19046, Curitiba, PR., Brazil (81.531-990)

Funded by:

Conselho Nacional de Desenvolvimento Científico e Tecnológico -

CNPq; Grant Number: 30.0738/87, 52.1478/96

Keywords

citrinin • mycotoxin • rat liver mitochondria • superoxide

dismutase • catalase • glutathione reductase • glutathione

peroxidase • transhydrogenase • superoxide anion

Abstract

The effects of citrinin in the maintenance of the homeostasis of the

reactive oxygen species in rat liver cells were evaluated. Citrinin

(CTN) modifies the antioxidant enzymatic defences of cells through

the inhibition of GSSG-reductase and transhydrogenase. No effect was

observed on GSH-peroxidase, catalase, glucose 6-phosphate and 6

phosphogluconate dehydrogenases, and superoxide dismutase. The

mycotoxin increased the generation of reactive oxygen species,

stimulating the production of the superoxide anion in the

respiratory chain. The results suggest that oxidative stress is an

important mechanism, side by side with other effects previously

shown, in the establishment of the cytotoxicity and cellular death

provoked by CTN in several tissues. © 1997 Wiley & Sons, Ltd.

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