The inhibition by citrinin (CTN) of lipid peroxidation of mitochondria, sub-mitochondrial particles (SMP) and microsomes was studied. This eect was reversed by the presence of high concentrations of Fe 3 (0 . 4 and 0 . 5 mM), suggesting chelation of the mycotoxin with iron or interference in the red
Mechanism of citrinin-induced dysfunction of mitochondria. V. Effect on the homeostasis of the reactive oxygen species
✍ Scribed by Sonia M. R. Ribeiro; Generoso M. Chagas; Annibal P. Campello; Ma. Lúcia W. Kluppel
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 149 KB
- Volume
- 15
- Category
- Article
- ISSN
- 0263-6484
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✦ Synopsis
The eects of citrinin in the maintenance of the homeostasis of the reactive oxygen species in rat liver cells were evaluated. Citrinin (CTN) modi®es the antioxidant enzymatic defences of cells through the inhibition of GSSGreductase and transhydrogenase. No eect 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 eects previously shown, in the establishment of the cytotoxicity and cellular death provoked by CTN in several tissues.
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