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Mechanism of citrinin-induced dysfunction of mitochondria iii. Effects on renal cortical and liver mitochondrial swelling

✍ Scribed by Generoso M. Chagas; Ma. Benigna M. Oliveira; Annibal P. Campello; Ma. Lúcia W. Klüppel


Publisher
John Wiley and Sons
Year
1995
Tongue
English
Weight
497 KB
Volume
15
Category
Article
ISSN
0260-437X

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✦ Synopsis


The effects of the mycotoxin citrinin on renal cortical and liver mitochondrial swelling were studied. Citrinin decreases the rate of swelling induced by the valinomycin-K+ complex, suggesting that the mycotoxin interferes with the mitochondrial membrane fluidity. Citrinin promotes reduction of the amplitude of swelling in the presence of Na+ ions. This alteration reflects interference with complex I of the respiratory chain and ATP synthase complex activity without disarranging the inner mitochondrial membrane, in view of the fact that the shrinkage was not affected. The effect increases with citrinin concentration. Renal tissue is more susceptible than hepatic tissue.


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Mechanism of citrinin-induced dysfunctio
✍ Generoso M. Chagas; Annibal P. Campello; Ma. Lúcia W. Klüppel 📂 Article 📅 1992 🏛 John Wiley and Sons 🌐 English ⚖ 604 KB

Citrinin depresses the phosphorylation efficiency of rat renal cortical mitochondria, as inferred from the decrease of the respiratory control coefficient (RC) and ADP/O ratios. The transmembrane potential (A+) developed by energized mitochondria and the depolarization upon ADP addition are also dec

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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 dysfunctio
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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, catal