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Mechanism of citrinin‐induced dysfunction of mitochondria. I. Effects on respiration, enzyme activities and membrane potential of renal cortical mitochondria
Author(s) -
Chagas Generoso M.,
Campello Annibal P.,
Klüppel Ma. Lúcia W.
Publication year - 1992
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550120209
Subject(s) - citrinin , mitochondrion , membrane potential , cytochrome c oxidase , depolarization , succinate dehydrogenase , enzyme , biochemistry , respiratory chain , respiration , mechanism of action , biology , chemistry , biophysics , anatomy , in vitro , mycotoxin , botany
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 (Δψ) developed by energized mitochondria and the depolarization upon ADP addition are also decreased. Citrinin (1.0 mM) inhibits almost all enzymes linked to the respiratory chain and increases the activity of succinate cytochrome c reductase and succinate oxidase (coupled). Malate and glutamate dehydrogenases are also inhibited. The inhibitory action of citrinin on phosphoryiation efficiency could be related to the following findings: the effect on complex I; the action on the ATP synthetase complex; the partial inhibition of the transmembrane potential.