Abstract

Mitochondrial damage was evident in the earliest lesions in cardiac muscle of rabbits poisoned by coffee senna (Cassia occidentalis), suggesting that mitochondria might be the target for the toxic action of coffee senna. Oxidative phosphorylation by mitochondria isolated from poisoned rabbits was uncoupled, and in more severely affected rabbits mitochondrial respiration was depressed. The activities of myocardial malic dehydrogenase, isocitric dehydrogenase and lactic dehydrogenase were increased, glycogen was depleted, and lactate accumulated in poisoned rabbits. The toxin(s) of coffee senna induced uncoupling of oxidative phosphorylation in myocardial mitochondria. Thus, the mitochondria, deprived of their ability to convert the energy derived from respiration into adenosine triphosphate, were unable to maintain ionic gradients and became swollen. This caused progressive failure of respiration with subsequent disruption of myocardial mitochondrial structure and myocardial degeneration.

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