The effects of acute and long‐term exposure to CS 2 on oxidation and phosphorylation processes in brain mitochondria of rats were studied. Although rats developed different symptoms of poisoning, depending on the type of exposure, the brain mitochondria of both groups of animals exhibited the same types of disturbances in oxidative phosphorylation. The main characteristic of these disturbances was the uncoupling of oxidative phosphorylation indicated by lower respiratory control indices due to stimulation of oxidation of respiratory substrates by mitochondria in the metabolic state 4. This effect was accompanied by a decreased P:O ratio and a lower ATP‐Pi exchange rate. An inhibitory effect of CS 2 on the energy transfer processes is also suggested. The observed changes in oxidative phosphorylation were more distinct in the case of acute poisoning, with a longer period of an uninterrupted exposure enabling a more complete tissue saturation with CS 2 , than in the case of long‐term exposure with shorter periods of intoxication within the day.
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Tarkowski et al. (1971) studied this question.
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