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EC number: 904-290-8 | CAS number: -
CS2 intoxication exerted different signs of toxicity depending on the duration of treatment. After the 10-month exposure the animals experienced loss of motor equilibrium, muscular weakness, and hind-limb paresis. The acute challenging caused severe narcosis, reduced cardiac and respiratory rate, straightening of hind limbs, and lower body temperature. Nonetheless, the effects on the brain mitochondria were of the same type at both cases: disturbances in oxidative phosphorylation-uncoupling of oxidative phosphorylation, decreased phosphorus-oxygen (P:O) ratio, and a lower ATP-inorganic phosphorus (ATP-Pi) exchange rate.
The effects of acute and long-term exposure to CS2, 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 CS2 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 CS2, than in the case of long-term exposure with shorter periods of intoxication within the day.
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