Effect of mercury compounds on cholineacetyl transferase.
Methylmercury poisoning exhibit prominent signs and symptoms of the central nervous system. In an attempt to study the mechanism of toxicity, mercuric chloride (HgCl2) and methyl mercury chloride (CH3HgCl) were given orally by gavage and through drinking water to male albino rats. Rats were sacrificed at appropriate time and brain and diaphragm were analyzed for cholineacetyltransferase (ChAT) activity, and also examined histopathologically. Both HgCl2 and CH3HgCl given orally by gavage significantly inhibited ChAT activity which was dose related. CH3HgCl produced greater inhibition than HgCl2. CH3HgCl through drinking water also significantly inhibited brain ChAT, however rats did not drink water containing HgCl2. Both HgCl2 and CH3HgCl also inhibited ChAT when incubated in vitro with rat brain homogenates. Histopathological studies revealed neural degeneration and necrosis in the cerebrum of rats treated with these mercurials. These results indicate the possible involvement of cholinergic system during mercury intoxication.
D000818:Animals; D001921:Brain / Q000201:enzymology; D002795:Choline O-Acetyltransferase / Q000037:antagonists & inhibitors*; D003964:Diaphragm / Q000201:enzymology; D008297:Male; D008628:Mercury / Q000494:pharmacology*; D008767:Methylmercury Compounds / Q000494:pharmacology; D051381:Rats
D008767:Methylmercury Compounds; D002795:Choline O-Acetyltransferase; D008628:Mercury