Barbiturate potentiation in mercury poisoning.
Barbiturate potentiation was observed in Japanese quail fed dietary levels of 4, 21, and 24 ppm Hg as methyl mercuric chloride. Gross symptoms of mercury poisoning were not observed until after BP was observed. After the initial increase in BP time was observed in the birds receiving 4 and 12 ppm mercury, there followed a plateau in response until those birds receiving 24 ppm Hg began to show gross symptoms of toxicity and the BP time markedly rose again. Pronounced BP persisted 7 weeks after removal of mercury from the diet reflecting the long biological half-life of mercury as the methyl derivative. Selenium effectively prevented BP after 7 days exposure to toxic levels of methyl mercury chloride. Therefore, results suggest that early toxic effects of mercury can be observed readily by BP and that this environmental contaminant may influence drug activity or increase the sensitivity of the nervous system to sodium pentobarbital.
D000818:Animals; D001463:Barbiturates / Q000494:pharmacology*; D001923:Brain Chemistry; D004357:Drug Synergism; D008099:Liver / Q000378:metabolism; D008297:Male; D008628:Mercury / Q000378:metabolism; D008630:Mercury Poisoning / Q000503:physiopathology*; D011784:Quail / Q000502:physiology*; D012643:Selenium / Q000506:poisoning; D012890:Sleep / Q000187:drug effects; D013997:Time Factors
D001463:Barbiturates; D008628:Mercury; D012643:Selenium