Barbiturate potentiation in mercury poisoning

Goldsmith, Robert H.; Soares, Joseph H.

doi:10.1007/bf01721945

Bull. Environ. Contam. Toxicol.

1975

DOI: 10.1007/bf01721945

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Barbiturate potentiation in mercury poisoning

Robert H. Goldsmith

Joseph H. Soares

Abstract: 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 mercur… Show more

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Cited by 5 publications

References 7 publications

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Potentiation of methylmercury toxicity by piperonyl butoxide

Friedman

Eaton

1978

Bull. Environ. Contam. Toxicol.

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Methylmercury (MeHg) is an extremely potent neurotoxin about 25% of which is degraded in vivo to inorganic mercury. Piperonyl butoxide (PB) is a widely used pesticidal synergist which inhibits many mammalian detoxification reactions. In a preliminary experiment with the high doses of PB and MeHg, PB induced a 12% decrease in mean survival time and a 20% decrease in mean latency time to neurotoxicity. The weight loss in PB-MeHg group was far greater than the control MeHg group. In a dose response experiment, mean survival times in rats fed 40 ppm MeHg-C1 were 5.75, 5.3, and 5.0 weeks at 0, 0.5, and 1% PB, respectively. By the ninth week 25% of rats fed 20 ppm MeHg-C1 showed neurotoxicity and 63% of the 0.5% PB fed showed neurotoxicity with some mortality. In experiments at 20 ppm MeHg-C1 both PB fed groups weighted considerably less than corresponding controls.

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Potentiation of methylmercury toxicity by piperonyl butoxide

Friedman

Eaton

1978

Bull. Environ. Contam. Toxicol.

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Influence of acetaldehyde, dietary protein, carbon tetrachloride and butylatedhydroxytoluene on the toxicity of methylmercury in rats

Bailey

1978

Bull. Environ. Contam. Toxicol.

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The influence of environmental or dietary factors on the toxicity of methylmercury (MeHg) was investigated due to possibilities that humans exposed to methylmercury may have been sensitized. Groups of 8 rats were exposed to 0, 20 or 40 ppm MeHg in a semisynthetic diet and fed 0.5% BHT, 5% protein (instead of 15%), or injected with 250 mg/kg CC14 or acetaldehyde. In control rats neurotoxicity occurred at 4 weeks and 9 weeks with 40 and 20 ppm MeHg, respectively. Mortality was observed at 6 weeks with 40 ppm and 1 rat died in week 9 with 20 ppm MeHg. Acetaldehyde injected rats died at week 4 and 6 when fed 40 or 20 ppm MeHg. Neurotoxicity was observed in week 3 and 5 in these groups, respectively. Treating rats with the low protein or BHT accelerated neurotoxicity and mortality by 1 week with 40 ppm MeHg. These agents had killed all test animals within 7 weeks at 20 ppm MeHg. Neither acetaldehyde nor BHT influenced 0 ppm MeHg controls while 5% protein induced precipitous weight loss. In the case of CC14, the rats lived longer in combination experiments than one would have expected from the individual treatments.

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Attenuation by methyl mercury and mercuric sulfide of pentobarbital induced hypnotic tolerance in mice through inhibition of ATPase activities and nitric oxide production in cerebral cortex

Chuu

Huang

et al. 2007

Arch Toxicol

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This study is aimed at exploring the possible mechanism of hypnosis-enhancing effect of HgS or cinnabar (a traditional Chinese medicine containing more than 95% HgS) in mice treated with pentobarbital. We also examined whether the effect of HgS is different from that of the well-known methyl mercury (MeHg). After a short period (7 days) of oral administration to mice, a nontoxic dose (0.1 g/kg) of HgS not only significantly enhanced pentobarbital-induced hypnosis but also attenuated tolerance induction; while a higher dose (1 g/kg) of HgS or cinnabar exerted an almost irreversible enhancing effect on pentobarbital-hypnosis similar to that of MeHg (2 mg/kg) tested, which was still effective even after 10 or 35 days cessation of administration. To study comparatively the effects of different mercury forms from oral administration of MeHg and HgS on membrane ATPase activities of experimental mice, analysis of the Hg content in the cerebral cortex revealed that correlated with the decrease of Na(+)/K(+)-ATPase and Ca(2+)-ATPase activities. Furthermore, NO levels of blood but not that of cerebral cortex were also decreased by mercuric compounds. Although pentobarbital alone enhanced cytochrome p450-2C9 in time dependent manner, all of mercurial compounds tested had no such effect. All of these findings indicated that the mercurial compounds including cinnabar, HgS and MeHg exert a long-lasting enhancing hypnotic activity without affecting pentobarbital metabolism, which provides evidence-based sedative effect of cinnabar used in Chinese traditional medicine for more than 2,000 years. The nontoxic HgS dosing (0.1 g/kg/day) for consecutive 7 days is perhaps useful for delaying or preventing pentobarbital-tolerance.

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Barbiturate potentiation in mercury poisoning

Cited by 5 publications

References 7 publications

Potentiation of methylmercury toxicity by piperonyl butoxide

Potentiation of methylmercury toxicity by piperonyl butoxide

Influence of acetaldehyde, dietary protein, carbon tetrachloride and butylatedhydroxytoluene on the toxicity of methylmercury in rats

Attenuation by methyl mercury and mercuric sulfide of pentobarbital induced hypnotic tolerance in mice through inhibition of ATPase activities and nitric oxide production in cerebral cortex

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