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 me...

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Veröffentlicht in:Bull. Environ. Contam. Toxicol.; (United States) 1975-06, Vol.13 (6), p.737-740
Hauptverfasser: Goldsmith, R.H, Soares, J.H. Jr
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container_title Bull. Environ. Contam. Toxicol.; (United States)
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Soares, J.H. Jr
description 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.
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Jr</creatorcontrib><creatorcontrib>Univ. of Maryland, College Park</creatorcontrib><title>Barbiturate potentiation in mercury poisoning</title><title>Bull. Environ. Contam. Toxicol.; (United States)</title><addtitle>Bull Environ Contam Toxicol</addtitle><description>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. 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POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT</topic><topic>RADICALS</topic><topic>SELENIUM</topic><topic>Selenium - poisoning</topic><topic>SEMIMETALS</topic><topic>SLEEP</topic><topic>Sleep - drug effects</topic><topic>Time Factors</topic><topic>TOXICITY</topic><topic>VERTEBRATES</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Goldsmith, R.H</creatorcontrib><creatorcontrib>Soares, J.H. Jr</creatorcontrib><creatorcontrib>Univ. of Maryland, College Park</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><collection>OSTI.GOV</collection><jtitle>Bull. 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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.</abstract><cop>United States</cop><pmid>1139056</pmid><doi>10.1007/BF01721945</doi><tpages>4</tpages></addata></record>
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subjects 560300 - Chemicals Metabolism & Toxicology
ALKYL RADICALS
ANIMALS
AZINES
BARBITURATES
Barbiturates - pharmacology
BIOLOGICAL EFFECTS
BIOLOGICAL HALF-LIFE
BIRDS
BODY
BRAIN
Brain Chemistry
CENTRAL NERVOUS SYSTEM
Drug Synergism
DRUGS
ELEMENTS
HETEROCYCLIC COMPOUNDS
HYPNOTICS AND SEDATIVES
INGESTION
INTAKE
Liver - metabolism
Male
MERCURY
Mercury - metabolism
Mercury Poisoning - physiopathology
METALS
METHYL RADICALS
NERVOUS SYSTEM
ORGANIC COMPOUNDS
ORGANIC NITROGEN COMPOUNDS
ORGANIC OXYGEN COMPOUNDS
ORGANS
PYRIMIDINES
Quail - physiology
quails
RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT
RADICALS
SELENIUM
Selenium - poisoning
SEMIMETALS
SLEEP
Sleep - drug effects
Time Factors
TOXICITY
VERTEBRATES
title Barbiturate potentiation in mercury poisoning
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