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THE ROLE OF HOMOCYSTINE IN PROTECTING PROTEIN-DEPLETED DOGS EXPOSED TO FATAL DOSES OF CHLOROFORM

In dogs maintained on low protein diets and subjected to phlebotomy over a long period of time, the inhalation of chloroform, for 30 minutes, produced uniform fatality within 48 hours. The histological changes of massive hepato-cellular destruction were observed at autopsy. Homocystine, in the amoun...

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Detalles Bibliográficos
Autores principales: Vennart, George P., McKee, Frank W.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1955
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136449/
https://www.ncbi.nlm.nih.gov/pubmed/13233445
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author Vennart, George P.
McKee, Frank W.
author_facet Vennart, George P.
McKee, Frank W.
author_sort Vennart, George P.
collection PubMed
description In dogs maintained on low protein diets and subjected to phlebotomy over a long period of time, the inhalation of chloroform, for 30 minutes, produced uniform fatality within 48 hours. The histological changes of massive hepato-cellular destruction were observed at autopsy. Homocystine, in the amount of 2.0 gm., given orally 2 hours after or 2 hours prior to the administration of chloroform, protected dogs against the lethal action of the toxin. Inconstant changes in fibrinogen and icteric indices were observed in the protected animals, indicating some mild liver damage, but this was not correlated with the length of the previous depletion period, the phase of the experiment, or any other factor. No evidence was obtained that methyl groups are necessary for the protection of the liver by homocystine.
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spelling pubmed-21364492008-04-17 THE ROLE OF HOMOCYSTINE IN PROTECTING PROTEIN-DEPLETED DOGS EXPOSED TO FATAL DOSES OF CHLOROFORM Vennart, George P. McKee, Frank W. J Exp Med Article In dogs maintained on low protein diets and subjected to phlebotomy over a long period of time, the inhalation of chloroform, for 30 minutes, produced uniform fatality within 48 hours. The histological changes of massive hepato-cellular destruction were observed at autopsy. Homocystine, in the amount of 2.0 gm., given orally 2 hours after or 2 hours prior to the administration of chloroform, protected dogs against the lethal action of the toxin. Inconstant changes in fibrinogen and icteric indices were observed in the protected animals, indicating some mild liver damage, but this was not correlated with the length of the previous depletion period, the phase of the experiment, or any other factor. No evidence was obtained that methyl groups are necessary for the protection of the liver by homocystine. The Rockefeller University Press 1955-01-31 /pmc/articles/PMC2136449/ /pubmed/13233445 Text en Copyright © Copyright, 1955, by The Rockefeller Institute for Medical Research New York This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Vennart, George P.
McKee, Frank W.
THE ROLE OF HOMOCYSTINE IN PROTECTING PROTEIN-DEPLETED DOGS EXPOSED TO FATAL DOSES OF CHLOROFORM
title THE ROLE OF HOMOCYSTINE IN PROTECTING PROTEIN-DEPLETED DOGS EXPOSED TO FATAL DOSES OF CHLOROFORM
title_full THE ROLE OF HOMOCYSTINE IN PROTECTING PROTEIN-DEPLETED DOGS EXPOSED TO FATAL DOSES OF CHLOROFORM
title_fullStr THE ROLE OF HOMOCYSTINE IN PROTECTING PROTEIN-DEPLETED DOGS EXPOSED TO FATAL DOSES OF CHLOROFORM
title_full_unstemmed THE ROLE OF HOMOCYSTINE IN PROTECTING PROTEIN-DEPLETED DOGS EXPOSED TO FATAL DOSES OF CHLOROFORM
title_short THE ROLE OF HOMOCYSTINE IN PROTECTING PROTEIN-DEPLETED DOGS EXPOSED TO FATAL DOSES OF CHLOROFORM
title_sort role of homocystine in protecting protein-depleted dogs exposed to fatal doses of chloroform
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136449/
https://www.ncbi.nlm.nih.gov/pubmed/13233445
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