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Potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls.

Mice ingesting a standard rodent diet supplemented with polybrominated biphenyls (PBBs) were more susceptible to chlorinated hydrocarbon solvent-induced renal and hepatic damage, as well as the lethal effects of CHCl3 and CCl4, than were mice consuming control diet. As little as 0.025 ml/kg CHCl3 ca...

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Autores principales: Kluwe, W M, McCormack, K M, Hook, J B
Formato: Texto
Lenguaje:English
Publicado: 1978
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637459/
https://www.ncbi.nlm.nih.gov/pubmed/209982
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author Kluwe, W M
McCormack, K M
Hook, J B
author_facet Kluwe, W M
McCormack, K M
Hook, J B
author_sort Kluwe, W M
collection PubMed
description Mice ingesting a standard rodent diet supplemented with polybrominated biphenyls (PBBs) were more susceptible to chlorinated hydrocarbon solvent-induced renal and hepatic damage, as well as the lethal effects of CHCl3 and CCl4, than were mice consuming control diet. As little as 0.025 ml/kg CHCl3 caused a significant increase in serum glutamic oxaloacetic transaminase (SGOT) and blood urea nitrogen (BUN) and a significant decrease in renal cortical slices accumulation of p-aminohippurate (PAH) in PBB-pretreated but not control mice. SGOT and serum glutamic pyruvate transaminase (SGPT) were greater in PBB-pretreated mice than in control mice after 0.125 and 0.005 ml/kg CCl4, respectively. Renal cortical PAH accumulation was greatly reduced in PBB-pretreated but not control mice aftter 0.125 ml/kg CCl4. The solvent-induced decrease in PAH accumulation was also greater in PBB-pretreated mice than in control mice following administration of 1.0 ml/kg trichloroethylene (TRI) and 0.15 ml/kg 1,1,2-trichloroethane (TCE).
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spelling pubmed-16374592006-11-17 Potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls. Kluwe, W M McCormack, K M Hook, J B Environ Health Perspect Research Article Mice ingesting a standard rodent diet supplemented with polybrominated biphenyls (PBBs) were more susceptible to chlorinated hydrocarbon solvent-induced renal and hepatic damage, as well as the lethal effects of CHCl3 and CCl4, than were mice consuming control diet. As little as 0.025 ml/kg CHCl3 caused a significant increase in serum glutamic oxaloacetic transaminase (SGOT) and blood urea nitrogen (BUN) and a significant decrease in renal cortical slices accumulation of p-aminohippurate (PAH) in PBB-pretreated but not control mice. SGOT and serum glutamic pyruvate transaminase (SGPT) were greater in PBB-pretreated mice than in control mice after 0.125 and 0.005 ml/kg CCl4, respectively. Renal cortical PAH accumulation was greatly reduced in PBB-pretreated but not control mice aftter 0.125 ml/kg CCl4. The solvent-induced decrease in PAH accumulation was also greater in PBB-pretreated mice than in control mice following administration of 1.0 ml/kg trichloroethylene (TRI) and 0.15 ml/kg 1,1,2-trichloroethane (TCE). 1978-04 /pmc/articles/PMC1637459/ /pubmed/209982 Text en
spellingShingle Research Article
Kluwe, W M
McCormack, K M
Hook, J B
Potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls.
title Potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls.
title_full Potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls.
title_fullStr Potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls.
title_full_unstemmed Potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls.
title_short Potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls.
title_sort potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637459/
https://www.ncbi.nlm.nih.gov/pubmed/209982
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