Potentiation of hepatic and renal toxicity of various compounds by prior exposure to polybrominated biphenyls
| Autor: | K.M. McCormack, Jerry B. Hook, W M Kluwe |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 1978 |
| Předmět: |
Male
Health Toxicology and Mutagenesis Polybrominated Biphenyls Pharmacology Kidney Drug synergism Mice Hepatic damage polycyclic compounds medicine Hydrocarbons Chlorinated Animals Chemistry Biphenyl Compounds Body Weight Public Health Environmental and Occupational Health Long-term potentiation Drug Synergism Organ Size Animal Feed Hydrocarbons.chlorinated Biphenyl compound medicine.anatomical_structure Biochemistry Liver Toxicity Blood Chemical Analysis Research Article |
| Zdroj: | Environmental Health Perspectives |
| ISSN: | 0091-6765 |
| Popis: | 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). |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|