Effects of polybrominated biphenyls, "beta"-naphthoflavone and phenobarbital on arylhydrocarbon hydroxylase activities and chloroform-induced nephrotoxicity and hepatotoxicity in male C57BL/6J and DBA/2J mice
Ahmadizadeh, M; Kuo, CH; Echt, R; Hook, JB
| HERO ID | 9959 |
|---|---|
| In Press | No |
| Year | 1984 |
| Title | Effects of polybrominated biphenyls, "beta"-naphthoflavone and phenobarbital on arylhydrocarbon hydroxylase activities and chloroform-induced nephrotoxicity and hepatotoxicity in male C57BL/6J and DBA/2J mice |
| Authors | Ahmadizadeh, M; Kuo, CH; Echt, R; Hook, JB |
| Journal | Toxicology |
| Volume | 31 |
| Issue | 3 |
| Page Numbers | 343-352 |
| Abstract | The effects of polybrominated biphenyls (PBB), beta-naphthoflavone (6051872) (NF), and phenobarbital (50066) on the activity of arylhydrocarbon-hydroxylase (AHH) in liver and kidney were studied in male C57BL/6J-mice (C57-mice) and male DBA/2J-mice (DBA-mice). The effect of these compounds on chloroform (67663) induced hepatotoxicity and nephrotoxicity was also examined. NF was fed to C57-mice and DBA-mice at a concentration of 1 gram per kilogram of diet for 5 days before exposure to chloroform. Control animals received regular diet. Another group of mice was fed 0 or 100 parts per million PBB for 28 days before chloroform exposure. Phenobarbital was injected in another group at the rate of 80 milligrams per kilogram body weight intraperitoneally (ip) on 3 consecutive days. Twenty four hours after the final injection, mice were exposed to chloroform. After pretreatment with NF, PBB, or phenobarbital, mice received 0.025, 0.05, 0.1, or 0.25 milliliter of chloroform per kilogram body weight ip in peanut oil. Controls were injected with peanut oil alone. All animals were killed after 24 hours. Blood, liver, and kidneys were removed from each animal and used to assay for serum glutamic-pyruvic-transaminase (SGPT) activity, blood urea nitrogen (BUN), and the ability to accumulate organic cations as tetraethylammonium (66400) (TEA), and organic anions as para-aminohippurate (61789) (PAH). A dose related increase in SGPT activity was observed in previously untreated mice following exposure to chloroform. Administration of chloroform to phenobarbital or PBB treated C57-mice or DBA-mice caused a marked increase in SGPT activity. After a single dose of chloroform, accumulation of PAH and TEA was depressed in a dose related manner. Dietary PBB enhanced this depression in C57-mice only. A dose dependent increase in BUN was observed after exposure to chloroform. Only PBB treatment of C57-mice enhanced this response. AHH activity was stimulated in liver after treatment of both strains with phenobarbital and PBB. The authors conclude that the nephrotoxic metabolite of chloroform is generated in the kidneys. |
| Is Certified Translation | No |
| Dupe Override | No |
| Comments | substitute Greek character for "beta" in title; 1984b in 027,05.Toxicology 31: 343-352. |
| Is Public | Yes |
| Keyword | <?xml version="1.0" encoding="UTF-8"?><kw>DCN-130347</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Biphenyls</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Naphthalenes</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Aromatic hydrocarbons</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Comparative toxicology</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Enzyme activity</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Detoxification</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Physiological chemistry</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Animal studies</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Rodents</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Kidney toxins</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Hepatotoxicity</kw>; <?xml version="1.0" encoding="UTF-8"?><kw>Metabolites</kw> |
| Relationship(s) |
|