| First Author | Jeong TC | Year | 1999 |
| Journal | Toxicol Lett | Volume | 105 |
| Issue | 1 | Pages | 39-46 |
| PubMed ID | 10092055 | Mgi Jnum | J:54172 |
| Mgi Id | MGI:1334170 | Doi | 10.1016/s0378-4274(98)00386-5 |
| Citation | Jeong TC, et al. (1999) Pretreatment of male BALB/c mice with beta-ionone potentiates thioacetamide-induced hepatotoxicity. Toxicol Lett 105(1):39-46 |
| abstractText | A possible role of metabolic activation by cytochrome P450 (P450) in thioacetamide-induced hepatotoxicity was investigated in male BALB/c mice. The mice were pretreated with the P450 inducer, beta-ionone, subcutaneously at 600 mg/kg, 72 and 48 h prior to an intraperitoneal administration of either 100 or 200 mg/kg of thioacetamide. The elevated activities of serum alanine aminotransferase and serum aspartate aminotransferase by thioacetamide were greatly potentiated by the pretreatment with beta-ionone. Moreover, the potentiation of thioacetamide-induced hepatotoxicity was also observed in the histopathological examination of livers. The hepatic necrosis by thioacetamide was potentiated when mice were pretreated with beta-ionone. In liver microsomes, the activities of P450 2B-specific pentoxyresorufin O-depentylase and benzyloxyresorufin O-debenzylase were significantly induced by the treatment with beta-ionone. Beta-ionone also induced other P450-associated monooxygenases. Because the pretreatment with beta-ionone was not hepatotoxic at the dose inducing P450s. our present results suggest that beta-ionone may be a useful model inducer of P450 enzyme(s) in studying toxic mechanism of certain chemicals which require metabolic activation by P450s in mice. |
