Inhibition by the bioflavonoid ternatin of aflatoxin B-1-induced lipid peroxidation in rat liver

Aflatoxin B-1, a metabolite of Aspergillus flavus is a potent hepatotoxic a nd hepatocarcinogenic mycotoxin. Lipid peroxidation and oxidative DNA damag e are the principal manifestations of aflatoxin B1 induced toxicity which c ould be mitigated by antioxidants. Many plant constituents, e.g. flavonoids , lignans and spice principles (capsaicin, curcumin, eugenol, etc.) have be en reported to prevent liver damage associated with lipid peroxidation, In this study we investigated ternatin, a tetramethoxyflavone isolated from Eg letes viscosa, for possible protection against liver injury induced by afla toxin B-1 in rats. Seventy two hours after a single intraperitoneal dose of aflatoxin B-1 (1 m g kg(-1)), the concentration of malondialdehyde, the product of lipid perox idation in liver homogenates, and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly elevated (P < 0.01). Subcutaneous ternatin (25 mg kg(-1)) pretreatment greatly reduced a flatoxin B-1-induced increases in the levels of serum enzymes (ALT from 507 1 +/- 763 to 293 +/- 66 international units L-1 and AST from 4241 +/- 471 t o 449 +/- 108 international units L-1) and elevated malondialdehyde levels (from 11.37 +/- 1.27 to 0.79 +/- 0.22 nmol (mg wet tissue)(-1)) in a manner similar to oral vitamin E (300 mg kg(-1)), a standard antioxidant. Further , histological changes induced by aflatoxin B-1 such as hepatocellular necr osis and bile-duct proliferation were markedly inhibited in animals pretrea ted with ternatin or vitamin E. These data provide evidence that ternatin inhibits lipid peroxidation and a ffords protection against liver damage induced by aflatoxin B-1. Ternatin m ight, therefore, be a suitable candidate for the chemoprevention of aflatox icosis associated liver cancer.