Mf. Souza et al., Inhibition by the bioflavonoid ternatin of aflatoxin B-1-induced lipid peroxidation in rat liver, J PHARM PHA, 51(2), 1999, pp. 125-129
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.