Beta-Carotene partially prevents the damage induced by 1,4-dimethylaminoazobenzene in mice.

Abstract

Hepatocarcinogenesis (HC) induced by various carcinogens such as 1,4-dimethylaminoazobenzene (DAB) is a multistep and complex process. The anticancer efficacy of beta-carotene (beta C) was evaluated by estimating some biochemical parameters during the initiation stage of HC. beta C dietary supplementation partially prevented the rise in delta-aminolevulinate synthetase activity. P 450 levels were dramatically enhanced in all groups studied. beta C administration did not overcome catalase inactivation due to DAB treatment; however, superoxide dismutase activity levels showed to be less decreased in the DAB + beta C animals in comparison to the DAB group. The great enhancement provoked by DAB of glutathione S-transferase, a proposed marker of HC, was partially reversed by beta C. In conclusion, heme pathway regulation, drug metabolism, and natural oxidative defence systems, strikingly modified in DAB fed animals, were partially controlled by provitamin A. The potential use of beta C in preventing carcinogenesis is suggested.