The effect of dietary carotenoid-rich extracts of carrots, tomatoes, and orange juice on rat liver gamma-glutamyl transpeptidase-positive preneoplastic foci induced by aflatoxin B1 was investigated. Organic extracts were prepared from the foods, dissolved in tricaprylin oil to equivalent concentrations of the major food-specific carotenoids, and fed by intubation to Fischer 344 male rats. The extracts were administered during the 2-week aflatoxin-dosing (initiation) period of the study or during the subsequent 12-week post-dosing (promotion) period. Vitamin status and antioxidant activities were measured in blood and liver. Extract feeding caused an accumulation of carotenoids in the liver, a substantial decrease in spontaneous erythrocyte hemolysis, and lowered plasma glutathione, blood superoxide dismutase, and blood catalase. Differences in foci development among the three extracts were not as consistent or profound as differences between initiation and promotion dosing. The number of gamma-glutamyl transpeptidase-positive foci was decreased by extract feeding during the initiation period, whereas extract feeding during the promotion period caused a decrease in the average diameter of the foci. The total volume of foci was markedly reduced by extract feeding during either period. Extracts were compared with purified carotenoids and alpha-tocopherol in their ability to affect in vitro antioxidation activity and were nearly as effective as the pure compounds. In summary, carotenoid-rich extracts of these three foods substantially inhibited biochemical and cellular events thought to play a role in the early stages of hepatocarcinogenesis.

The effects of beta-carotene, canthaxanthin, and extracts of tomato paste (containing lycopene) and orange juice (containing cryptoxanthin) on aflatoxin B1 (AFB1)-induced mutagenesis in S. typhimurium TA 100 and TA 98 were investigated. Inhibition of mutagenesis was studied during and following completion of AFB1 metabolism (i.e., after the addition of menadione), thereby permitting separate examination of the metabolic activation and phenotypic expression phases. Each experimental carotenoid, except lycopene, inhibited AFB1-induced mutagenesis in both tester strains. Cryptoxanthin was the most potent inhibitor, being at least an order of magnitude more potent than the other carotenoids. Inhibition by beta-carotene and canthaxanthin was more prominent during the activation phase, whereas cryptoxanthin was more effective during the subsequent phenotypic expression phase. These inhibitory effects were not dependent on conversion to retinol.

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