This study investigated the effects of consumption of various carotenoids on oral carcinogenesis and the activity of antioxidative enzymes in male hamsters. In the first 4 weeks, the right buccal pouch of each animal was daubed with 9,1 0-dimethyl-l ,2-benz-anthracene (DMBA) three times a week, and in the following 12 weeks the right buccal pouch was daubed with betel quid extract (BOE) and the rats were fed different experimental diets. Diets of the experimental groups were individually supplemented with 0, 1 % of β-carotene, lycopene, lutein, canthaxanthin, or equal amount of these four carotenoids (0,025% each) during the following 12 weeks. The results indicate that plasma and liver carotenoid levels of experimental groups were significantly higher than those of the control group (p < 0,05). Red blood cell (RBC) superoxide dismutase (SOD) activities of the lycopene and mixture groups were significantly lower than the control group, as was liver SOD activity of the canthaxanthin and mixture groups. Liver glutathione peroxidase (GPx) activities of the lutein, canthaxanthin, and mixture groups were significantly lower than that of the control group; however there was no difference between the activity of RBC GPx in each group. The plasma malondialdehyde (MDA) level in the mixture group was significantly lower than in the control group (p < 0.05); furthermore, hepatic MDA levels of the carotenoid treated groups were all significantly lower than that of the control group (p < 0,05). The number and volume of the tumor burden of the experimental groups were significantly lower than those of the control group. In conclusion, carotenoids provide an inhibitory capability on BQE-induced hamster oral carcinogenesis. The carotenoids significantly reduced the plasma and liver MDA levels and decreased the BQE-induced tumor burden in hamsters, especially in groups treated with lycopene, canthaxanthin, and a mixture of carotenoids.
This study investigated the effects of consumption of various carotenoids on oral carcinogenesis and the activity of antioxidative enzymes in male hamsters. In the first 4 weeks, the right buccal pouch of each animal was daubed with 9,1 0-dimethyl-l ,2-benz-anthracene (DMBA) three times a week, and in the following 12 weeks the right buccal pouch was daubed with betel quid extract (BOE) and the rats were fed different experimental diets. Diets of the experimental groups were individually supplemented with 0, 1 % of β-carotene, lycopene, lutein, canthaxanthin, or equal amount of these four carotenoids (0,025% each) during the following 12 weeks. The results indicate that plasma and liver carotenoid levels of experimental groups were significantly higher than those of the control group (p < 0,05). Red blood cell (RBC) superoxide dismutase (SOD) activities of the lycopene and mixture groups were significantly lower than the control group, as was liver SOD activity of the canthaxanthin and mixture groups. Liver glutathione peroxidase (GPx) activities of the lutein, canthaxanthin, and mixture groups were significantly lower than that of the control group; however there was no difference between the activity of RBC GPx in each group. The plasma malondialdehyde (MDA) level in the mixture group was significantly lower than in the control group (p < 0.05); furthermore, hepatic MDA levels of the carotenoid treated groups were all significantly lower than that of the control group (p < 0,05). The number and volume of the tumor burden of the experimental groups were significantly lower than those of the control group. In conclusion, carotenoids provide an inhibitory capability on BQE-induced hamster oral carcinogenesis. The carotenoids significantly reduced the plasma and liver MDA levels and decreased the BQE-induced tumor burden in hamsters, especially in groups treated with lycopene, canthaxanthin, and a mixture of carotenoids.
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