[Effect of beta-carotene on sister chromatid exchanges induced by MNNG and aflatoxin B1 in V79 cells].
In order to elucidate the mechanism of tumor prevention of beta-carotene, its effect on sister chromatid exchanges (SCE) induced by MNNG in cultured V79 cells, under condition free of the enzyme system to convert beta-carotene into vitamin A, was studied. It was found that SCE level was significantly increased by high doses beta-carotene (10(-5)-10(-4) M) and the enhancement of SCE was restored to its original level by addition of alpha-tocopherol (final concentration 2 micrograms/ml). This may be due to the latter inhibiting the oxidation of beta-carotene and reducing the amount of oxidated carotene, which is toxic for cultured cells. Combination of beta-carotene and alpha-tocopherol at low doses inhibited SCE induced by MNNG (P less than 0.05) but no protective activity was observed when used separately. It was also found that beta-carotene (2 x 10(-7) M) and retinol (16 micrograms/ml) inhibited SCE induced by aflatoxin B1, which is activated by S-9 mixture. The present data clearly show that the antitumor activity of beta-carotene may be attributed to both itself and its degraded compound vitamin A, and may take part in the initiation of carcinogenesis. Combination of beta-carotene and other cancer preventive drugs is more effective and safer than it used individually.
Deng
D J
DJ
Cancer Institute, Chinese Academy of Medical Sciences, Beijing.
Hu
G G
GG
Luo
X M
XM
D016604:Aflatoxin B1; D000348:Aflatoxins; D002273:Carcinogens; D002338:Carotenoids / Q000494:pharmacology*; D002478:Cells, Cultured; D008769:Methylnitronitrosoguanidine; D012854:Sister Chromatid Exchange / Q000187:drug effects*; D014810:Vitamin E / Q000494:pharmacology; D019207:beta Carotene
D000348:Aflatoxins; D002273:Carcinogens; D019207:beta Carotene; D008769:Methylnitronitrosoguanidine; D014810:Vitamin E; D002338:Carotenoids; D016604:Aflatoxin B1