Rossman T G, Klein C B, Naslund M
Carcinogenesis. 1986 May;7(5):727-32. doi: 10.1093/carcin/7.5.727.
Ascorbic acid (vitamin C) causes an increase in the mutation frequency of u.v.-irradiated Escherichia coli WP2. The enhancement occurs at all u.v. fluences, and is dependent upon the ascorbate concentration in the medium. A maximum effect (approximately 8- to 13-fold) is seen at 100-150 micrograms/ml, although some enhancement can be seen even at 10 micrograms/ml. The comutagenic effect of ascorbate with u.v. in E. coli is dependent upon peptone, a constituent of nutrient broth. The enhancement of u.v.-mutagenesis by ascorbate is absent in strains WP2s (uvrA) and WP6 (polA), suggesting that ascorbate affects the repair of pyrimidine dimers. The opposite results are observed for u.v.-mutagenesis in Chinese hamster V79 cells. The presence of ascorbate (50 micrograms/ml) during u.v. irradiation does not enhance the u.v. effect, but rather decreases it approximately 30%. These results are discussed with regard to differences in the mechanism of u.v.-mutagenesis and DNA repair in bacterial and mammalian cells.
抗坏血酸（维生素C）会使经紫外线照射的大肠杆菌WP2的突变频率增加。这种增强作用在所有紫外线通量下都会出现，并且取决于培养基中抗坏血酸盐的浓度。在100 - 150微克/毫升时可观察到最大效应（约8至13倍），不过即使在10微克/毫升时也能看到一些增强作用。抗坏血酸盐与紫外线在大肠杆菌中的共诱变作用取决于蛋白胨，它是营养肉汤的一种成分。在WP2s（uvrA）和WP6（polA）菌株中，抗坏血酸盐对紫外线诱变的增强作用不存在，这表明抗坏血酸盐会影响嘧啶二聚体的修复。在中国仓鼠V79细胞中，紫外线诱变则出现相反的结果。在紫外线照射期间存在抗坏血酸（50微克/毫升）并不会增强紫外线的效应，反而会使其降低约30%。针对细菌和哺乳动物细胞中紫外线诱变及DNA修复机制的差异，对这些结果进行了讨论。
