Shinohara K, Matsudaira H
Chem Biol Interact. 1976 Jan;12(1):53-63. doi: 10.1016/0009-2797(76)90066-1.
The effects of methylazoxymethanol (MAM) acetate on colony survival, cell proliferation and DNA synthesis of murine lymphoma L5178Y cells are studied. Decreased sensitivity and immediate depression of cell proliferation and DNA synthesis were found in L5178Y cells in contrast to the reports on HeLa cells. Pre-labelling with 5-bromodeoxyuridine (BUdR) did not enhance significantly the carcinogen-induced cell lethality. Post-treatment with caffeine greatly enhanced cell lethality and depression of cell proliferation. These effects of caffeine were diminished when the cells had passed through two generations following the MAM acetate treatment. Experiments with synchronized cells showed that the action of caffeine was located primarily in S phase following the MAM acetate-treatment. These results strongly suggest that in L5178Y cells, MAM acetate induces damage, which is repaired by a mechanism analogous to post-replication repair of UV light-induced damage.
研究了乙酸甲基偶氮甲醇（MAM）对鼠淋巴瘤L5178Y细胞集落存活、细胞增殖和DNA合成的影响。与关于HeLa细胞的报道相反，在L5178Y细胞中发现细胞增殖和DNA合成的敏感性降低以及立即受到抑制。用5-溴脱氧尿苷（BUdR）进行预标记并没有显著增强致癌物诱导的细胞致死率。用咖啡因进行后处理大大增强了细胞致死率并抑制了细胞增殖。当细胞在乙酸MAM处理后经过两代时，咖啡因的这些作用减弱。同步化细胞实验表明，咖啡因的作用主要位于乙酸MAM处理后的S期。这些结果强烈表明，在L5178Y细胞中，乙酸MAM诱导损伤，该损伤通过类似于紫外线诱导损伤的复制后修复机制进行修复。
