Schuster C, Rode G, Rabes H M
J Cancer Res Clin Oncol. 1985;110(2):98-102. doi: 10.1007/BF00402719.
O6-Methylguanine DNA transferase activity was investigated in liver proteins obtained at various intervals after partial hepatectomy and/or after hydroxyurea-induced synchronization of the liver cell cycle. Liver proteins were incubated with 3H-methylated calf thymus DNA as previously described by Pegg et al. (1981). The loss of O6-methylguanine was measured by radiochromatography of DNA hydrolysates. The extent of O6-methylguanine repair differed during the cell cycle: the activity increased in late G1, reached a maximum in early S phase and declined in late S phase and G2M. These results indicate that hepatocytes are endowed with an increased DNA repair capacity for this promutagenic lesion during the period of highest transformation sensitivity in the cell cycle. Though increased, however, this repair potential does not, because of its exhaustibility, appear to be sufficient to prevent initiation of transformation after high doses of alkylating carcinogens.
在部分肝切除术后和/或羟基脲诱导肝细胞周期同步化后的不同时间点获取肝脏蛋白质，研究其中O6-甲基鸟嘌呤DNA转移酶的活性。如Pegg等人（1981年）先前所述，将肝脏蛋白质与3H-甲基化的小牛胸腺DNA一起孵育。通过DNA水解产物的放射色谱法测量O6-甲基鸟嘌呤的损失。在细胞周期中，O6-甲基鸟嘌呤的修复程度有所不同：活性在G1晚期增加，在S期早期达到最大值，在S期晚期和G2M期下降。这些结果表明，在细胞周期中转化敏感性最高的时期，肝细胞对这种促突变损伤具有增强的DNA修复能力。然而，尽管这种修复能力有所增强，但由于其可耗尽性，在高剂量烷基化致癌物作用后，似乎不足以防止转化的起始。
