Gábelová A, Bacová G, Slamenová D, Périn F
Department of Mutagenesis and Carcinogenesis, Cancer Research Institute, Bratislava, Slovak Republic.
Acta Biochim Pol. 1998;45(1):203-8.
Several repair endonucleases were used to characterize and quantify various types of DNA damage induced by 7H-dibenzo[c,g]carbazole (DBC) and its methyl derivative, N-methyldibenzo[c,g]carbazole (MeDBC). Differences in the DNA damage profile induced by these two derivatives were found to be related to their chemical structure and dependent on the way of their metabolic activation. Different ways of activation gave rise to different numbers of single strand breaks and DNA modifications or, at least, to different ratios of common modifications. DBC induced the highest level of breaks in human hepatal cell line Hep G2, while MeDBC induced most of the breaks in V79 cell line with stable expression of human cytochrome P4501A1. Our results support the idea of two different pathways of biotransformation of DBC and MeDBC.
使用了几种修复核酸内切酶来表征和量化由7H-二苯并[c,g]咔唑(DBC)及其甲基衍生物N-甲基二苯并[c,g]咔唑(MeDBC)诱导的各种类型的DNA损伤。发现这两种衍生物诱导的DNA损伤谱差异与其化学结构有关,并取决于它们的代谢活化方式。不同的活化方式导致不同数量的单链断裂和DNA修饰,或者至少导致不同的常见修饰比例。DBC在人肝癌细胞系Hep G2中诱导的断裂水平最高,而MeDBC在稳定表达人细胞色素P4501A1的V79细胞系中诱导的断裂最多。我们的结果支持了DBC和MeDBC两种不同生物转化途径的观点。