Wang Jianshuang, Wang Yinsheng
Department of Chemistry, University of California, Riverside, CA 92521-0403, USA.
Nucleic Acids Res. 2009 Feb;37(2):336-45. doi: 10.1093/nar/gkn946. Epub 2008 Nov 28.
Humans are exposed to N-nitroso compounds from both endogenous and exogenous sources. Many N-nitroso compounds can be metabolically activated to give diazoacetate, which can result in the carboxymethylation of DNA. The remarkable similarity in p53 mutations found in human gastrointestinal tumors and in shuttle vector studies, where the human p53 gene-containing vector was treated with diazoacetate and propagated in yeast cells, suggests that diazoacetate might be an important etiological agent for human gastrointestinal tumors. The O(6)-carboxymethyl-2'-deoxyguanosine was previously detected in isolated DNA upon exposure to diazoacetate and in blood samples of healthy human subjects. The corresponding modifications of thymidine and 2'-deoxyadenosine have not been assessed, though significant mutations at A:T base pairs were found in the p53 tumor suppressor gene in human gastrointestinal tumors and in shuttle vector studies. To understand the implications of the carboxymethylation chemistry of thymidine in the observed mutations at A:T base pairs, here we synthesized authentic N3-carboxymethylthymidine (N3-CMdT) and O(4)-carboxymethylthymidine (O(4)-CMdT), incorporated them into DNA, and demonstrated, for the first time, that they were the major carboxymethylated derivatives of thymidine formed in calf thymus DNA upon exposure to diazoacetate. The demonstration of the formation of N3-CMdT and O(4)-CMdT in isolated DNA upon treatment with diazoacetate, together with the preparation of authentic oligodeoxyribonucleotide substrates housing these two lesions, laid the foundation for investigating the replication and repair of these lesions and for understanding their implications in the mutations observed in human gastrointestinal tumors.
人类会通过内源性和外源性来源接触到N-亚硝基化合物。许多N-亚硝基化合物可经代谢激活生成重氮乙酸酯,这可能导致DNA的羧甲基化。在人类胃肠道肿瘤中发现的p53突变与穿梭载体研究中的显著相似性表明,重氮乙酸酯可能是人类胃肠道肿瘤的一种重要病因。在穿梭载体研究中,将含有人p53基因的载体用重氮乙酸酯处理并在酵母细胞中繁殖。此前在分离的DNA暴露于重氮乙酸酯时以及健康人类受试者的血液样本中检测到了O(6)-羧甲基-2'-脱氧鸟苷。虽然在人类胃肠道肿瘤和穿梭载体研究中,在p53肿瘤抑制基因中发现了A:T碱基对处的显著突变,但尚未评估胸苷和2'-脱氧腺苷的相应修饰。为了了解胸苷羧甲基化化学在A:T碱基对处观察到的突变中的意义,我们在此合成了真实的N3-羧甲基胸苷(N3-CMdT)和O(4)-羧甲基胸苷(O(4)-CMdT),将它们掺入DNA中,并首次证明它们是小牛胸腺DNA暴露于重氮乙酸酯时形成的胸苷的主要羧甲基化衍生物。在用重氮乙酸酯处理后在分离的DNA中形成N3-CMdT和O(4)-CMdT的证明,以及包含这两种损伤的真实寡脱氧核糖核苷酸底物的制备,为研究这些损伤的复制和修复以及理解它们在人类胃肠道肿瘤中观察到的突变中的意义奠定了基础。