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Reactive oxygen species (ROS) can be induced by both endogenous and exogenous processes, and they can damage biological molecules including nucleic acids. Exposure of isolated DNA to X/gamma-rays and Fenton reagents was shown to lead to the formation of intrastrand cross-link lesions where the neighboring nucleobases in the same DNA strand are covalently bonded. By employing HPLC coupled with tandem mass spectrometry (LC-MS/MS) with the isotope dilution method, we assessed quantitatively the formation of a guanine-cytosine (G[8-5]C) intrastrand cross-link lesion in HeLa-S3 cells upon exposure to gamma-rays. The yield of the G[8-5]C cross-link was 0.037 lesions per 10(9) nucleosides per Gy, which was approximately 300 times lower than that of 5-formyl-2'-deoxyuridine (0.011 lesions per 10(6) nucleosides per Gy) under identical exposure conditions. We further constructed a single-stranded M13 genome harboring a site-specifically incorporated G[8-5]C lesion and developed a novel mass spectrometry-based method for interrogating the products emanating from the replication of the genome in Escherichia coli cells. The results demonstrated that G[8-5]C blocked considerably DNA replication as represented by a 20% bypass efficiency, and the lesion was significantly mutagenic in vivo, which included a 8.7% G--&gt;T and a 1.2% G--&gt;C transversion mutations. DNA replication in E. coli hosts deficient in SOS-induced polymerases revealed that polymerase V was responsible for the error-prone translesion synthesis in vivo.

Formation and genotoxicity of a guanine–cytosine intrastrand cross-link lesion in vivo