| First Author | Wang J | Year | 2012 |
| Journal | Nucleic Acids Res | Volume | 40 |
| Issue | 15 | Pages | 7368-74 |
| PubMed ID | 22581771 | Mgi Jnum | J:197766 |
| Mgi Id | MGI:5494512 | Doi | 10.1093/nar/gks357 |
| Citation | Wang J, et al. (2012) Endogenous formation and repair of oxidatively induced G[8-5 m]T intrastrand cross-link lesion. Nucleic Acids Res 40(15):7368-74 |
| abstractText | Exposure to reactive oxygen species (ROS) can give rise to the formation of various DNA damage products. Among them, d(G[8-5 m]T) can be induced in isolated DNA treated with Fenton reagents and in cultured human cells exposed to gamma-rays, d(G[8-5m]T) can be recognized and incised by purified Escherichia coli UvrABC nuclease. However, it remains unexplored whether d(G[8-5 m]T) accumulates in mammalian tissues and whether it is a substrate for nucleotide excision repair (NER) in vivo. Here, we found that d(G[8-5 m]T) could be detected in DNA isolated from tissues of healthy humans and animals, and elevated endogenous ROS generation enhanced the accumulation of this lesion in tissues of a rat model of Wilson's disease. Additionally, XPA-deficient human brain and mouse liver as well as various types of tissues of ERCC1-deficient mice contained higher levels of d(G[8-5 m]T) but not ROS-induced single-nucleobase lesions than the corresponding normal controls. Together, our studies established that d(G[8-5 m]T) can be induced endogenously in mammalian tissues and constitutes a substrate for NER in vivo. |
