Endogenous formation and repair of oxidatively induced G[8-5 m]T intrastrand cross-link lesion.

Nucleic Acids Research
Jin WangYinsheng Wang

Abstract

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 γ-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.

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Citations

Dec 12, 2012·Antioxidants & Redox Signaling·Joost P M MelisMirjam Luijten
Feb 23, 2013·Mechanisms of Ageing and Development·James E CleaverEric J Huang
Dec 19, 2012·DNA Repair·Raffaele SaccoRebecca R Laposa
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Nov 25, 2020·Seminars in Cell & Developmental Biology·Gustavo Satoru KajitaniCarlos Frederico Martins Menck

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