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Endogenous formation and repair of oxidatively induced g (8-5m) T intrastrand cross-link lesion

Academic Article
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Overview

authors

  • Wang, J.
  • Cao, H. C.
  • You, C. J.
  • Yuan, B. F.
  • Bahde, R.
  • Gupta, S.
  • Nishigori, C.
  • Niedernhofer, Laura
  • Brooks, P. J.
  • Wang, Y. S.

publication date

  • August 2012

journal

  • Nucleic Acids Research  Journal

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 ?-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.
  • 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.

subject areas

  • Animals
  • DNA
  • DNA Damage
  • DNA Repair
  • Guanine
  • Hepatolenticular Degeneration
  • Humans
  • Liver
  • Mice
  • Oxidation-Reduction
  • Rats
  • Thymine
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Identity

PubMed Central ID

  • PMC3424544

International Standard Serial Number (ISSN)

  • 0305-1048

Digital Object Identifier (DOI)

  • 10.1093/nar/gks357

PubMed ID

  • 22581771
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Additional Document Info

start page

  • 7368

end page

  • 7374

volume

  • 40

issue

  • 15

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