DNA damage induced by endogenous aldehydes: Current state of knowledge

Georgia Persephoni Voulgaridou, Ioannis Anestopoulos, Rodrigo Franco-Cruz, Mihalis I. Panayiotidis, Aglaia Pappa

Research output: Contribution to journalReview article

142 Scopus citations

Abstract

DNA damage plays a major role in various pathophysiological conditions including carcinogenesis, aging, inflammation, diabetes and neurodegenerative diseases. Oxidative stress and cell processes such as lipid peroxidation and glycation induce the formation of highly reactive endogenous aldehydes that react directly with DNA, form aldehyde-derived DNA adducts and lead to DNA damage. In occasion of persistent conditions that influence the formation and accumulation of aldehyde-derived DNA adducts the resulting unrepaired DNA damage causes deregulation of cell homeostasis and thus significantly contributes to disease phenotype. Some of the most highly reactive aldehydes produced endogenously are 4-hydroxy-2-nonenal, malondialdehyde, acrolein, crotonaldehyde and methylglyoxal. The mutagenic and carcinogenic effects associated with the elevated levels of these reactive aldehydes, especially, under conditions of stress, are attributed to their capability of causing directly modification of DNA bases or yielding promutagenic exocyclic adducts. In this review, we discuss the current knowledge on DNA damage induced by endogenously produced reactive aldehydes in relation to the pathophysiology of human diseases.

Original languageEnglish (US)
Pages (from-to)13-27
Number of pages15
JournalMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Volume711
Issue number1-2
DOIs
StatePublished - Jun 3 2011

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Keywords

  • 4-Hydroxy-2-nonenal (4-HNE)
  • 4-Oxo-trans-2-nonenal (4-ONE)
  • Acetaldehyde (AA)
  • Acrolein
  • Aldehydes
  • Crotonaldehyde (Cr)
  • DNA damage
  • Formaldehyde (FA)
  • Glyceraldehyde (GA)
  • Glyoxal
  • Malondialdehyde (MDA)
  • Methylglyoxal (MG)
  • Oxidative stress

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Health, Toxicology and Mutagenesis

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