Dicarbonyl stress in cell and tissue dysfunction contributing to ageing and disease

Biochem Biophys Res Commun. 2015 Mar 6;458(2):221-6. doi: 10.1016/j.bbrc.2015.01.140. Epub 2015 Feb 7.


Dicarbonyl stress is the abnormal accumulation of dicarbonyl metabolites leading to increased protein and DNA modification contributing to cell and tissue dysfunction in ageing and disease. Enzymes metabolising dicarbonyls, glyoxalase 1 and aldoketo reductases, provide an efficient and stress-response enzyme defence against dicarbonyl stress. Dicarbonyl stress is produced by increased formation and/or decreased metabolism of dicarbonyl metabolites, and by exposure to exogenous dicarbonyls. It contributes to ageing, disease and activity of cytototoxic chemotherapeutic agents.

Keywords: Cardiovascular disease; Diabetes; Glycation; Hypoxia; Inflammation; Oxidative stress.

Publication types

  • Review

MeSH terms

  • Aging / metabolism*
  • Aldehydes / metabolism*
  • Cardiovascular Diseases / metabolism*
  • Deoxyglucose / analogs & derivatives
  • Deoxyglucose / metabolism
  • Diabetes Mellitus / metabolism*
  • Glyoxal / metabolism
  • Humans
  • Inflammation / metabolism*
  • Kidney Diseases / metabolism*
  • Models, Biological
  • Oxidative Stress
  • Pyruvaldehyde / metabolism
  • Stress, Physiological


  • Aldehydes
  • Glyoxal
  • Pyruvaldehyde
  • Deoxyglucose
  • 3-deoxyglucosone