Homocysteine and endothelial dysfunction: a link with cardiovascular disease

J Nutr. 2000 Feb;130(2S Suppl):369S-372S. doi: 10.1093/jn/130.2.369S.

Abstract

The nature of the link between homocysteine and cardiovascular disease has not yet been clearly established. Impaired endothelium-independent vasodilatation is an early feature of vascular disease. In human studies, methionine loading, which acutely elevates plasma homocysteine, induces endothelial dysfunction. Folate therapy, which lowers homocysteine, enhances endothelial function. This is consistent with, but not proof of, homocysteine toxicity to endothelium in vivo. Homocysteine, in high concentration, can induce endothelial dysfunction in vitro. This is accompanied by increased superoxide production, which when inhibited, restores normal endothelial function. These observations suggest that homocysteine may induce vascular endothelial dysfunction by a mechanism involving reactive oxygen species.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cardiovascular Diseases / chemically induced*
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / metabolism*
  • Folic Acid / therapeutic use
  • Homocysteine / adverse effects*
  • Homocysteine / blood
  • Humans
  • Methionine / blood
  • Methionine / metabolism
  • Reactive Oxygen Species / metabolism

Substances

  • Reactive Oxygen Species
  • Homocysteine
  • Folic Acid
  • Methionine