Biochemistry (Moscow)

, Volume 74, Issue 6, pp 589–598

Molecular mechanisms of homocysteine toxicity

Review

DOI: 10.1134/S0006297909060017

Cite this article as:
Boldyrev, A.A. Biochemistry Moscow (2009) 74: 589. doi:10.1134/S0006297909060017

Abstract

Hyperhomocysteinemia is a risk factor for a number of cardiovascular and neurodegenerative processes as well as a complicating factor in normal pregnancy. Toxic effects of homocysteine and the product of its spontaneous oxidation, homocysteic acid, are based on their ability to activate NMDA receptors, increasing intracellular levels of ionized calcium and reactive oxygen species. Even a short-term exposure of cells to homocysteic acid at concentrations characteristic of hyperhomocysteinemia induces their apoptotic transformation. The discovery of NMDA receptors both in neuronal tissue and in several other tissues and organs (including immunocompetent cells) makes them a target for toxic action of homocysteine. The neuropeptide carnosine was found to protect the organism from homocysteine toxicity. Treatment of pregnant rats with carnosine under conditions of alimentary hyperhomocysteinemia increases viability and functional activity of their progeny.

Key words

homocysteinehomocysteic acidNMDA receptorsneuronslymphocytesneutrophils

Abbreviations

DCF

2′,7′-dichlorodihydrofluorescein

fMLP

fMet-Leu-Phe

HC

homocysteine

HCA

homocysteic acid

ROS

reactive oxygen species

Copyright information

© Pleiades Publishing, Ltd. 2009

Authors and Affiliations

  1. 1.Biological FacultyLomonosov Moscow State UniversityMoscowRussia
  2. 2.Research Center of NeurologyRussian Academy of Medical SciencesMoscowRussia