ORAL-ADMINISTRATION OF HOMOCYSTEINE LEADS TO INCREASED PLASMA TRIGLYCERIDES AND HOMOCYSTEIC ACID - ADDITIONAL MECHANISMS IN HOMOCYSTEINE INDUCED ENDOTHELIAL DAMAGE

Increased plasma homocyst(e)ine is strongly correlated with occlusive arterial diseases. A series of different hypotheses have been reported including involvement of free oxygen radicals and therefore oxidative stress. We determined plasma homocyst(e)ine and homocysteic acid leve ls after oral low dose homocysteine thiolactone administration to rats for a period of six weeks plasma levels of homocyst(e)ine and triglyc erides were significantly elevated in the group fed homocysteine thiol actone. GC/MS determination of ketone body formation showed that the u nderlying mechanism for the increase of triglycerides seems to be inhi bition of fatty acid oxidation. Homocysteic acid was detected in the e xperimental group exclusively. The present study showing a homocyst(e) ine correlated increase of plasma triglycerides by the inhibition of f atty acid oxidation may well propose an additional role of triglycerid es for vascular pathology. The presence of homocysteic acid in the exp erimental group only would support the free oxygen radical hypothesis for the development of vascular changes but homocysteic acid as a pote nt neurotransmitter could play an independent role in the pathogenesis .