X-Message-Number: 13999 From: Date: Sat, 24 Jun 2000 22:13:37 EDT Subject: telomeres and homocysteine If these guys are right (and if they used a physiological level of homocysteine in their in vitro experiment) then the blood homocysteine level might be even more important than formerly believed. Not only does homocysteine cause atherosclerosis (this is already established by other work), but it might cause other cells to age. The good news is that homocysteine level is easily controlled in most people with vitamins and trimethylglycine; the bad news is that you don't know what the levels are without blood tests, and some people need more supplementation than others. There are good clinical tests for homocysteine, but most doctors still don't know why they should order them. (I think it costs about $70 to buy the test yourself, so it's not really a problem for the motivated person. Guess I'll have to spring for one; right now I just take a moderate dose of TMG and hope for the best... not very scientific.) ------------------------------------------------------------------------ 1:FEBS Lett 2000 Mar 17;470(1):20-4 Homocysteine accelerates endothelial cell senescence. Xu D, Neville R, Finkel T Laboratory of Molecular Biology, NHLBI, NIH, Bldg 10/7B-15, 10 Center Drive, Bethesda, MD 20892-1650, USA. In this study we demonstrate that exposure of cultured endothelial cells to homocysteine significantly accelerates the rate of endothelial senescence. Examination of telomere length demonstrates that homocysteine increases the amount of telomere length lost per population doubling. The effects of homocysteine on both senescence and telomere length are inhibited by treatment with the peroxide scavenger catalase. Chronic exposure of endothelial cells to homocysteine also increases the expression of two surface molecules linked to vascular disease, intracellular adhesion molecule-1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1). Interestingly, the level of expression of both ICAM-1 and PAI-1 correlates with the degree of endothelial senescence. Taken together, these results suggest that homocysteine accelerates the rate of cellular senescence through a redox-dependent pathway. In addition, it suggests that chronic oxidative stress in the vessel wall may hasten the rate of senescence and that the senescent endothelial cell may in turn be pro-atherogenic. PMID: 10722838, UI: 20189826 Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=13999