X-Message-Number: 13999
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 

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