2016, Number 1
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RCAN 2016; 26 (1)
On the metabolism of homocysteine. Implications for nutrition
Rosabal NEL
Language: Spanish
References: 70
Page: 157-171
PDF size: 424.20 Kb.
ABSTRACT
Homocysteine (Hcy) is a risk factor for
endothelial damage and ischemic disease
independent in its behavior from other
traditional ones such as serum lipids.
Homocysteine originates from metionine within
alternate metabolic routes of transsulfuration
and remethylation. Defficient folate states
represent an important cause of
hyperhomocisteinemia. Hyperhomocisteinemia is
associated with increased incidence of
myocardial infarction, vascular (arterial |
venous) thrombosis, and other territorial |
systemic ischemic accidents. Supplementation
with folic acid is the main nutritional
intervention in the hyperhomocisteinemia states.
Consumption of folic acid “megadoses” might
result in reduction of Hcy serum levels without
affecting the rate of DNA methylation: an event
implicated in thrombotic damage. Evidences
accumulated up to this day are not conclusive
regarding the benefits of folic acid
supplementation upon incidence of ischemic
and/or thrombotic episodes.
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