On the high-Hyperhomocysteinemia and birth defects.docVIP

 PAGE \* MERGEFORMAT 15 On the high-Hyperhomocysteinemia and birth defects Paper Keywords birth defects; homocysteine; high hyperhomocysteinemia. Abstracts are the birth defects in babies born in any form of structure and function abnormalities, affecting the quality of the population is an important factor, in which the incidence of congenital heart disease top the list. Birth defects and abnormalities of homocysteine metabolism in the relationship between the more and more attention. In this paper, the metabolism of homocysteine, high production of hyperhomocysteinemia, homocysteine-induced birth defects in the mechanism of high-Hyperhomocysteinemia prevention and treatment of research are reviewed. In recent years, studies have shown that high-Hyperhomocysteinemia is induced by fetal blood vessel diseases and birth defects (birth defects BD) is an independent risk factor, and that of homocysteine (homocysteine HCY) metabolic abnormalities in children with congenital heart disease (congenital heart defects, CHD) in the pathogenesis plays an important role [1]. 1HCY metabolism HCY derived from dietary intake of methionine, is in the liver, muscle and other tissues generated by the demethylation of methionine as a sulfur-containing amino acid methionine in the body is almost all the tissues of metabolic intermediate, which has a number of substances in vivo a methyl group. HCY in the normal human body mainly in the form of the protein binding, free of HCY few. The specific metabolic processes are as follows: 1.1HCY re-methylation of methionine generated to complete the methionine cycle. In this process, HCY in the 5 - methyl-tetrahydrofolate transferase (also known as methionine synthase, MS) and methyl cobalamin (vitamin B12 in activated form) catalyzed by 5 - methyl - to provide methyl tetrahydrofolate, the reaction can occur in a variety of organizations. 5 - methyl-tetrahydrofolate from folic acid metabolism, from