防治高同型半胱氨酸血症的新策略

Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. At present, the main therapeutic provision is to supply vitamin B 6, B 12 and folic acids, and the toxic and ill effect have been reported. Homocysteine, taurine, hydrogen sulfide and metallothionein are metabolic products from methionine. Homocysteine induces necrosis of endothelium, proliferation of vascular smooth muscle cells, proliferation and activation of vascular fibroblast cells and mitochondrial structural destruction and dysfunction of myocardium cells. Taurine, an end metabolic product of homocysteine, obviously reduces cardiovascular injury induced by homocysteine. The possible mechanism of antagonism by reducing oxidative stress and endoplasmic reticulum stress has been proved. Hydrogen sulfide, another end metabolic product of homocysteine, obviously reducing cardiovascular injury of homocysteine by scavenging oxidative radicals has been found. Metallothionein a derivant production of homocysteine metabolism, antagonism to homocysteine injury to cardiovascular system been discussed. Homocysteine, taurine, hydrogen sulfide and metallothionein, as a metabolic product of methionine, interactive antagonism and interactive biological influence have been reviewed. Induced endogenous or exogenous supply of taurine, hydrogen sulfide and metallothionein might resist cardiovascular injury induced by hyperhomocysteinemia. According to the methionine metabolic cycle, using endogenous antagonistic substances might be a new clinical preventive and treatment target of homocystinemia.