Hydrogen sulfide (H 2S) may be endogenously produced by cystathionine β lyase (CBS) and cystathionine γ lyase (CSE) as a cardiovascular physiological functional factor. On the hypoxic pulmonary hypertension (HPH) an...Hydrogen sulfide (H 2S) may be endogenously produced by cystathionine β lyase (CBS) and cystathionine γ lyase (CSE) as a cardiovascular physiological functional factor. On the hypoxic pulmonary hypertension (HPH) animal model, the plasma H 2S concentration, the gene expression and the activity (CSE) were decreased in lung tissues In L -NAME induced hypertension and spontaneous hypertension rats (SHR) models, the plasma H 2S concentration, vascular CSE activity and mRNA expression were obviously decreased. When H 2S was exogenously supplied, systolic pressure obviously decrease. These studies suggested that CSE/H 2S pathway participated in the pathophysiological development of hypertension. The endogenous level of H 2S produced by some arterial tissues increased in both septic and endotoxic shock rats. The level of H 2S highly correlated with the endogenous level of NO These results suggest that H 2S may be a novel cardiovascular functional regulator.展开更多
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 reporte...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.展开更多
文摘Hydrogen sulfide (H 2S) may be endogenously produced by cystathionine β lyase (CBS) and cystathionine γ lyase (CSE) as a cardiovascular physiological functional factor. On the hypoxic pulmonary hypertension (HPH) animal model, the plasma H 2S concentration, the gene expression and the activity (CSE) were decreased in lung tissues In L -NAME induced hypertension and spontaneous hypertension rats (SHR) models, the plasma H 2S concentration, vascular CSE activity and mRNA expression were obviously decreased. When H 2S was exogenously supplied, systolic pressure obviously decrease. These studies suggested that CSE/H 2S pathway participated in the pathophysiological development of hypertension. The endogenous level of H 2S produced by some arterial tissues increased in both septic and endotoxic shock rats. The level of H 2S highly correlated with the endogenous level of NO These results suggest that H 2S may be a novel cardiovascular functional regulator.
文摘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.
