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自1963年初次报道同型胱氨酸尿症后,人们注意到这种病人有广泛的血管病变,常死于严重的动脉粥样硬化。造成血管病变的主要原因是同型半胱氨酸血症,而同型半胱氨酸则来自甲硫氨酸。所以有的学者提出,虽然脂类和糖代谢的异常是动脒粥样硬化已确定的危险因素,而蛋白质代谢的改变、过多摄入甲硫氨酸也可能是引起血管损伤的重要附加因素。甲硫氨酸是人体的必需氨基酸之一。它在体内先活化成S-腺苷甲硫氨酸(活性甲硫氨酸),供出甲基生成S-腺苷同型半胱氨酸,再水解成同型半胱氨酸和腺苷。同型半胱氨酸处于代谢分枝点上。它有两条去路:
Since the first report of homocystinuria in 1963, it has been observed that this patient has extensive vascular lesions and often dies of severe atherosclerosis. The main cause of vascular disease is homocysteine, while homocysteine is derived from methionine. Therefore, some scholars have suggested that while abnormalities in lipid and glucose metabolism are risk factors for the determination of amidine-induced atherosclerosis and changes in protein metabolism, excessive intake of methionine may also be an important additional factor causing vascular damage . Methionine is one of the essential amino acids in the body. It is activated in vivo to S-adenosylmethionine (an active methionine) for methyl generation to S-adenosylhomocysteine and then to homocysteine and adenosine. Homocysteine is at the metabolic branch point. It has two ways to go: