Tsuji M, Kodama K, Oguchi K
Department of Pharmacology, School of Medicine, Showa University, Tokyo, Japan.
Jpn J Pharmacol. 1990 Jan;52(1):45-9. doi: 10.1254/jjp.52.45.
Effects of S-adenosyl-L-methionine disulfate tosylate salt (SAMe-ST) and L-methionine (L-Met) on rat erythrocytes and primary cultured hepatocytes were studied. SAMe-ST in concentrations of 0.2 to 5.0 mg/ml protected erythrocytes from hypotonic hemolysis. Almost an identical level of protection was provided by SAMe chloride, suggesting that this protective effect is due to the SAMe moiety itself but not its sulfate or tosylate moiety. L-Met also showed a slight protective effect, but at higher concentrations, it slightly enhanced hemolysis. When the cultured hepatocytes were treated with SAMe-ST, the leakage of enzymes from the hepatocytes were significantly decreased compared with that in the control. L-Met also showed similar protective effects, but to a lesser degree than in the case of SAMe-ST. SAMe-ST significantly increased Na+.K(+)-ATPase activity. The present results indicate that SAMe remarkably inhibits hypotonic hemolysis and enzyme leakage from cultured hepatocytes and that its mechanism is probably related to a change in the membrane property.
研究了对甲苯磺酸S-腺苷-L-蛋氨酸盐（SAMe-ST）和L-蛋氨酸（L-Met）对大鼠红细胞和原代培养肝细胞的影响。浓度为0.2至5.0mg/ml的SAMe-ST可保护红细胞免受低渗溶血。氯化SAMe提供了几乎相同水平的保护，这表明这种保护作用是由于SAMe部分本身，而不是其硫酸盐或对甲苯磺酸盐部分。L-Met也显示出轻微的保护作用，但在较高浓度下，它会轻微增强溶血作用。当用SAMe-ST处理培养的肝细胞时，与对照组相比，肝细胞的酶泄漏显著减少。L-Met也显示出类似的保护作用，但程度低于SAMe-ST。SAMe-ST显著增加了Na+.K(+)-ATP酶活性。目前的结果表明，SAMe显著抑制低渗溶血和培养肝细胞的酶泄漏，其机制可能与膜性质的改变有关。
