Sakaida I, Nagatomi A, Okita K
First Department of Internal Medicine, School of Medicine, Yamaguchi University, Japan.
J Gastroenterol. 1996 Oct;31(5):684-90. doi: 10.1007/BF02347617.
The killing of cultured hepatocytes by cyanide accelerated phospholipid metabolism, with a reduction in cytoplasmic pH, but did not accelerate proteolysis. Alkalinization of the cytoplasm by monensin, a protonsodium exchange ionophore, enhanced the loss of viability and acceleration of phospholipid metabolism caused by cyanide. Thus, acidification of the cytoplasm appears to protect against the toxic effects of cyanide. Glycine reduced the killing of hepatocytes, concomitant with reduced phospholipid metabolism. The protective effect of glycine neither enhanced the reduction in cytoplasmic pH nor prevented the depletion of adenosine triphosphate (ATP) by cyanide. The mechanism of the protection exerted by glycine against chemical ischemia can be attributed neither to changes in cytoplasmic pH nor to the prevention of ATP depletion, but appears to be due to other mechanisms that have yet to be identified.
氰化物对培养的肝细胞的杀伤作用加速了磷脂代谢，同时细胞质pH值降低，但并未加速蛋白质水解。莫能菌素（一种质子-钠交换离子载体）使细胞质碱化，增强了氰化物导致的细胞活力丧失和磷脂代谢加速。因此，细胞质酸化似乎可抵御氰化物的毒性作用。甘氨酸减少了肝细胞的杀伤，同时伴随着磷脂代谢的降低。甘氨酸的保护作用既未增强细胞质pH值的降低，也未阻止氰化物导致的三磷酸腺苷（ATP）耗竭。甘氨酸对化学性缺血的保护机制既不能归因于细胞质pH值的变化，也不能归因于对ATP耗竭的预防，而似乎是由于尚未确定的其他机制。
