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半乳糖胺诱导的肝细胞死亡中早期可逆的质膜损伤

Early, reversible plasma membrane injury in galactosamine-induced liver cell death.

作者信息

El-Mofty S K, Scrutton M C, Serroni A, Nicolini C, Farber J L

出版信息

Am J Pathol. 1975 Jun;79(3):579-96.

Abstract

Administration to rats of D-galactosamine (400 mg/kg) produces liver cell death that develops during the first 24 hours. Plasma membranes isolated within the first few hours from these animals show a 40% reduction in 5'-nucleotidase activity and a two-fold increase in maximum negative ellipticity determined by circular dichroism. Simultaneous administration of uridine prevents liver cell death and these early alterations in the plasma membranes. Uridine also prevents cell death if administered for up to 3 hours after galactosamine. The 5'nucleotidase activity reduced when uridine is administered for up to 2-1/2 hours after galactosamine. Changes in the liver calcium ion concentration accompany these plasma membrane alterations. Uridine will prevent and reverse the changes in calcium content in parallel to its ability to reverse the membrane alterations. The significance of these findings with respect to the mechanism of galactosamine-induced liver cell death is discussed.

摘要

给大鼠注射D-半乳糖胺(400毫克/千克)会导致肝细胞死亡,这种死亡在最初24小时内发生。在最初几个小时内从这些动物身上分离出的质膜显示,5'-核苷酸酶活性降低了40%,并且通过圆二色性测定的最大负椭圆率增加了两倍。同时给予尿苷可防止肝细胞死亡以及质膜的这些早期变化。如果在给予半乳糖胺后长达3小时内给予尿苷,也可防止细胞死亡。在给予半乳糖胺后长达2.5小时内给予尿苷,5'-核苷酸酶活性会降低。这些质膜变化伴随着肝脏钙离子浓度的变化。尿苷能够防止并逆转钙含量的变化,这与其逆转膜变化的能力是并行的。文中讨论了这些发现对于半乳糖胺诱导肝细胞死亡机制的意义。

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Mechanisms of cell death in acute liver failure.急性肝衰竭中的细胞死亡机制。
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