Effects of urease-induced hyperammonemia in mouse liver
Effects of urease-induced hyperammonemia in mouse liver
复制标题
DOI：
10.1007/bf02890308
复制
发表时间：
1984
期刊：
影响因子：
--
通讯作者：
J. O'connor;J. Renau‐Piqueras;S. Grisolía
中科院分区：
文献类型：
--
作者：
J. O'connor;J. Renau‐Piqueras;S. Grisolía
腹腔注射尿素酶可引起小鼠明显而持续的高氨血症。尿素酶处理小鼠肝细胞的超微结构和体视学分析显示，线粒体、粗面内质网、滑面内质网和溶酶体发生了显著变化。因此，线粒体变得更大，更圆，并包含一个较低的电子密度矩阵，虽然它们的体积密度保持类似于对照细胞。此外，还观察到平滑和粗面网以及溶酶体隔室增加。尿素酶处理的小鼠肝脏的生化分析显示，细胞内的水和lipids.Although氨诱导这些变化的机制尚不清楚，这些发现和那些在人类和实验动物的肝脏中所描述的持续高氨血症的条件下的可能的关系进行了讨论。
Intraperitoneal injections of urease induced a marked and sustained hyperammonemia in mice. Ultrastructural and stereologic analysis of hepatocytes from urease-treated mice showed striking changes in the mitochondria, rough and smooth endoplasmic reticulum and lysosomes. Thus, mitochondria became larger and rounder, and contained a less electron-dense matrix although their volume density remained similar to that of control cells. In addition, increases in the smooth and rough reticulum and the lysosomal compartment, were observed. Biochemical analysis of the livers from urease-treated mice revealed a significant increase in the intracellular content of water and lipids.Although the mechanism by which ammonia induces these changes remains unclear, the possible relationship between these findings and those described in the liver of humans and experimental animals in conditions of sustained hyperammonemia is discussed.