The role of phospholipid metabolism in bromobenzene- and carbon tetrachloride-dependent hepatocyte injury.
The role of phospholipid metabolism in bromobenzene- and carbon tetrachloride-dependent hepatocyte injury.
复制标题
磷脂代谢在溴苯和四氯化碳依赖性肝细胞损伤中的作用。
DOI：
10.1016/0041-008x(84)90187-x
复制
发表时间：
1984
影响因子：
3.8
通讯作者：
McGuffin,MA
中科院分区：
文献类型：
--
作者：
Lamb,RG;McCue,SB;Taylor,DR;McGuffin,MA
Sprague-Dawley rats and cultured rat hepatocytes exposed to bromobenzene (BB) and carbon tetrachloride (CCl4) display rapid and significant increases and decreases in hepatic phospholipase C (PLC) and sn-glycerol-3-phosphate acyltransferase (GPAT) activities, respectively. Primary cultures of adult rat hepatocytes were used to determine if the BB- and CCl4-dependent alterations in phospholipid metabolism were related to the hepatotoxicity of these agents. Cultured hepatocytes exposed to BB and CCl4exhibited a rapid (1 to 5 min), PLC-mediated reduction (20 to 80%) in [32P]phosphatidylserine content. Other phospholipids were also reduced; however, phosphatidylserine was preferentially degraded by hepatotoxin-activated PLC. A time course of CCl4-and BB-induced cellular events showed that these agents (1) rapidly activate liver cell PLC activity; (2) accelearate86Rb release; (3) decrease GPAT acyltransferase activity; and (4) cause a release of intracellular enzymes (GOT and GPT). All of these BB- and CCl4-mediated effects on the functional integrity of liver cells were blocked or reduced by agents (EDTA and chlorpromazine) that reduce the BB- and CCl4-dependent rise in PLC activity. Therefore, BB- and CCl4-dependent alterations in the functional and structural integrity of liver cells may be a result of accelerated phospholipid degradation and a corresponding inability of the cell to repair injured membranes by generating new phospholipids.
