Rossi M A, Pagliuca C, Flaccavento C, Torrielli M V
Boll Soc Ital Biol Sper. 1979 Sep 30;55(18):1870-6.
The content of hepatic GSH was evaluated in rats after poisoning with white phosphorus. In addition, liver damage following the administration of the hepatotoxin was assessed by determining hepatic triglyceride accumulation. Experiments in parallel were carried out in an attempt to evaluate the enhanced susceptibility of hepatic tissue to peroxidative decomposition of unsaturated lipids 'in vitro', as measured by the production of TBA-reacting substances. Our data indicate that only in the early stage of intoxication is it possible to detect a slight decrease of GSH content in the liver, while during the subsequent stages the concentration of GSH was unaffected. At 6 hours of intoxication the level of hepatic triglycerides was significantly increased. Pretreatment with GSH was followed by an amelioration of fatty infiltration, but the content of hepatic GSH was unchanged. The production of TBA-reacting products was found enhanced only at 6 hours of intoxication. These results are discussed in relation to the role of lipid peroxidation in liver injury by white phosphorus.
对用白磷中毒后的大鼠肝脏谷胱甘肽(GSH)含量进行了评估。此外,通过测定肝脏甘油三酯蓄积情况来评估给予肝毒素后肝脏的损伤。同时进行了实验,试图评估肝组织在“体外”对不饱和脂质过氧化分解的易感性增强情况,这通过硫代巴比妥酸反应性物质的产生来衡量。我们的数据表明,仅在中毒早期可检测到肝脏中GSH含量略有下降,而在随后阶段GSH浓度未受影响。中毒6小时时肝脏甘油三酯水平显著升高。用GSH预处理后脂肪浸润有所改善,但肝脏GSH含量未变。仅在中毒6小时时发现硫代巴比妥酸反应产物的产生增加。结合脂质过氧化在白磷所致肝损伤中的作用对这些结果进行了讨论。