Brown P L, Jeffires C D
Infect Immun. 1975 Jan;11(1):8-13. doi: 10.1128/iai.11.1.8-13.1975.
The decrease in the level of liver glutathione (GSH) in endotoxin-treated mice was in part due to formation of glutathione disulfide (GSSG). An electron-generating system (EGS) had no effect when incubated with soluble liver extracts from normal controls but resulted in recovery of GSH amounting to 25% in endotoxin-treated animals. Incubation in the absence of the EGS caused a decline of 16% in the GSH in extracts from normal animals compared with a 50% decrease in endotoxin-treated animals. Exclusion of nicotinamide adenine dinucleotide phosphate (NADP) from the EGS resulted in a slight decline in the GSH of the extract from the normal controls but 25% for the endotoxin-treated animals. Reduction of exogenous GSSG by the liver extracts required that exogenous NADP be added to ghe incubation mixtures.
内毒素处理小鼠肝脏中谷胱甘肽（GSH）水平的降低部分归因于二硫化谷胱甘肽（GSSG）的形成。电子发生系统（EGS）与正常对照的可溶性肝脏提取物一起孵育时没有效果，但在内毒素处理的动物中可使GSH含量恢复至25%。在没有EGS的情况下孵育，正常动物提取物中的GSH下降了16%，而内毒素处理的动物下降了50%。从EGS中排除烟酰胺腺嘌呤二核苷酸磷酸（NADP）导致正常对照提取物中的GSH略有下降，但内毒素处理的动物下降了25%。肝脏提取物对外源性GSSG的还原需要向孵育混合物中添加外源性NADP。
