Estrela J M, Gil F, Vila J M, Viña J
Departamento de Fisiología, Facultad de Medicina, Universidad de Valencia, Spain.
Am J Physiol. 1988 Dec;255(6 Pt 1):E801-5. doi: 10.1152/ajpendo.1988.255.6.E801.
Glutathione metabolism was studied in isolated hepatocytes from 48-h starved rats. Phenylephrine (10 microM, final concentration) was incubated in the presence of a mixture of L-glutamine, glycine, L-serine, and L-methionine (at 10 times their normal plasma concentration). Alpha-adrenergic stimulation provoked a decrease in glutathione (GSH) synthesis. This effect was accompanied by an enhanced efflux of glutathione from the cells. Phenylephrine stimulated the rate of glutathione disulfide (GSSG) formation; however, this effect was clearly insufficient to explain the disappearance of GSH. Our results suggest that the decrease in cellular GSH levels observed under conditions of shock, stress, or peripheral inflammation can be explained by a dual effect, i.e., an increase in glutathione efflux and an inhibition of its synthesis.
在48小时饥饿大鼠的分离肝细胞中研究了谷胱甘肽代谢。将去氧肾上腺素（终浓度10微摩尔）与L-谷氨酰胺、甘氨酸、L-丝氨酸和L-甲硫氨酸的混合物（浓度为正常血浆浓度的10倍）一起孵育。α-肾上腺素能刺激导致谷胱甘肽（GSH）合成减少。这种效应伴随着谷胱甘肽从细胞中的外流增加。去氧肾上腺素刺激了谷胱甘肽二硫化物（GSSG）的形成速率；然而，这种效应显然不足以解释GSH的消失。我们的结果表明，在休克、应激或外周炎症条件下观察到的细胞内GSH水平降低可以通过双重作用来解释，即谷胱甘肽外流增加和其合成受到抑制。
