Zlokovic B V, Mackic J B, McComb J G, Weiss M H, Kaplowitz N, Kannan R
Department of Neurological Surgery, Children's Hospital, Los Angeles, USC School of Medicine 90033.
Biochem Biophys Res Commun. 1994 May 30;201(1):402-8. doi: 10.1006/bbrc.1994.1715.
Using a vascular brain perfusion model in the guinea-pig, the net uptake of [35S]-GSH by the brain was found to be linear and similar in various regions during 10 min perfusion. Dual labeled [35S and 3H] GSH taken up by the brain had the same isotope ratio as the injected stock whether or not gamma- glutamyl transferase was inhibited. Greater than 96% of brain uptake of [35S]-cysteine-labeled GSH and [3H]-glycine-labeled GSH were in intact form. Transcytosis of [35S]-GSH from lumen into brain parenchyma was demonstrated using a capillary depletion technique. Both GSH and GSH-monoethyl ester inhibited [35S]-GSH transport. Thus, we have demonstrated blood-brain barrier extraction of circulating GSH in a brain perfusion model, and the transcytosis of intact GSH into the brain parenchyma without breakdown.
在豚鼠的血管脑灌注模型中，发现大脑对[35S]-谷胱甘肽（GSH）的净摄取在10分钟灌注期间呈线性，且在各个区域相似。无论γ-谷氨酰转移酶是否被抑制，大脑摄取的双标记[35S和3H] GSH与注射原液具有相同的同位素比率。大脑对[35S]-半胱氨酸标记的GSH和[3H]-甘氨酸标记的GSH的摄取中，超过96%为完整形式。使用毛细血管耗竭技术证明了[35S]-GSH从管腔向脑实质的转胞吞作用。GSH和GSH-单乙酯均抑制[35S]-GSH的转运。因此，我们在脑灌注模型中证明了循环GSH的血脑屏障摄取，以及完整GSH进入脑实质而不分解的转胞吞作用。
