Favilli F, Marraccini P, Iantomasi T, Vincenzini M T
Dipartimento di Scienze Biochimiche, Università di Firenze, Italy.
Br J Nutr. 1997 Aug;78(2):293-300. doi: 10.1079/bjn19970147.
The present study reports data on absorption of orally administered glutathione (GSH) in rat jejunum and in other organs, and the possible role of specific transport systems of GSH and gamma-glutamyltranspeptidase (EC 2.3.2.1; gamma-GT) activity. GSH levels were measured simultaneously in various organs after oral GSH administration to untreated rats and rats treated with L-buthionine sulfoximine (BSO) or acivicin (AT125). BSO selectively inhibits GSH intracellular synthesis and AT125 is a specific inhibitor of gamma-GT activity. GSH levels were also measured after oral administration of an equivalent amount of the constituent amino acids of GSH to untreated and BSO-treated rats. Significant increases in GSH levels were found in jejunum, lung, heart, liver and brain after oral GSH administration to untreated rats. GSH increases were also obtained in all organs, except liver, when GSH was administered to rats previously GHS-depleted by treatment with BSO. The analysis of all results allowed us to distinguish between the increase in GSH intracellular levels due to intact GSH uptake by specific transporters, and that due to GSH degradation by gamma-GT activity and subsequent absorption of degradation products with intracellular resynthesis of GSH; both these mechanisms seemed to be involved in increasing GSH content in heart after oral GSH administration. Jejunum, lung and brain took up GSH mostly intact, by specific transport systems, while in liver GSH uptake occurred only by its breakdown by gamma-GT activity followed by intracellular resynthesis.
本研究报告了口服谷胱甘肽（GSH）在大鼠空肠及其他器官中的吸收数据，以及GSH特定转运系统和γ-谷氨酰转肽酶（EC 2.3.2.1；γ-GT）活性的可能作用。在给未处理的大鼠以及用L-丁硫氨酸亚砜胺（BSO）或阿西维辛（AT125）处理的大鼠口服GSH后，同时测定各器官中的GSH水平。BSO选择性抑制GSH的细胞内合成，而AT125是γ-GT活性的特异性抑制剂。还对未处理和经BSO处理的大鼠口服等量GSH组成氨基酸后测定了GSH水平。给未处理的大鼠口服GSH后，空肠、肺、心脏、肝脏和大脑中的GSH水平显著升高。当给先前用BSO处理而使GSH耗竭的大鼠口服GSH时，除肝脏外，所有器官中的GSH水平也都有升高。对所有结果的分析使我们能够区分由于特定转运蛋白完整摄取GSH导致的GSH细胞内水平升高，以及由于γ-GT活性降解GSH并随后吸收降解产物并在细胞内重新合成GSH导致的升高；口服GSH后，这两种机制似乎都参与了心脏中GSH含量的增加。空肠、肺和大脑主要通过特定转运系统完整摄取GSH，而在肝脏中，GSH仅通过γ-GT活性将其分解，随后在细胞内重新合成来摄取。
