谷胱甘肽(GSH)和抗坏血酸(维生素C)化合物对绵羊肝脏中纯化的葡萄糖-6-磷酸脱氢酶(G6PD)酶的抑制作用。

IF 2.7 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Zehra Bas, Vedat Turkoglu
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引用次数: 0

摘要

目的:葡萄糖-6-磷酸脱氢酶(G6PD)是一种具有多种重要生化功能的酶。然而,在各种癌症疾病中,G6PD活性的增加导致癌细胞生长,因此G6PD抑制剂已成为癌症治疗的一个重要研究领域。材料和方法:用亲和层析法从羊肝脏中提取2',5'-ADP Sepharose 4B,纯化G6PD 4530倍。探讨还原型谷胱甘肽(GSH)和抗坏血酸(维生素C)对G6PD活性的影响。结果与讨论:GSH和抗坏血酸对G6PD有显著抑制作用,IC50值分别为0.37µM和34.66µM。Lineweaver-Burk图显示,这些化合物的抑制类型为非竞争性抑制。计算GSH和抗坏血酸的Ki值分别为0.48µM和30.47µM。结论:本研究观察到谷胱甘肽和抗坏血酸抗氧化化合物对G6PD具有抑制作用,可能具有保护和预防癌症的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The inhibitory impact of glutathione (GSH) and ascorbic acid (vitamin C) compounds on glucose-6-phosphate dehydrogenase (G6PD) enzyme purified from sheep liver.

Objective: Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme with many essential biochemical functions. However, in various cancer diseases, increased activity of G6PD causes cancer cells to grow, so G6PD inhibitors have become a significant area of research in cancer treatment.

Materials and methods: Here, G6PD was purified 4530-fold with affinity chromatography using 2',5'-ADP Sepharose 4B from sheep liver. The effects of reduced glutathione (GSH) and ascorbic acid (vitamin C) on G6PD activity were explored.

Results and discussion: GSH and ascorbic acid showed a significant inhibitory effect on G6PD, and IC50 values were found as 0.37 µM and 34.66 µM, respectively. The inhibition type from Lineweaver-Burk plots of these compounds was identified as non-competitive inhibition. The Ki values of GSH and ascorbic acid were calculated as 0.48 µM and 30.47 µM, respectively.

Conclusion: In this study, it was observed that GSH and ascorbic acid antioxidant compounds exhibit an inhibitory effect on G6PD and may be protective and preventive against cancer.

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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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