谷胱甘肽还原酶催化机制的生物物理数学模型。

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-10-09 DOI:10.1016/j.freeradbiomed.2013.10.001
Venkat R Pannala, Jason N Bazil, Amadou K S Camara, Ranjan K Dash
{"title":"谷胱甘肽还原酶催化机制的生物物理数学模型。","authors":"Venkat R Pannala,&nbsp;Jason N Bazil,&nbsp;Amadou K S Camara,&nbsp;Ranjan K Dash","doi":"10.1016/j.freeradbiomed.2013.10.001","DOIUrl":null,"url":null,"abstract":"<p><p>Glutathione reductase (GR) catalyzes the reduction of oxidized glutathione (GSSG) to reduced glutathione (GSH) using NADPH as the reducing cofactor, and thereby maintains a constant GSH level in the system. GSH scavenges superoxide (O2(*-)) and hydroxyl radicals (OH) nonenzymatically or by serving as an electron donor to several enzymes involved in reactive oxygen species (ROS) detoxification. In either case, GSH oxidizes to GSSG and is subsequently regenerated by the catalytic action of GR. Although the GR kinetic mechanism has been extensively studied under various experimental conditions with variable substrates and products, the catalytic mechanism has not been studied in terms of a mechanistic model that accounts for the effects of the substrates and products on the reaction kinetics. The aim of this study is therefore to develop a comprehensive mathematical model for the catalytic mechanism of GR. We use available experimental data on GR kinetics from various species/sources to develop the mathematical model and estimate the associated model parameters. The model simulations are consistent with the experimental observation that GR operates via both ping-pong and sequential branching mechanisms based on relevant concentrations of its reaction substrate GSSG. Furthermore, we show the observed pH-dependent substrate inhibition of GR activity by GSSG and bimodal behavior of GR activity with pH. The model presents a unique opportunity to understand the effects of products on the kinetics of GR. The model simulations show that under physiological conditions, where both substrates and products are present, the flux distribution depends on the concentrations of both GSSG and NADP(+), with ping-pong flux operating at low levels and sequential flux dominating at higher levels. The kinetic model of GR may serve as a key module for the development of integrated models for ROS-scavenging systems to understand protection of cells under normal and oxidative stress conditions.</p>","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1385-1397"},"PeriodicalIF":0.0000,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.10.001","citationCount":"29","resultStr":"{\"title\":\"A biophysically based mathematical model for the catalytic mechanism of glutathione reductase.\",\"authors\":\"Venkat R Pannala,&nbsp;Jason N Bazil,&nbsp;Amadou K S Camara,&nbsp;Ranjan K Dash\",\"doi\":\"10.1016/j.freeradbiomed.2013.10.001\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Glutathione reductase (GR) catalyzes the reduction of oxidized glutathione (GSSG) to reduced glutathione (GSH) using NADPH as the reducing cofactor, and thereby maintains a constant GSH level in the system. GSH scavenges superoxide (O2(*-)) and hydroxyl radicals (OH) nonenzymatically or by serving as an electron donor to several enzymes involved in reactive oxygen species (ROS) detoxification. In either case, GSH oxidizes to GSSG and is subsequently regenerated by the catalytic action of GR. Although the GR kinetic mechanism has been extensively studied under various experimental conditions with variable substrates and products, the catalytic mechanism has not been studied in terms of a mechanistic model that accounts for the effects of the substrates and products on the reaction kinetics. The aim of this study is therefore to develop a comprehensive mathematical model for the catalytic mechanism of GR. We use available experimental data on GR kinetics from various species/sources to develop the mathematical model and estimate the associated model parameters. The model simulations are consistent with the experimental observation that GR operates via both ping-pong and sequential branching mechanisms based on relevant concentrations of its reaction substrate GSSG. Furthermore, we show the observed pH-dependent substrate inhibition of GR activity by GSSG and bimodal behavior of GR activity with pH. The model presents a unique opportunity to understand the effects of products on the kinetics of GR. The model simulations show that under physiological conditions, where both substrates and products are present, the flux distribution depends on the concentrations of both GSSG and NADP(+), with ping-pong flux operating at low levels and sequential flux dominating at higher levels. The kinetic model of GR may serve as a key module for the development of integrated models for ROS-scavenging systems to understand protection of cells under normal and oxidative stress conditions.</p>\",\"PeriodicalId\":505743,\"journal\":{\"name\":\"Free radical biology & medicine\",\"volume\":\" \",\"pages\":\"1385-1397\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2013-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.10.001\",\"citationCount\":\"29\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Free radical biology & medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.freeradbiomed.2013.10.001\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2013/10/9 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Free radical biology & medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.freeradbiomed.2013.10.001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2013/10/9 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 29

摘要

谷胱甘肽还原酶(GR)利用NADPH作为还原辅助因子,催化氧化谷胱甘肽(GSSG)还原为还原性谷胱甘肽(GSH),从而维持系统中恒定的谷胱甘肽水平。谷胱甘肽非酶性清除超氧化物(O2(*-))和羟基自由基(OH)或作为参与活性氧(ROS)解毒的几种酶的电子供体。在这两种情况下,谷胱甘肽都会氧化为GSSG,并随后在GR的催化作用下再生。尽管在不同底物和产物的各种实验条件下,对GR的动力学机制进行了广泛的研究,但还没有一个能解释底物和产物对反应动力学影响的机理模型来研究其催化机理。因此,本研究的目的是为GR的催化机理建立一个综合的数学模型。我们使用来自不同物种/来源的GR动力学实验数据来建立数学模型并估计相关的模型参数。模型模拟结果与实验观察结果一致,GR通过乒乓和顺序分支机制进行反应,该机制基于其反应底物GSSG的相关浓度。此外,我们还展示了观察到的ph依赖性底物GSSG对GR活性的抑制以及GR活性随ph的双峰行为。该模型为理解产物对GR动力学的影响提供了独特的机会。模型模拟表明,在底物和产物同时存在的生理条件下,通量分布取决于GSSG和NADP(+)的浓度。乒乓通量在低水平起作用,顺序通量在高水平起主导作用。GR的动力学模型可以作为开发ros清除系统综合模型的关键模块,以了解正常和氧化应激条件下细胞的保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

A biophysically based mathematical model for the catalytic mechanism of glutathione reductase.

A biophysically based mathematical model for the catalytic mechanism of glutathione reductase.

A biophysically based mathematical model for the catalytic mechanism of glutathione reductase.

A biophysically based mathematical model for the catalytic mechanism of glutathione reductase.

Glutathione reductase (GR) catalyzes the reduction of oxidized glutathione (GSSG) to reduced glutathione (GSH) using NADPH as the reducing cofactor, and thereby maintains a constant GSH level in the system. GSH scavenges superoxide (O2(*-)) and hydroxyl radicals (OH) nonenzymatically or by serving as an electron donor to several enzymes involved in reactive oxygen species (ROS) detoxification. In either case, GSH oxidizes to GSSG and is subsequently regenerated by the catalytic action of GR. Although the GR kinetic mechanism has been extensively studied under various experimental conditions with variable substrates and products, the catalytic mechanism has not been studied in terms of a mechanistic model that accounts for the effects of the substrates and products on the reaction kinetics. The aim of this study is therefore to develop a comprehensive mathematical model for the catalytic mechanism of GR. We use available experimental data on GR kinetics from various species/sources to develop the mathematical model and estimate the associated model parameters. The model simulations are consistent with the experimental observation that GR operates via both ping-pong and sequential branching mechanisms based on relevant concentrations of its reaction substrate GSSG. Furthermore, we show the observed pH-dependent substrate inhibition of GR activity by GSSG and bimodal behavior of GR activity with pH. The model presents a unique opportunity to understand the effects of products on the kinetics of GR. The model simulations show that under physiological conditions, where both substrates and products are present, the flux distribution depends on the concentrations of both GSSG and NADP(+), with ping-pong flux operating at low levels and sequential flux dominating at higher levels. The kinetic model of GR may serve as a key module for the development of integrated models for ROS-scavenging systems to understand protection of cells under normal and oxidative stress conditions.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信