马维兴,雷质文,唐 静,马 云,贾俊涛,赵丽青,林 超,晏良军,刘均洪.葡萄糖诱导的线粒体蛋白氧化应激及调控机制概述[J].食品安全质量检测学报,2020,11(3):715-720
葡萄糖诱导的线粒体蛋白氧化应激及调控机制概述
Overview of regulation mechanism of mitochondrial proteins on glucose-induced oxidative stress
投稿时间:2019-10-21  修订日期:2020-01-13
DOI:
中文关键词:  能量代谢  葡萄糖  线粒体  氧化应激  蛋白质
英文关键词:energy metabolism  glucose  mitochondria  oxidative stress  proteins
基金项目:山东检验检疫局科研项目(SK201705)
作者单位
马维兴 青岛海关技术中心;北得州大学健康科学中心药学院;青岛科技大学化工学院 
雷质文 青岛海关技术中心 
唐 静 青岛海关技术中心 
马 云 青岛海关技术中心 
贾俊涛 青岛海关技术中心 
赵丽青 青岛海关技术中心 
林 超 青岛海关技术中心 
晏良军 北得州大学健康科学中心药学院 
刘均洪 青岛科技大学化工学院 
AuthorInstitution
MA Wei-Xing Technical Center of Qingdao Customs;Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center;College of Chemical Engineering, Qingdao University of Science and Technology 
LEI Zhi-Wen Technical Center of Qingdao Customs 
TANG Jing Technical Center of Qingdao Customs 
MA Yun Technical Center of Qingdao Customs 
JIA Jun-Tao Technical Center of Qingdao Customs 
ZHAO Li-Qing Technical Center of Qingdao Customs 
LIN Chao Technical Center of Qingdao Customs 
YAN Liang-Jun Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center 
LIU Jun-Hong College of Chemical Engineering, Qingdao University of Science and Technology 
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中文摘要:
      食品中的葡萄糖是人体细胞获取能量的重要来源, 细胞中的线粒体是重要的能量代谢场所, 在维持人体正常生理代谢功能中起重要作用。但葡萄糖代谢异常会导致线粒体功能紊乱, 这是通过葡萄糖诱导的氧化应激导致的线粒体蛋白功能异常, 进而引发相关疾病, 例如糖尿病、阿尔茨海默症和脑中风。所以维持线粒体生理功能, 研究氧化应激调控机制, 探究相关疾病更有效的治疗手段至关重要。本文综述了氧化应激涉及的主要线粒体蛋白(包括顺乌头酸酶、腺嘌呤核苷酸转位酶、二氢硫辛酰胺脱氢酶、线粒体蛋白复合物I、雌激素受体β、热休克转录因子1和缺氧诱导因子2α)、氧化应激调控机制(包括丙酮酸调节、线粒体蛋白之间的协同调节)和人工干预过程(包括乙醇戒断、亚甲蓝作电子受体和5-甲氧基吲哚-2-羧酸预处理)。
英文摘要:
      The glucose ingested from food is the critical resource of energy acquisition for human cells. Mitochondria, as a vital organelle for energy metabolism in cells, plays an important role in maintaining normal metabolic processes. However, aberrant glucose metabolism can lead to mitochondrial dysfunction, which is a mitochondrial proteins dysfunction caused by glucose-induced oxidative stress and then contributes to related diseases such as diabetes mellitus, Alzheimer's disease and stroke. Therefore, maintaining mitochondrial metabolic processes and investigating the regulation mechanism on oxidative stress is crucial to exploring more efficient approaches to treatment of related diseases. This paper summarized the major mitochondrial proteins (including aconitase, adenine nucleotide translocase, dihydrolipoamide dehydrogenase, mitochondrial complex I, estrogen receptor β, heat shock transcription factor 1 and hypoxia-inducible factor 2α), and elaborated the regulation mechanism on oxidative stress (including pyruvate regulation and synergistic regulation of related mitochondrial proteins) as well as manual intervention process (including Ethanol Withdrawal, methylene blue as an electron acceptor and 5-methoxyindole-2-carboxylic acid pre-conditioning).
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