Antioxidant effects of Se-glutathione peroxidase in alcoholic liver disease

作者全名："Shen, Yingyan; Huang, Hanmei; Wang, Yunhong; Yang, Rongping; Ke, Xiumei"

作者地址："[Shen, Yingyan] Chengdu Univ Tradit Chinese Med, Key Lab Breeding Base Systemat Res & Utilizat Chin, Med Resources Cofounded Sichuan Prov & Minist Sci, Chengdu, Peoples R China; [Huang, Hanmei; Yang, Rongping] Southwest Univ, Chongqing Key Lab Chinese Med New Drug Screening, Chongqing, Peoples R China; [Wang, Yunhong] Chongqing Acad Chinese Mat Med, Chongqing, Peoples R China; [Ke, Xiumei] Chongqing Med Univ, Chongqing Key Lab Tradit Chinese Med Prevent & Cur, Chongqing, Peoples R China; [Yang, Rongping] Southwest Univ, 2 Tiansheng Rd, Chongqing 400715, Peoples R China; [Ke, Xiumei] Chongqing Med Univ, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China"

通信作者："Yang, RP (通讯作者)，Southwest Univ, 2 Tiansheng Rd, Chongqing 400715, Peoples R China.; Ke, XM (通讯作者)，Chongqing Med Univ, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China."

来源：JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY

ESI学科分类：BIOLOGY & BIOCHEMISTRY

WOS号：WOS:000848772000004

JCR分区：Q3

影响因子：3.5

年份：2022

卷号：74

期号：　

开始页：　

结束页：　

文献类型：Review

关键词：Alcoholic liver disease; Oxidative damage; Se; Glutathione peroxidase

摘要："Oxidative damage induced by ethanol and its metabolites is one of the factors that fuels the development of alcoholic liver disease (ALD). Selenium (Se) is an effective cofactor for glutathione peroxidase (GPx), and has antioxidant effects that improve ALD. In patients with ALD, ethanol-induced oxidative damage inhibits the synthesis of related Se-containing proteins such as: selenoprotein P (Sepp1), albumin (ALB), and GPx in the liver, thus decreasing the overall Se level in patients. Both Se deficiency and excess can affect the expression of GPx, resulting in damage to the antioxidant defense system. This damage enhances oxidative stress by increasing the levels of reactive oxygen species (ROS) in the body, which aggravates the inflammatory response, lipid meta-bolism disorder, and lipid peroxidation and worsens ALD symptoms. A cascade of oxidative damages caused by ALD will deplete selenium deposition in the body, stimulate the expression of Gpx1, Sepp1, and Gpx4, and thus mobilize systemic selenoproteins, which can restore GPx activity in the hepatocytes of ALD patients, reduce the levels of reactive oxygen species and alleviate oxidative stress, the inflammatory response, lipid metabolism disorder, and lipid peroxidation, thus helping to mitigate ALD. This review provides a reference for future ALD studies that evaluate the regulation of Se levels and contributes to studies on the potential pathological mech-anisms of Se imbalance in ALD."

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