Oxidative stress, antioxidants and intestinal calcium absorption
作者机构：Laboratorio“Dr.Fernando Canas”Cátedra de Bioquímica y Biología MolecularFacultad de Ciencias MédicasINICSA(CONICET-Universidad Nacional de Córdoba)Pabellón ArgentinaCiudad UniversitariaCórdoba 5000Argentina
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2017年第23卷第16期
页 面：2841-2853页
核心收录：
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
基 金：Supported by Dr.Nori Tolosa de Talamoni from CONICET No.PIP 2013-2015 and No.SECYT(UNC)2016 Argentina
主 题：Transcellular and paracellular Ca2+pathways DL-buthionine-S R-sulfoximine Menadione Sodium deoxycholate Lithocholic acid Ursodeoxycholic acid Melatonin
摘 要：The disequilibrium between the production of reactive oxygen(ROS) and nitrogen(RNS) species and their elimination by protective mechanisms leads to oxidative stress. Mitochondria are the main source of ROS as by-products of electron transport chain. Most of the time the intestine responds adequately against the oxidative stress, but with aging or under conditions that exacerbate the ROS and/or RNS production, the defenses are not enough and contribute to developing intestinal pathologies. The endogenous antioxidant defense system in gut includes glutathione(GSH) and GSH-dependent enzymes as major components. When the ROS and/or RNS production is exacerbated, oxidative stress occurs and the intestinal Ca2+ absorption is inhibited. GSH depleting drugs such as DLbuthionine-S,R-sulfoximine, menadione and sodium deoxycholate inhibit the Ca2+ transport from lumen to blood by alteration in the protein expression and/or activity of molecules involved in the Ca2+ transcellular and paracellular pathways through mechanisms of oxidative stress, apoptosis and/or autophagy. Quercetin, melatonin, lithocholic and ursodeoxycholic acids block the effect of those drugs in experimental animals by their antioxidant, anti-apoptotic and/or anti-autophagic properties. Therefore, they may become drugs of choice for treatment of deteriorated intestinal Ca2+ absorption under oxidant conditions such as aging, diabetes, gut inflammation and other intestinal disorders.
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