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World J Gastroenterol. Apr 28, 2017; 23(16): 2841-2853
Published online Apr 28, 2017. doi: 10.3748/wjg.v23.i16.2841
Oxidative stress, antioxidants and intestinal calcium absorption
Gabriela Diaz de Barboza, Solange Guizzardi, Luciana Moine, Nori Tolosa de Talamoni
Gabriela Diaz de Barboza, Solange Guizzardi, Luciana Moine, Nori Tolosa de Talamoni, Laboratorio “Dr. Fernando Cañas”, Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, INICSA (CONICET-Universidad Nacional de Córdoba), Pabellón Argentina, Ciudad Universitaria, Córdoba 5000, Argentina
Author contributions: Diaz de Barboza G, Guizzardi S, Moine L and Tolosa de Talamoni N participated in information collection, analysis, information organization, writing, figure design, and final editing.
Supported by Dr. Nori Tolosa de Talamoni from CONICET, No. PIP 2013-2015 and No. SECYT (UNC) 2016, Argentina.
Conflict-of-interest statement: No conflicts of interest, financial or otherwise, are declared by the authors.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Nori Tolosa de Talamoni, Professor, Laboratorio “Dr. Fernando Cañas”, Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, INICSA (CONICET-Universidad Nacional de Córdoba), Pabellón Argentina, 2do. Piso, Ciudad Universitaria, Córdoba 5000, Argentina. ntolosatalamoni@yahoo.com.ar
Telephone: +54-351-4333024 Fax: +54-351-4333024
Received: January 7, 2017
Peer-review started: January 9, 2017
First decision: February 9, 2017
Revised: March 1, 2017
Accepted: March 30, 2017
Article in press: March 30, 2017
Published online: April 28, 2017
Processing time: 111 Days and 7.6 Hours
Abstract

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 DL-buthionine-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.

Keywords: Transcellular and paracellular Ca2+pathways; DL-buthionine-S,R-sulfoximine; Menadione; Sodium deoxycholate; Lithocholic acid; Ursodeoxycholic acid; Melatonin

Core tip: Glutathione depleting drugs inhibit the intestinal Ca2+ absorption by alteration in the protein expression and/or activity of molecules involved in the transcellular and paracellular Ca2+ 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 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.