Oxidativestress,antioxidantsandintestinalcalciumabsorption

摘要： Thedisequilibriumbetweentheproductionofreactiveoxygen(ROS)andnitrogen(RNS)speciesandtheireliminationbyprotectivemechanismsleadstooxidativestress.MitochondriaarethemainsourceofROSasby-productsofelectrontransportchain.Mostofthetimetheintestinerespondsadequatelyagainsttheoxidativestress,butwithagingorunderconditionsthatexacerbatetheROSand/orRNSproduction,thedefensesarenotenoughandcontributetodevelopingintestinalpathologies.Theendogenousantioxidantdefensesystemingutincludesglutathione(GSH)andGSH-dependentenzymesasmajorcomponents.WhentheROSand/orRNSproductionisexacerbated,oxidativestressoccursandtheintestinalCa2+absorptionisinhibited.GSHdepletingdrugssuchasDLbuthionine-S,R-sulfoximine,menadioneandsodiumdeoxycholateinhibittheCa2+transportfromlumentobloodbyalterationintheproteinexpressionand/oractivityofmoleculesinvolvedintheCa2+transcellularandparacellularpathwaysthroughmechanismsofoxidativestress,apoptosisand/orautophagy.Quercetin,melatonin,lithocholicandursodeoxycholicacidsblocktheeffectofthosedrugsinexperimentalanimalsbytheirantioxidant,anti-apoptoticand/oranti-autophagicproperties.Therefore,theymaybecomedrugsofchoicefortreatmentofdeterioratedintestinalCa2+absorptionunderoxidantconditionssuchasaging,diabetes,gutinflammationandotherintestinaldisorders. ... （共13頁）