%0 Journal Article
%T AutophagypreventsautophagiccelldeathinTetrahymenainresponsetooxidativestress
%A Si-Wei ZHANG
%A Jiang-Nan FENG
%A Yi CAO
%A Li-Ping MENG
%A Shu-Lin WANG
%J 动物学研究
%P 167-173
%D 2015
%X Autophagyisamajorcellularpathwayusedtodegradelong-livedproteinsororganellesthatmaybedamagedduetoincreasedreactiveoxygenspecies(ROS)generatedbycellularstress.Autophagytypicallyenhancescellsurvival,butitmayalsoacttopromotecelldeathundercertainconditions.Themechanismunderlyingthisparadox,however,remainsunclear.WeshowedthatTetrahymenacellsexertedincreasedmembrane-boundvacuolescharacteristicofautophagyfollowedbyautophagiccelldeath(referredtoascelldeathwithautophagy)afterexposuretohydrogenperoxide.Inhibitionofautophagybychloroquineor3-methyladeninesignificantlyaugmentedautophagiccelldeathinducedbyhydrogenperoxide.BlockageofthemitochondrialelectrontransportchainorstarvationtriggeredactivationofautophagyfollowedbycelldeathbyinducingtheproductionofROSduetothelossofmitochondrialmembranepotential.ThisindicatedaregulatoryroleofmitochondrialROSinprogrammingautophagyandautophagiccelldeathinTetrahymena.Importantly,suppressionofautophagyenhancedautophagiccelldeathinTetrahymenainresponsetoelevatedROSproductionfromstarvation,andthiswasreversedbyantioxidants.Therefore,ourresultssuggestthatautophagywasactivateduponoxidativestresstopreventtheinitiationofautophagiccelldeathinTetrahymenauntiltheaccumulationofROSpassedthepointofnoreturn,leadingtodelayedcelldeathinTetrahymena.
%K Autophagy
%K Autophagiccelldeath
%K Lysosome
%K Mitochondria
%K Reactiveoxygenspecies
%K Tetrahymena
%U http://www.zoores.ac.cn/CN/abstract/abstract3643.shtml