title: Influence of platelet γ-glutamyltransferase on oxidative stress and apoptosis in the presence of holo-transferrin.
abstract: Several studies have documented that formation           of oxidant mediators may induce apoptosis in           nucleated and anucleated cells by modulating intracellular           signalling pathways. Reactive oxygen species           (ROS) play a very important role in the platelet function.           γ-Glutamyltransferase (GGT), a novel source of           cellular production of oxidants in the presence of           iron and reduced glutathione (GSH), is also found on           platelets. The role of platelet-bound GGT in platelet           apoptosis and oxidative stress is unknown. The aim           of our study was to determine the effects of platelet           GGT activity on oxidative stress and apoptotic events           in vitro via determination of lipid peroxidation           (LPO), protein oxidation, GSH, catalase, caspase-3           activation and phosphatidylserine (PS) exposure in           the presence of holo-transferrin (Tf). Stimulation of           platelet GGT activity with GSH and glycylglycine           (GlyGly) increased caspase-3 activation and PS exposure.           A significant increase in lipid and protein           oxidation and decrease in GSH and catalase levels           was also observed in platelets with stimulation of GGT activity in the presence of Tf. Inhibition of           GGT activity effectively reduced all the markers.           These results suggest that generation of ROS by the           GGT/GSH/Tf system can modify the platelets' redox           environment and induce apoptosis in in vitro conditions.
authors.affiliation: Biochemistry Department, Faculty of Pharmacy, Marmara University, Istanbul, Turkey. azizesener@hotmail.com
authors.forename: A
authors.initials: A
authors.lastname: Sener
authors.forename: O
authors.initials: O
authors.lastname: Cevik
authors.forename: G
authors.initials: G
authors.lastname: Yanikkaya-Demirel
authors.forename: S
authors.initials: S
authors.lastname: Apikoglu-Rabus
authors.forename: D
authors.initials: D
authors.lastname: Ozsavci
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D001792:Blood Platelets / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology*; D053148:Caspase 3 / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004151:Dipeptides / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D010718:Phosphatidylserines / Q000378:metabolism; D050050:Protein Carbonylation / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000378:metabolism; D014168:Transferrin / Q000494:pharmacology*; D005723:gamma-Glutamyltransferase / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D004151:Dipeptides; D004791:Enzyme Inhibitors; D010718:Phosphatidylserines; D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds; D014168:Transferrin; C110714:holotransferrin; C028505:cysteinylglycine; D002374:Catalase; D005723:gamma-Glutamyltransferase; D053148:Caspase 3; D005978:Glutathione