TURKISH JOURNAL OF BIOCHEMISTRY-TURK BIYOKIMYA DERGISI, cilt.36, sa.3, ss.200-206, 2011 (SCI-Expanded)
Objective: There are various studies that have been published indicating that reactive oxygen species are produced in large quantities in post-ischemic reperfusion and this oxidative burst mediates the severity of the damage. It has been previously suggested that monoamine oxidase (MAO) is a potential source of hydrogen peroxide (H2O2) in early reperfusion; and mitochondrial hydroxyl radicals generated from H2O2 during MAO metabolism serve as a contributor to tissue injury. The aim of this study was to investigate the possible contribution of elevated activities of MAO isoforms to the generation of reactive oxygen species and lipid peroxidation in hepatic ischemia-reperfusion injury in mice.