Interaction of Singlet Oxygen with 5-Nucleotidase in Rat Hearts

This study was aimed to determine whether singlet oxygen (1O2) attenuates 5-nucleotidase activity in the ischemic myocardium. Isolated rat hearts were exposed to either exogenous1O2produced by irradiating rose bengal or 40-min ischemia and reperfusion. Ecto-5-nucleotidase activity was inhibited by exogenous1O2(3.74±0.38μmol/min/g dry weight), when compared with normal control (7.52±0.41μmol/min/g dry weight;P<0.05). The enzymatic activity was significantly preserved by histidine (25 m ) – a1O2scavenger (7.04±0.61μmol/min/g dry weight;P<0.05vrose bengal group). After ischemia, the activity of ecto-5-nucleotidase was greatly reduced (2.51±0.25μmol/min/g dry weight), when compared with normal control. Histidine significantly enhanced ecto-5-nucleotidase activity (6.55±0.52μmol/min/g dry weight,P<0.05vischemic control). Adenosine release was consistent with ecto-5-nucleotidase activity. The time course studies of effects of1O2on coronary flow, cardiac function, and LDH release revealed that the damage by1O2to ecto-5-nucleotidase activity and adenosine release primarily accounted for impaired coronary flow, cardiac dysfunction, and impaired cardiac metabolism. Lipid peroxidation induced by exogenous1O2or ischemia was in parallel with ecto-5-nucleotidase deactivation by1O2. It is concluded that1O2causes inactivation of ecto-5-nucleotidase and attenuation of adenosine release which could possibly be one of the important mechanisms of oxygen radical-mediated myocardial injury.