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 exogenous 1O2 produced by irradiating rose bengal or 40-min ischemia and reperfusion. Ecto-5′-nucleotidase activity was inhibited by exogenous 1O2 (3.74 ± 0.38 μmol/min/g dry weight), when compared with normal control (7.52 ± 0.41 μmol/min/g dry weight; P < 0.05). The enzymatic activity was significantly preserved by histidine (25 mM) - a 1O2 scavenger (7.04 ± 0.61 μmol/min/g dry weight; P < 0.05 v rose bengal group). After ischemia, the activity of ecto-5′-nucleotidase was greatly reduced (2.51 ± 0.25 μmol/min/g dry weight), when compared with normal control. Histidine significantly enhanced ecto-5′-nucleotidase activity (6.55 ± 0.52 μmol/min/g dry weight, P < 0.05 v ischemic control). Adenosine release was consistent with ecto-5′-nucleotidase activity. The time course studies of effects of 1O2 on coronary flow, cardiac function, and LDH release revealed that the damage by 1O2 to ecto-5′-nucleotidase activity and adenosine release primarily accounted for impaired coronary now cardiac dysfunction, and impaired cardiac metabolism. Lipid peroxidation induced by exogenous 1O2 or ischemia was in parallel with ecto-5′-nucleotidase deactivation by 1O2. It is concluded that 1O2 causes 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.
- Rose bengal
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine