AN EXPERIMENTAL STUDY ON THE INDUCTIONMECHANISM OF SUPEROXIDE DISMUTASE IN CULTURED CARDIOMYOCYTES DURING HEAT SHOCK

AN EXPERIMENTAL STUDY ON THE INDUCTION MECHANISM OF SUPEROXIDE DISMUTASE IN CULTURED CARDIOMYOCYTES DURING HEAT SHOCK

Objective To explore the role of reaction oxygen species (ROS) in heat shock (HS) on the tolerance of cardiomyocytes to anoxia - reoxygenation (AO - RO) injury and on the activity of superoxide dismutase (SOD).Methods Cultured neonatal myocytes of rats were divided into 5 groups: normal control, anoxic control, HS,HS- SOD pretreated and exogenous ROS pretreated (n= 6). Results Compared with the 2 control groups, ROS release in HS and ROS pretreated groups increased mildly, but after experiencing 3h anoxia/lh reoxygenation 24hlater, ROS release of the two groups decreased significantly, which was accompanied by enhanced SOD activities and less myocytes damage. Opposite results were found when SOD was insituted during HS. Conclusion HS did enhance myocardial tolerance to AO-RO injury. The mild release of ROS during HS may trigger delayed myocardial protection by altering SOD activity.