Akademik Veri Yönetim Sistemi
Fabad Journal of Pharmaceutical Sciences, cilt.29, sa.2, ss.63-70, 2004 (Scopus)
Recent studies have been focused on the protective role of ischemic preconditioning (IP) against ischemia reperfusion (I/R) injury of the lung occurring following cardiopulmonary bypass or lung transplantation. Although reactive oxygen species (ROS) production has been postulated to play a crucial role in I/R, the sources of ROS during I/R are still unclear. Since it has been previously described that monoamine oxidases (MAOs) are a potential source of hydrogen peroxide (H2O2) generation in early reperfusion following ischemia, the present study aimed to investigate the possible contribution of MAO to ROS generation and lipid peroxidation during I/R and IP protocols in the lung. Male Wistar rats were randomly divided into three groups: control lungs were subjected to 30 min. of perfusion; lungs of the I/R group were subjected to 2 h of cold ischemia following 30 min. of perfusion; and in the third group IP was performed by two cycles of 5 min. ischemia followed by 5 min. of reperfusion prior to 2 h of cold ischemia and then reperfusion. MAO-A and B activities, lipid peroxidation, reduced (GSH) and oxidized (GSSG) glutathione levels, H2O2 release and catalase activity were determined in tissue samples. MAO-A and B activities, lipid peroxidation, GSSG content and H2O2 release were found to be increased, while GSH content, GSH/GSSG ratio and catalase activity were decreased in lung tissues of the I/R group when compared with those of the control group. MAO-A and B activities, lipid peroxidation, GSSG content and H2O 2 release were found to be decreased, while GSH content, GSH/GSSG ratio and catalase activity were increased in lung tissues of the IP group when compared with those of the I/R group. Strong positive correlations were found between MAO activity and H2O2 release in lung tissues of I/R and IP groups, suggesting that MAO is a potential source of H 2O2 generation during reperfusion and that IP protects the lung against oxidative damage via diminishing MAO-mediated excess H 2O2 formation. Although the present study is preliminary by design, we suggest that MAO isoforms may contribute to ROS generation during I/R, and that MAO inhibitors may be used together with IP to protect against lung injury during I/R.