An examination of the effects of thioredoksin and l-name on liver injury in the experimental liver ischemia/reperfusion model

The phisio-phatalogy of I/R injury has not been fully understood. Moreover, it becomes more complex by the discovery of new molecules, genes, and various factors everyday. Altough the mechanism of this multi-step injury has been explained completely, the obtained evidences point out that reactive oxygen products play a key role in the injury.In this study the affects of Trx and L-name on liver injury have been investigated by giving them to rats in which partial liver I/R was generated. It was observed that in reperfusion while Trx increases the hepatic blood flow, L-name causes a decrease. When liver enzyme values were examined in the study groups the ALT, AST, LDH, GGT, NO, MDA, HAE, P-selektin and Endotelin-1 values increased in the ischemia group while on the other hand there were decreases in these values in groups which were given Trx, L-name, and Trx-L-name together. It was observed that GPx and SOD enzymes, and total glutation (tGSH) significantly decreased in ischemia group as compared to the sham group. On the contrary there was an increase in groups which were given Trx, L-name, and Trx-L-name. Furthermore, these substances also decreases the ratios of apopitosis. When the corelations are examined there are observed corelations of especially P-selektin and NO with ALT, LDH, ALP, GGT, P-selektin, ET-1, GPx, tGSH, SOD, MDA, HAE, and apopitosis (p<0.05).When the obtained results are evaluated it is determined that there were decreases in liver cell injury, generation of ROS and lipid peroxidation products,release of adhesion molecules, and apopitosis ratios. At the same time it was also shown through this study that there were increases in antioxidant enzymes and substances at the cellular level in livers. By obstructing extra NO production as a result of inhibition of NOS with L-name it was observed that there exist Trx like effects.