Sodium nitrite-derived nitric oxide protects rat testes against ischemia/reperfusion injury

摘要

Testicular torsion,a common urologic emergency,is primarily caused by ischemia/reperfusion (I/R)injury of the testis.Nitric oxide (NO)-derived from nitrite (NO2-)has been reported to have prominent therapeutic effects on I/R injury in the heart,liver,and brain;however,its effects on testicular I/R injury have not been evaluated.This study,therefore,investigated whether NO from NO2^-is beneficial in a rat model of testicular I/R injury which eventually results in impaired spermatogenesis.Male Sprague-Dawley rats were assigned to the following seven groups:group A,sham-operated control group;Group B,I/R with no treatment;Groups C, D,and E,I/R followed by treatment with three different doses of NO2^-;Group F,I/R followed by administration of NO2-and NO scavenger (2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide potassium salt [C-PTIO]);and Group G,I/R followed by administration of nitrate (NO3^-).NO2^-,NO3^-,and C-PTIO were intravenously administered.Histological examination of the testes and the western blot analysis of caspase-3 were performed.Levels of antioxidant enzymes and lipid peroxidation were measured. Germ cell apoptosis,oxidative stress,antioxidant enzymatic function,and lipid peroxidation in Group B were significantly higher than those in Group A.Group B exhibited an abnormal testicular morphology and impaired spermatogenesis.In contrast,testicular damages were attenuated in the NO2^-treatment groups,which were caused by reduction in superoxide and peroxynitrite levels and an inhibition of caspase-3-dependent apoptosis.The results of this study suggest NO2^-to be a promising therapeutic agent with anti-oxidant and anti-apoptotic properties in testicular I/R injury.