Histological and biochemical investigation of possible effects of carvacrol on experimental testis ischemia reperfusion model in rats

Testicular torsion is a urological problem that causes subfertility and testicular damage in young males and newborns. Following the testis torsion, detorsion leads to ischemia reperfusion injury in the testis. Testicular ischemia reperfusion injury causes increase of reactive oxygen species, oxidative stress and germ cell apoptosis. The opening of ATP-dependent potassium channels protects the tissue against ischemia reperfusion injury. In this study, it was aimed to investigate the possible protective effects of carvacrol against the testicular ischemia reperfusion injury and effects on Kir6.2 channels which is a member of ATP-dependent potassium channels. In this study 36 male 2-4 months old male Albino Wistar rats were used. Experimental groups were determined as Sham, Control+DMSO, Control+Carvacrol, IR, IR+DMSO and Treatment groups. The left testis was rotated counter-clockwise at 720º for testicular torsion for 2 hours, and detorsion for 2 hours following torsion were performed for experimental testicular ischemia reperfusion model. In treatment group, carvacrol was dissolved in 5% DMSO at a dose of 73 mg/kg and half hour before detorsion, and 0.2 ml dose was administered intraperitoneally. Histologically, congestion, edema, structural disturbance in seminiferous tubules and cell debris were very common in the IR group, but minimal in the treatment group. Apoptotic cell counts and serum MDA levels were significantly decreased (p≤0.05) and Kir6.2 activation was significantly increased in the treatment group when compared to IR group (p≤0.05).