Effect of vitamin E on oxidative stress in the contralateral testis of neonatal and pubertal hemicastrated rats

Abstract

ObjectiveTo evaluate whether the antioxidant vitamin E can prevent the harmful effects of reactive oxidative stress (ROS) that occur during compensatory testicular hypertrophy (CTH). Materials and methodsThirty Sprague–Dawley rats were divided into six equal groups: neonatal hemicastrated vitamin E (NH_Vit E/NH) and sham surgical controls (NC), and pubertal hemicastrated vitamin E (PH_Vit E/PH) and sham surgical controls (PC). Vitamin E was administered orally to the NH_Vit E and PH_Vit E groups three times a week from week 3–12 prior to sacrifice. Antioxidant enzymes were measured in testis samples from each animal. ResultsDifferences in superoxide dismutase activity were observed between the NH (21.04 ± 0.48) and NH_Vit E (22.62 ± 0.64) groups (P = 0.008); the PH (20.59 ± 0.11) and PC (20.91 ± 0.20) groups (P = 0.032); and the PH (20.59 ± 0.11) and PH_Vit E (22.32 ± 1.01) groups (P = 0.008). Thiobarbituric acid-reactive substance in the PH and PH_Vit E groups was 0.097 ± 0.022 and 0.036 ± 0.004 (P = 0.008), respectively; and in the NH and NH_Vit E groups it was 0.135 ± 0.02 and 0.039 ± 0.003 (P = 0.008), respectively. ConclusionsThese results suggest that CTH is not associated with reducing oxidative injury, nor does it prevent ROS-induced cell damage. However, administration of vitamin E does reduce oxidative injury and prevent ROS-induced cell damage in a hemicastrated rat model.