Objective: To 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 methods: Thirty 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. Results: Differences 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. Conclusions: These 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.
All Science Journal Classification (ASJC) codes
- Pediatrics, Perinatology, and Child Health