Vasectomy induces oxidative stress and up-regulates the expression of peroxiredoxins in mouse testis in short and early periods after surgery.

We investigated oxidative damage caused by and antioxidant responses to peroxiredoxins in the mouse testis at different time points after vasectomy. Mice were divided into a sham operated control group and a vasectomized group. Testicular samples were collected 2 to 120 days postoperatively. Histology and cell apoptosis were evaluated by hematoxylin and eosin staining, and TUNEL assay, respectively. Oxidative damage was determined using a commercial malondialdehyde kit. The expression of peroxiredoxin and other antioxidant enzyme mRNAs was detected by reverse transcriptase-polymerase chain reaction. Western blot and immunohistochemistry were performed to examine peroxiredoxin protein expression. Histology revealed severe damage in vasectomized testes with high malondialdehyde levels. The alteration in malondialdehyde was in parallel with the process of histological injury and apoptosis. Germ cell apoptosis developed in a time dependent and cell specific manner. The expression of peroxiredoxin 1, 2 and 3, especially peroxiredoxin 2, was significantly up-regulated at the mRNA and protein levels in the testis after vasectomy, which subsequently ameliorated testicular damage toward the control level. In addition, other related antioxidant enzymes, such as Cat and Sod3, showed decreased expression at the mRNA level in vasectomized testes. This study shows that vasectomy induces oxidative stress in the mouse testis in the short-term early period after surgery, resulting in histological injury and germ cell apoptosis. Peroxiredoxins may have important roles as antioxidant defenses in vasectomized testis and provide new prevention and therapy alternatives for testicular damage after vasectomy.