The present study is undertaken to evaluate the protective effects of vitamin C (VC) against methomyl-induced oxidative stress and testicular injures in Wister rat. Male rats were randomly divided into 4 groups of 6 rats each. The route of application selected for the study was oral gavage for 28 consecutive days. Group 1 was served as a control, whereas group 2 was supplemented with VC (200 mg kg-1 body weight, bw). Group 3 was administered with a dose of methomyl equivalent to 1/10 LD50 (2.034 mg kg-1 bw), whereas group 4 was co-administered VC and methomyl as the same dose of groups 2 and 3, respectively. Sub-acute exposure of rats to methomyl for 28 consecutive days resulted in a significant increase in testicular lipid peroxidation (LPO) and a decrease in glutathione (GSH) level. In addition, the testicular activities of catalase (CAT), superoxide dismutase (SOD) and glutathione-S-transferase (GST) enzymes were significantly decline in response to methomyl exposure. Furthermore, histopathological studies in testis of rats treated with methomyl exhibited incomplete spermatogenic series in seminiferous tubules and necrosis of spermatogoneal cells lining seminiferous tubules. Notably, the co-administration of VC modulated the biochemical parameters and the intensity of histopathological findings. The effect of VC on transcriptional activity of four key stress and apoptosisrelated genes (CASP3, CASP9, Tp53 and Bcl2), in response to methomyl exposure in rats, was investigated. Results revealed a significant up-regulation in the level of the expression for the tested genes, however supplementation of VC to methomyl-treated rats modulated the observed significant up-regulation in the level of the expression for those genes, indicative of an protective interfering role in the signaling transduction process of methomyl-mediated toxicity. In conclusion, these data suggested that administration of VC may partially protect against methomyl induced testicular oxidative damage and apoptosis-related genes.