Cadmium (Cd) is an inorganic heavy metal which is of significant occupational concern, has been classified as human carcinogen. Administration of Cd in animals results in multiple organ tumorigenesis. Evidences indicate that the oxidative stress plays an important role in Cd carcinogenesis. Cd exposure has been related to human diseases such as cancer and studies have shown the adverse effects of different doses of cadmium chloride (CdCl2) on reproductive functions in male. Studies have shown that CdCl2-induced testicular and spermatozoa toxicity associated with the oxidative stress in male downregulating the apoptotic genes and up regulating gonadotropins and anti-apoptotic genes. CdCl2 toxicity significantly decreases the reproductive organ weights, epididymal sperm concentration, motility and B-cell lymphoma 2 (BCL 2) positive anti-apoptotic cell rate, whereas it caused significant increases in level of lipid peroxidation and abnormal sperm rates. BAX gene expression has been detected in leydig cells, indicating that BAX gene is a promotor of cell death is often positively regulated by the tumour suppressor gene p53 and may also cause the formation of multinucleated giant cells which is caused by additional DNA replication of the primary spermatocytes that fail to undergo meiosis. Thus, this article reviews some of the molecular toxicity mechanism of Cd and its effect on the testis which will be helpful in anticipation and deterrence of Cd-induced testicular toxicity.