Although testicular cancer is the most common oncological diagnosis in young males of reproductive age, treatments for this condition are extremely effective leading to survival rates that approach 100%. As a result, concerns have been raised about the subsequent fertility of men following cancer treatment as well as the health and wellbeing of their offspring. Existing data on this issue are inconclusive, so an analysis has been undertaken of sperm quality and fertility of mice exposed to a chemotherapeutic regime including bleomycin, etoposide and cis-platinum (BEP). By conducting these studies in the Big Blue® transgenic mouse, the mutational load carried by the testes and offspring of treated males has also been quantified. A 3-week exposure to BEP induced complete azoospermia associated with a loss of developing germ cells and extensive vacuolization of Sertoli cell cytoplasm. Following cessation of treatment, spermatozoa first appeared in the caput epididymis after 6 weeks and by 12 weeks motile spermatozoa could be recovered from the cauda. However, relative to control animals, the motility of these cells was significantly impaired and mitochondrial superoxide generation was significantly elevated. Despite this increase in free radical generation, no evidence of chromatin instability in these spermatozoa was detected. Furthermore, embryos obtained from females mated at this 12-week time point showed no evidence of an increased mutational load. We conclude that, notwithstanding the damaging impact of BEP therapy on spermatogenesis and sperm quality, the absence of an increased mutational load in the offspring represents encouraging news for men contemplating a family following chemotherapy for testicular cancer.