Male infertility is a common condition affecting at least 1 in 20 of the male population. However, despite its prevalence, the aetiology of this condition remains poorly understood. Genetic factors play a minor role accounting for around 25% of cases of azoospermia and 10% of cases with idiopathic infertility. Aside from chromosomal disorders such as Klinefelter syndrome and rare single gene mutations, the most common genetic lesions responsible for male infertility are Y-chromosome deletions. Such minor causes aside, the causative factors underpinning a vast majority of male infertility remain unknown. In most infertile males sufficient numbers of spermatozoa are present to achieve fertilization, however the functional competence of these cells has, for some reason, become compromised. Such a dramatic loss of sperm function has been shown to involve a high incidence of oxidative stress affecting the ability of the spermatozoa to swim, interact with the zona pellucida, acrosome react and fuse with the vitelline membrane of the oocyte. In addition, oxidative stress compromises the integrity of DNA in the male germ line and thereby impacts the mutational load carried by children. This is a serious problem for the ART industry, particularly when ICSI is used as the preferred method of insemination. Oxidative DNA damage in spermatozoa targets areas of the genome involved in a variety of brain disorders (eg. autism, spontaneous schizophrenia and bipolar disease) the incidence which may become elevated in the offspring of patients treated for infertility associated with oxidative stress. The recent evidence indicating an increased risk of autism in ICSI children is a case in point. We must be careful that the uncontrolled use of such technology does not ultimately create a health burden for future generations to solve.