Spermatozoa with numerical chromosomal abnormalities are more prone to be retained by Annexin V-MACS columns.
Nuclear DNA damage in spermatozoa could potentially have a major impact on the fertilizing capacity of these cells, their ability to establish a normal pattern of embryonic development as well as the health and wellbeing of subsequent offspring. Many laboratory techniques have been developed to assess this damage focusing on strand breaks, chromatin stability following exposure to extreme pH conditions and the formation of DNA adducts. Of particular importance may be the dominant role played by oxidative stress in the etiology of defective sperm function and DNA damage. The oxidative base lesions created via this mechanism have the potential to generate genetic and epigenetic mutations in the offspring that could have a profound impact on the latter's long-term health trajectory. Moreover if oxidative stress is the cause of DNA damage in spermatozoa then there is a potential role for antioxidant therapy in the resolution of this problem, which deserves investigation.