Origins and effects of variations in spermatozoal quality.

A traditional view of mammalian fertilization is that the active component of the process, the spermatozoon, by virtue of its progressive motility and acrosomal enzymes, penetrates an otherwise passive oocyte. This concept has placed bias on spermatozoal normality as largely determining the outcome of fertilization. Once this has been achieved, the contribution of the spermatozoon is often forgotten, and attention switches to the maternally derived "blue-print" for early embryonic development. Paternal genomic contribution is known to start at the 8-cell stage in the human, but this is usually after the early cleavage stage embryos are transferred in human reproductive technologies, such as in vitro fertilization (IVF). Hence, any fundamental abnormal contribution to embryogenesis derived from the fertilizing spermatozoon is not seen. IVF has permitted far greater powers of analysis of fertilization in the human, and fertilization success appears to be determined in this system by three main factors: spermatozoal quality, oocyte quality, and the quality of the in vitro culture conditions (the gamete environment). If the second two factors are more carefully controlled than the first, as is the usual emphasis in IVF practice, then any large variation in fertilization rates that is also related to embryonic viability and ultimate pregnancy outcome may be thought to be more directly associated with original quality of the fertilizing spermatozoon. If this hypothesis is accepted, we should drastically alter our concept of the spermatozoon as a robust simple initiator of embryonic development, and embrace the idea of the vulnerability of such germ cells both during and after their production, and how detrimental influences on this may profoundly affect embryogenesis after fertilization.