ORIGINS AND EFFECTS OF VARIATIONS IN SPERMATOZOAL QUALITY

A traditional view of mammalian fertilization is that the active compo nent of the process, the spermatozoon, by virtue of its progressive mo tility and acrosomal enzymes, penetrates an otherwise passive oocyte. This concept has placed bias on spermatozoal normality as largely dete rmining the outcome of fertilization. Once this has been achieved, the contribution of the spermatozoon is often forgotten, and attention sw itches to the maternally derived ''blue-print'' for early embryonic de velopment. Paternal genomic contribution is known to start at the 8-ce ll stage in the human, but this is usually after the early cleavage st age embryos are transferred in human reproductive technologies, such a s in vitro fertilization (IVF). Hence, any fundamental abnormal contri bution to embryogenesis derived from the fertilizing spermatozoon is n ot seen. IVF has permitted far greater powers of analysis of fertiliza tion in the human, and fertilization success appears to be determined in this sytem by three main factors: spermatozoal quality, oocyte qual ity, and the quality of the in vitro culture conditions (the gamete en vironment). If the second two factors are more carefully controlled th an the first, as is the usual emphasis in IVF practice, then any large variation in fertilization rates that is also related to embryonic vi ability and ultimate pregnancy outcome may be thought to be more direc tly associated with original quality of the fertilizing spermatozoon. If this hypothesis is accepted, we should drastically alter our concep t of the spermatozoon as a robust simple initiator of embryonic develo pment, and embrace the idea of the vulnerability of such germ cells bo th during and after their production, and how detrimental influences o n this may profoundly affect embryogenesis after fertilization.