In light of this we have shown that semen with high CMA positivity leads to significantly lower fertilization rates when using subzonal sperm injection. When using the ICSI technique all sperm membraneoocyte interactions are superseded placing more importance on the quality of the sperm nucleus and the ability of the oocyte to initiate decondensation and pronuclear formation.The mean percentage of spermatozoa presenting normal morphology, chromomycin A or intracytoplasmic sperm injection. DNA and the use of ICSI to force fertilization in these patients may cause further uneasiness as to the fate of fertilized ICSI eggs.Here we therefore discuss whether the quality of a patients spermatozoa, in terms of chromatin anomalies, can influence the outcome of ICSI and present results comparing embryo development to the blastocyst stage of patients undergoing routine IVF and ICSI.When examining the above three parameters it could therefore be presumed that males with acceptable sperm parameters would present a normal morphology of, CMA fluorescence of and exhibit endogenous nicks in of their spermatozoa. The question therefore arises as to whether the above anomalies may influence fertilization after ICSI.To ascertain whether a relationship existed between the sperm chromatin parameters of the patients and the ability of spermatozoa to fertilize after ICSI we separated the patients according to their sperm morphology, CMA fluorescence, and the presence of endogenous nicks.When ICSI patients were separated according to these criteria no overall difference was observed in their ability to achieve fertilization. This may however mean that spermatozoa selected for ICSI were among those that did not possess anomalies in the sperm nucleus.In patients who had a lower percentage of anomalies in their chromatin a significantly lower number of spermatozoa remained condensed.In contrast, patients who had a high percentage of anomalies in their chromatin had more than double the number of unfertilized oocytes containing spermatozoa that had remained condensed.The percentage of unfertilized oocytes containing spermatozoa that had remained condensed did not differ in relation to the patients morphology.Once sperm decondensation had been initiated, no significant difference was observed between the patient groups.How anomalies in the sperm nuclear Targetmol’s Uridine structure can influence decondensation during fertilization is not established.They have shown that treatment of male rats with cyclophosphamide had little effect on the male reproductive system but caused single strand DNA breaks in the caudaepididymal spermatozoa. More disturbingly, similar treatment protocols using cyclophosphamide produce an increase in postimplantation loss and malformations. A number of studies have indicated that the oocyte has the capability to repair the damaged DNA of spermatozoa.A high level of abnormalities in the chromatin of a spermatozoa selected for ICSI may impede the completion or initiation of decondensation therefore leading to a failure of fertilization.This may occur even though the oocyte possesses the necessary mechanism to initiate decondensation.Although we do not postulate that the failure of fertilization is entirely due to a sperm defect it seems likely that poor chromatin packaging andor damaged DNA may contribute to a failure in the decondensation process.Furthermore, lower rates of development to the blastocyst stage by ICSI embryos compared to those developed after routine IVF indicate that a further selection may occur during the preimplantation stage.