Abstract
Both confirmatory and disputive evidence is presented on the hypothesis that spermatozoa aging in the female tract lose their ability to contribute to normal embryonic development before losing their capacity for fertilization. Studies of spermatozoa aging in female rats and guinea pigs have demonstrated no coincident increases in pre or postimplantation losses while other studies in rabbits have demonstrated such a relationship. One such study found that spermatozoa aging of 29 hours resulted in post implantation losses of 47% compared with 27% in controls. Another study observed an increase in chromosome anomalies at 30 hours aging. While the duration of fertilizing capacity of spermatozoa in the female tract varies widely within mammalian species spermatozoa generally maintain their motility much longer than their ability to fertilize ova. In mammals with estrus cycles and in induced ovulators the fertilizing life of spermatozoa is approximately equal to or greater than the maximum time between insemination and ovulation. Among mammals length of spermatozoan survival differs in different regions of the reproductive tract. In women the acidic vaginal milieu (pH 3 to 4) seems to limit spermatozoan life in the vagina. Hexosamines and carbohydrates in free or polysaccharide forms may contribute to the extended longevity of spermatozoa in the cervix. Estrogen (exogenous and endogenous) appears enhance spermatozoan survival in cervical secretions. Upon their deposition in the female reproductive tract spermatozoa are subjected to increased temperature changes in pH and great dilution and leukocyte invasion in the oviducts and uterus. Spermatozoa become highly motile. Capacitation and increased metabolism of spermatozoa may also limit survival. It is suggested that the ability of the spermatozoan aged in the male tract to contribute to a loss and a postimplantation loss. Aging in the male tract has been associated with an incidence of chromosomnomalies. Further study is required to determine wheter spermatozoan aging contributes significantly to reproductive failure in man.
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