Manganese (Mn2+) stimulated the progressive motility of human washed sperm in a time- and dose-dependent manner. This confirmed previous data indicating a capacity for activating the adenylyl cyclase of sperm homogenates in vitro. A maintained response was best seen with doses 0.2-1.0 mM. After an initial stimulation, higher concentrations of up to 20 mM were associated with a decline in the response to control levels. Magnesium ions (Mg2+) stimulated motility in the same dose range but to less than 50% of the Mn2+ response. Other divalent cations such as zinc (Zn2+), strontium (Sr2+), and Calcium (Ca2+) also exerted stimulatory effects to varying degrees in descending order. Metal ion effects on sperm motility may be mediated through a common cation-binding site on the adenylyl cyclase.
The properties (association and dissociation rates, affinity and specificity) of GnRH receptors in the rat pituitary and the Leydig cells are very similar. In addition, in vivo administration for 5 or 11 days of 10 micrograms of GnRH to adult rats resulted in an increase (p less than 0.01) in both Leydig cell and pituitary GnRH receptors. In contrast, the same treatment caused a significant decrease (p less than 0.01) of Leydig cell LH receptor number. Furthermore, testosterone propionate (500 micrograms/day), which had no effect on Leydig cell LH receptors, caused a significant increase (p less than 0.01) of testicular GnRH receptors but a decrease (p less than 0.01) of pituitary GnRH receptors. Estradiol 17 beta valerate (5 micrograms/day) reduced (p less than 0.01) both testicular (5 days) and pituitary (5 and 11 days) GnRH receptors. Such treatment for 5 days also decreased (p less than 0.05) the Leydig cell LH receptors. No effect of dexamethasone and 17-hydroxyprogesterone was seen after 5 or 11 days of treatment. Thus, although pituitary and Leydig cell receptors appear similar, their regulation by exogenous hormone treatments is different. Furthermore, the regulation of Leydig cell GnRH and LH receptors also appears very different, suggesting different roles of the receptors in the control of the Leydig cell function.
Prostatic secretory and basal or stem cells were isolated from rat ventral prostate lobes by collagenase dispersion and density centrifugation in a Percoll gradient. The membrane-bound adenylyl cyclase of secretory cells could be activated in a dose-dependent manner by vasoactive intestinal peptide (VIP ED50 10(-7)M) but not thyrotropin-releasing hormone (TRH). Conversely, only TRH could significantly stimulate the adenylyl cyclase in basal cell membranes (ED50 5 X 10(-7). In two separate studies enzyme activity was stimulated seven- and 13-fold by this peptide. This action of TRH on prostatic basal cells supports previous reports that high levels of immunologically active TRH have been found in prostate tissue and that TRH stimulates the growth of prostatic cancer cells in vitro.
Epididymal function was evaluated in normozoospermic men and men with asthenoteratozoospermia using alpha-glucosidase as a secretory parameter. No difference was observed in the total quantity of the enzyme secreted into the ejaculate in spite of major differences between the two groups in the proportion of spermatozoa exhibiting progressive motility and normal morphology. In general, the secretion of alpha-glucosidase was positively correlated with the sperm concentration in the normozoospermic group, but not in asthenozoospermic subjects. The total enzyme contents of the ejaculate were significantly greater in men with asthenoteratozoospermia (sperm concentrations, greater than 35 x 10(6)/ml) than in subjects with severe oligoasthenoteratozoospermia (sperm concentrations less than 10 x 10(6)/ml, P less than 0.01) indicating a higher incidence of epididymal occlusion and/or dysfunction in the latter group. Within normozoospermic individuals, extremes in progressive motility or abnormal morphology could not be related to the quantities of enzyme when expressed per million sperm cells. It is concluded that if alpha-glucosidase is a reliable parameter of human epididymal secretory function, variation in the secretory function of the epididymis cannot explain the poor sperm quality observed in asthenoteratozoospermic individuals.
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