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Five men with cystic fibrosis delivered semen samples which were analysed for the content of the four main groups of prostaglandins (PGs). No PGs could be found in any of the specimens. The results of the present study provide further evidence that the seminal vesicles constitute the dominant site of production of PGs in human semen.

A comparison of different procedures for adenosinetriphosphate (ATP) determination in whole ejaculates showed that it is advantageous to treat the specimens with trichloroacetic acid (TCA before quantification of ATP by bioluminescence). Semen samples from different men were found to cause varying degrees of inhibition of the luciferin-luciferase reaction. Hence, internal ATP standard had to be added to each sample to allow calculation of endogenous ATP. Mean recovery of ATP was 98.5%. The intrassay and interassay coefficients of variation were 3.0% and 3.9%, respectively. A correlation between the number of progressively motile spermatozoa and the ATP concentration was found (r = 0.89, P = 0.0005, n = 22). The mean level of ATP was 0.49 nmol/living sperm X 10(6) in semen with normal sperm motility and sperm density obtained from 22 men attending our fertility clinic. Seminal ATP was detected only in the spermatozoa.

A single 1 mg dose of prostaglandin (PG) E2 was given orally to 19 men. Ejaculates were obtained 90 minutes and 24 and 48 hours thereafter. Before treatment, each man delivered another three semen samples with the same time intervals as during the study period. PGE2 was also administered to seven men during naproxen treatment and ejaculates were sampled as above. PGE2 did not influence the 90 minutes' posttreatment ejaculates, but after 24 hours there was a significant (P less than 0.05) decrease in sperm counts as compared to the control samples. The change in sperm count was suggested to be due to an effect of PG on the contractile elements in the deferent duct. Sperm motility, viability, and morphology as well as semen volume and adenosine triphosphate (ATP) content remained unchanged. The total semen PGE content was increased 24 hours after treatment from 169 micrograms/ejaculate to 213 micrograms/ejaculate (P = 0.02). In the combined PGE2/naproxen treatment the PGE levels were significantly (P less than 0.05) elevated in the ejaculate 48 hours after treatment. The increase may indicate an increased de novo synthesis of prostaglandins. Based on the results from the analysis of the composition of the 19-hydroxy PGF-isomers with and without naproxen treatment, it is speculated that oral PGE2 influences the cyclo-oxygenase activity.

Whole ejaculates were examined for their content of prostaglandins (PGs) during medication with 250 mg naproxen three times daily for 2 weeks. Six volunteers delivered semen samples before, periodically during, and after the period of medication. During treatment with naproxen, the concentration of PGE, PGF, 19-hydroxy-PGE, and 19-hydroxy-PGF significantly decreased. One week after cessation of medication the PG concentration had returned almost to that found before treatment. The four 19-hydroxy-PGF compounds could be determined separately and the relation between them estimated. The proportion of 8 alpha-19-hydroxy-PGF2 alpha increased, whereas that of 8 beta-19-hydroxy-PGF1 alpha decreased significantly during the medication period. No significant influence of the treatment on sperm density or motility could be observed. It is concluded that treatment with naproxen, a potent inhibitor of PG synthesis, significantly reduces the concentration of all PGs present in human seminal fluid. The implication of the effect on human fertility is discussed.

Prostaglandins E, F, 19-hydroxy E, and 19-hydroxy F (PGE, PGF, 19-OH-PGE, and 19-OH-PGF) in human semen were determined by a new chemical method. The method allows liquefaction to occur, a prerequisite for simultaneous estimation of PG concentration and sperm characteristics in the same ejaculate. The present study showed also that the variation in PG concentration between different individuals was more pronounced than in repeated ejaculates from the same individual. Sperm density and sperm motility seemed related to PG concentration. A high density was associated with a low PG concentration. The concentration of 19-OH-PGE was higher and that of 19-OH-PGF lower in ejaculates with a normal sperm motility than in those with an abnormal motility. It seems that functional requisites of sperm depend upon optimal seminal PG concentration.

The aim of the present study was to evaluate the effect of addition of physiologic amounts of different prostaglandins normally present in semen, on sperm motility, on sperm penetration capacity in cervical mucus in vitro, and on the adenosine triphosphate (ATP) concentration in semen. Semen samples were obtained from volunteers who were attending the fertility outpatient clinic. Sperm motility was measured on a video recorder with a built-in timer, sperm penetration by the Kremer test, and ATP by bioluminescence assay. The addition of 19-hydroxy prostaglandin (PG) E to ejaculates positively stimulated sperm motility and sperm penetration capacity. The opposite effect was observed with 19-hydroxy PGF. PGE1, PGE2, and PGF2 alpha had no effect on either parameter, while PGF1 alpha reduced the sperm motility. The addition of 19-hydroxy PGE to ejaculates increased and the addition of 19-hydroxy PGF reduced semen concentrations of ATP. However, only the last-mentioned effect was statistically significant (P less than 0.05). It is suggested that, in particular, 19-hydroxy PGE and 19-hydroxy PGF are important regulators of sperm motility and that the effect may be mediated via effects on the ATP content in the spermatozoa.