Rapid and slow hydroxylators of seminal E prostaglandins among men in barren unions

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Abstract
E prostaglandins are formed in seminal vesicles and can be oxygenated by (omega-1)-hydroxylation catalysed by cytochrome P450 to 19(R)-hydroxy metabolites. The latter are not further metabolized. Prostaglandin E1 (PGE1), PGE2, 19-hydroxy-PGE1 and 19-hydroxy-PGE2 were measured in seminal fluid of 95 men, who attended the clinic for infertility. After extractive isolation, the E prostaglandins were converted to B prostaglandins by alkali treatment and analysed by high performance liquid chromatography on beta-cyclodextrin silica with 17-phenyl-PGE2 as an internal standard. The relative amount of 19-hydroxy E-prostaglandins varied between 26% and 97%. Most (86%) of the men were classified as rapid or normal hydroxylators with PGE/19-hydroxy PGE ratios below 0.75, while 14% were slow hydroxylators. The relative amount of 19-hydroxy E1 and 19-hydroxy E2 showed a 96% covariation, which supports that a common enzymatic mechanism is operating on both E1 and E2 prostaglandins and that this mechanism is the major determinant for formation of 19-hydroxy compounds. We conclude that the relative amounts of PGE1, PGE2, 19-hydroxy-PGE1 and 19-hydroxy-PGE2 in seminal fluid vary, possibly due to polymorphic expression of this enzymatic mechanism. Total output of 19-hydroxy-PGE compounds, but not the primary PGE compounds was correlated with the output of seminal fructose, supporting that the 19-hydroxy prostaglandins are the normal end products of the seminal vesicles. Low sperm concentration found among men with high output of E prostaglandins could here simply be explained by dilution of spermatozoa by a high output of seminal vesicular fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

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