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Rapid and slow hydroxylators of seminal E prostaglandins among men in barren unions
Author(s) -
Pourian M. R.,
Kvist U.,
Björndahl L.,
Oliw E. H.
Publication year - 2009
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/j.1439-0272.1995.tb01075.x
Subject(s) - prostaglandin e , chemistry , prostaglandin , dinoprostone , hydroxylation , seminal vesicle , prostaglandin e2 , medicine , endocrinology , sperm , enzyme , andrology , biochemistry , biology , prostate , cancer
Summary E prostaglandins are formed in seminal vesicles and can be oxygenated by (ω‐1)‐hydroxylation catalysed by cytochrome P450 to 19(R)‐hydroxy metabolites. The latter are not further metabolized. Prostaglandin E 1 (PGE 1 ), PGE 2 , 19‐hydroxy‐PGE 1 and 19‐hydroxy‐PGE 2 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 β‐cyclodextrin silica with 17‐phenyl‐PGE 2 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 E 1 and 19‐hydroxy E 2 showed a 96% covariation, which supports that a common enzymatic mechanism is operating on both E 1 and E 2 prostaglandins and that this mechanism is the major determinant for formation of 19‐hydroxy compounds. We conclude that the relative amounts of PGE 1 , PGE 2 , 19‐hydroxy‐PGE 1 and 19‐hydroxy‐PGE 2 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. Rapid and slow hydroxylators revealed no difference in time of abstinence or in total output of E prostaglandins, sperm number, semen volume or total output of fluid from the seminal vesicles and prostate. The physiological significance of the variation in seminal E prostaglandins and 19‐hydroxylation, respectively, remains unclear.