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Biomedical subjects

U Kvist

Publications and source records attributed to U Kvist.

42 records · Page 3Linked to original sources
PubMed1980

Rapid post-ejaculatory inhibitory effect of seminal plasma on sperm nuclear chromatin decondensation ability in man.

The stability of the nuclear chromatin in human spermatozoa soon after ejaculation was studied by exposing the cells to sodium dodecyl sulphate (SDS) one to 20 min after ejaculation. Semen samples were obtained both from men with apparently normal, and from men with impaired prostatic secretion (= subnormal seminal plasma [Zn]). The sperm nuclear resistance to decondensation in SDS increased in both groups during the first 15 min after ejaculation, but was significantly lower in the semen samples with subnormal [Zn]. This fast post-ejaculatory increment in sperm SDS resistance was significantly reduced by a 5-fold saline dilution of the semen at the time of ejaculation. It is discussed if the observed stabilization with time was illusory and that a prostatic component instead counteracted an intrinsic nuclear chromatin decondensation (NCD) process initiated by SDS derangement of spermatozoal membranes.

Chromatin↗
PubMed1980

Reversible inhibition of nuclear chromatin decondensation (NCD) ability of human spermatozoa induced by prostatic fluid.

In semen from donors with adequate secretory function of the prostate, spermatozoa in the first ("prostatic") portion of the ejaculate were more resistant to nuclear swelling in sodium dodecyl sulphate (SDS) than spermatozoa from the second ("vesicular") portion. No such difference was revealed by a donor with severely impaired prostatic function. This demonstrates that some sperm nuclear chromatin stabilizing factor(s) is present in normal prostatic fluid. The chromatin stabilizing factor(s) could largely be removed by washing the spermatozoa in saline containing albumin. Spermatozoa sensitized to SDS in this manner regained their SDS resistance upon exposure to normal (zinc-rich) "prostatic fluid". Such exposure also induced a high degree of resistance in natively SDS sensitive spermatozoa. The possibility is discussed that zinc of prostatic or other origin reversibly inhibits a nuclear chromatin decondensation ability (NCD-ability). It is suggested that such a mechanism may be of essential importance for male genome transfer.

Chromatin↗
PubMed1980

Importance of spermatozoal zinc as temporary inhibitor of sperm nuclear chromatin decondensation ability in man.

Nuclear chromatin decondensation (NCD) of ejaculated human spermatozoa was studied in vitro. Spermatozoa subjected to membrane disintegration induced by the detergent sodium dodecyl sulphate (SDS) were found to undergo NCD if previously or afterwards treated with substances known to deplete the spermatozoa of zinc (albumin and EDTA). Zn2+, but not other, "prostatic" cations (Ca2+, Mg2+), inhibited the experimentally induced NCD and the NCD of spermatozoa from men with impaired prostatic function. It is suggested that the human spermatozoon has an intrinsic mechanism for NCD, that is preserved by temporary zinc inhibition and might be reactivated by zinc removal within the female genital tract.

Cations↗
PubMed1976

A further contribution to the question of trophic and hormonal influences on the noradrenaline content of the male reproductive tract: effect of combined androgen and estrogen treatment of prepuberally castrated rats.

58 days old, prepuberally castrated, male rats were treated with estrogen, testosterone or a combination of both hormones for 18 days. The total noradrenaline (NA)-content of the male accessory glands was increased by the hormone treatments. This increase was smallest in the estrogen treated group and largest in the group treated with both estrogen and testosterone. The NA-concentration, however, followed the reversed picture i.e. it was largest in untreated castrated rats and smallest in the rats receiving both estrogen and testosterone. Neither treatment brought the NA-amount up to the level of uncastrated controls of the same age although the weights of the secondary sex glands of rats receiving both estrogen and testosterone exceeded those of uncastrated controls. Similar, but less definite changes were observed in vas deferens and cauda epididymidis. It is concluded that a developing target area exerts some trophic influence on the adrenergic neurons innervating it. However, the trophic influence exerted by the effector organ on the nerves is not of the kind, that the innervation density and NA-concentration of the organ always are maintained at a constant level.

Animals↗
PubMedDate not supplied

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

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)

Alprostadil↗