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1 Department of Obstétrics and
Gynecology, University of Essen, Essen,
West Germany
2 Department of
Obstetrics and Gynecology, University of
Chicago, Chicago, Illinois
3 Departments of Physiology and
Biophysics, and Obstetrics and
Gynecology, University of Illinois at the
Medical Center, Chicago, Illinois
The coagulation and liquefaction process of
human semen was studied in some detail. It
was found that contact of seminal vesicle fluid
with the other accessory sex gland secretions
or spermatozoa does not seem to be essential
for the formation of the coagulum, and that
heparin and sodium citrate do not affect coagulum formation, indicating a difference between
the seminal coagulation process and that of
the blood clot. Regarding the liquefaction
process of the seminal coagulum, it was shown
that 1) spermatozoa do not influence liquefaction; 2) that the seminal plasminogen activator,
lysozyme,
-amylase, pepsin, and neuraminidase are not the primary liquefying factors;
3) that the liquefying agent is present in the
first portion of a split ejaculate, is heat labile,
is partially destroyed by freezing at -20 C
but is stable to lyophilizatlon, is precipitable
with (NH4)2SO4, is not affected by serum or
EDTA, and is inhibited by rabbit bile but not by
the seminal plasma proteinase inhibitors, the
Kunitz pancreatic trypsin inhibitor, or epsilonaminocaproic acid (EACA). All of these properties are characteristics of the seminal enzyme, seminin. A partially purified preparation
of this enzyme enhanced liquefaction, and two
patients who had low seminin activity possessed poorly lysing coagula. These findings
confirm that seminin is the agent primarily responsible for liquefaction of the seminal
coagulum of man. The data further show that
liquefaction of the seminal coagulum occurs by
a different mechanism than that of the lysis of
the blood clot.
Key words: semen, coagulation, liquefaction, enzymes
Submitted on May 20, 1980
Revised on July 31, 1980
Accepted on July 31, 1980
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