Abstract

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, α‐amylase, pepsin, and neuramini dase 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 lyophilization, 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 epsilon‐aminocaproic acid (EACA). All of these prop erties are characteristics of the seminal en zyme, seminin. A partially purified preparation of this enzyme enhanced liquefaction, and two patients who had low seminin activity pos sessed poorly lysing coagula. These findings confirm that seminin is the agent primarily re sponsible 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.

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