Evolution of gonadotropin structure and function.
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Biomedical subjects
Publications and source records attributed to C H Muller.
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Sperm maturation antigen 4 (SMA-4) is a surface component of the mouse sperm tail. Previously, immunofluorescence studies indicated that SMA-4 may be secreted by principal cells of the distal caput epididymidis and bound to spermatozoa as they pass through that region of the duct. In the present study, detergent extracts of spermatozoa from the cauda epididymidis were subjected to polyacrylamide gel electrophoresis under reducing and denaturing conditions, transferred to nitrocellulose, and immunostained with a monoclonal antibody against SMA-4. A band of approximately 54,000 molecular weight was revealed. The band was also stained by the periodic acid-Schiff (PAS) procedure. This glycoprotein was not detected in extracts of spermatozoa from the proximal caput epididymidis or of spermatozoa from the cauda epididymidis that were preincubated for 4 hours in an in vitro fertilization environment. Blots of sperm-free fluid from the corpus and cauda epididymidis displayed an immunoreactive and PAS-positive band of about 85,000 molecular weight that was not observed in fluid from the caput epididymidis. The difference in the molecular weights of the antigen in the fluid and that in extracts of cauda spermatozoa suggests that SMA-4 may be modified chemically upon association with the sperm surface.
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Assuring the highest possible quality of care to the patient is the first goal of the andrology laboratory. Quality control and quality assurance as they apply to the andrology laboratory are outlined, and special problems in quality control for sperm function assays are addressed. An example of the patient review process is presented. Quality of care also depends on the ability of the laboratory to perform appropriate tests of sperm function that can diagnose sperm defects, predict success or failure of in vitro fertilization, and lead to rational therapies for sperm dysfunctions. Methods for, and diagnostic value of, sperm swim-out, enhanced sperm penetration assays, acrosome reaction assessment, motility analysis of capacitating sperm, and sperm-zona binding assays are reviewed. No single test, other than in vitro fertilization itself, is capable of providing a complete diagnosis or a highly accurate prediction. A battery of sperm function tests, arranged in an algorithm, is presented as a theoretically better approach.
A potentially important event during sperm capacitation is the loss of sperm membrane cholesterol. Although the exact mechanisms mediating this loss are not known, albumin and high density lipoprotein have been proposed as lipid acceptors. The authors propose that lipid transfer may be involved in capacitation as a specific mediator in the sequence of events leading to sperm membrane cholesterol loss. We present the first direct evidence of lipid transfer activity (LTA) in human follicular fluid (HFF). The redistribution of 14C-cholesteryl ester among human plasma lipoproteins was used as a measure of LTA (% Transfer [%T]). The HFF was fractionated by S-300 gel filtration chromatography and assayed for LTA. Three peaks of activity were consistently eluted from the column. Each peak of LTA also stimulated human sperm to penetrate zona-free hamster oocytes after short capacitating incubations. The peak with highest LTA (12.75 +/- 1.11%T) with an Mr approximately 68,000, gave the greatest stimulation (penetration index, PI: 3.34 +/- 0.96 fold increase above control, n = 4). The HFF also showed a significant dose response for both LTA and PI, whereas bovine serum albumin did not. These results demonstrate the existence of LTA in HFF and suggest that a specific lipid transfer protein may have a role in human sperm capacitation or acrosome reaction.
There is considerable confusion about the effects of prostatitis syndromes on male reproductive physiology. Therefore, we correlated findings on seminal fluid and expressed prostatic secretions from 100 men attending a special prostatitis clinic. These men had symptoms of prostatitis but no evidence of urethritis, acute or chronic bacterial prostatitis, or significant urological abnormalities. All subjects were evaluated following a standardized protocol, including lower urinary tract localization studies, expressed prostatic secretion analyses, and seminal fluid analyses with Bryan-Leishman staining. Seminal fluid findings were compared in men with inflammation (> or = 10(6) leukocytes/ml) in their expressed prostatic secretions, i.e., nonbacterial prostatitis, and men without inflammation in prostatic secretions, i.e., prostatodynia. Of 23 men with inflammation (> or = 10(6) leukocytes/ml) in their seminal fluid, 6 (26%) had nonbacterial prostatitis (mean leukocyte concentration 8.6 +/- 9.4 x 10(6)/ml of semen) and 17 (74%) had prostatodynia (mean leukocyte concentration 6.2 +/- 7.0 x 10(6)/ml, not significant). Of 77 men who did not have seminal inflammation, 15 (19%) had nonbacterial prostatitis (mean leukocyte concentration 0.1 +/- 0.2 x 10(6)/ml) and 62 (81%) had prostatodynia (mean leukocyte concentration 0.1 +/- 0.2 x 10(6)/ml, not significant). Men with nonbacterial prostatitis had lower values for several parameters associated with sperm motility, especially the proportion of motile sperm (45% compared with 60% for men with prostatodynia, P = 0.08) and sperm subjective speed score (median 3 compared to 4 for men with prostatodynia, P = 0.03). In summary, a minority of men had seminal inflammation, even among men with nonbacterial prostatitis. There was poor correlation between inflammation in the prostatic secretions and in the semen. Nonbacterial prostatitis, but not seminal inflammation, was associated with reduced sperm motility. Our findings highlight technical issues and the importance of investigating different sites and samples, including the urethra, expressed prostatic secretions, and seminal fluid.