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Reduced Sperm Counts (reduced + sperm_count)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Effect of textile waste water on the spermatogenesis of male albino rats

JOURNAL OF APPLIED TOXICOLOGY, Issue 3 2003
R. S. Gupta
Abstract Textile waste water released from dyeing and printing industries situated in Sanganer, Jaipur (India), brought about inhibition of spermatogenesis in male rats. Water analysis showed the presence of heavy metals at more than permissible limits. Oral administration of waste water to the rats at the dose level of 26.6 ml kg,1 body wt. significantly reduced the weights of testes, epididymides and seminal vesicle. Treated animals showed a notable depression of various stages of spermatogenesis. The production of spermatids was inhibited by 70.8% in waste-water-treated rats. The populations of spermatogonia, preleptotene spermatocytes and secondary spermatocytes were decreased by 67.2, 71.1 and 73.2%, respectively. The total number of Sertoli cells was affected after waste water treatment. Reduced sperm count and motility resulted in treated groups. A significant fall in the content of various biochemical parameters of reproductive tissues was observed after water treatment. Copyright © 2003 John Wiley & Sons, Ltd. [source]

How work-place conditions, environmental toxicants and lifestyle affect male reproductive function,

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 5 2002
Jens Peter Bonde
Summary Major temporal and geographical shifts in male reproductive function is presently an issue worldwide. The hormonal disruption hypothesis has achieved considerable attention but epidemiological evidence in support of the theory is lacking. Several occupational hazards to male reproductive function are known but exposure prevalences are hardly sufficient to play a role for reduced sperm count in the general male population. Sedentary work may be an exception. Perhaps prolonged time in the sedentary position exhausts the testicular heat regulation. But so far studies addressing implications of the heat hypothesis in the general population are few. Neither change of sexual behaviour nor reduced period of sexual continence seems to be a likely explanation. Tobacco smoking and consumption of caffeine and alcoholic beverages in adulthood have a rather marginal impact on spermatogenesis and can hardly explain major shifts or regional differences in male reproductive health. However, prenatal effects following smoking during pregnancy might play a role because we have witnessed a smoking epidemic among fertile women in some countries during the second half of the twentieth century. Moreover, if genetic factors play more than a marginal role for testicular function and sperm count, pregnancy planning resulting in reduced family size during the past 100 years could possibly explain a decline in semen quality because the most fertile part of the population reproduce less while the subfertile probably continue to get a limited number of children. [source]

Occupational risks for male fertility: an analysis of patients attending a tertiary referral centre

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 6 2001
Sebastian Kenkel
The impact of environment and occupation on male fertility is still under debate. We investigated whether certain occupations may be over- or under-represented among men attending our infertility clinic in relation to the entire population of the area. Diagnoses and semen parameters of 2054 infertile men from the district of Münster were analysed retrospectively. The patients were categorized into 29 occupational groups. The relative size of each group was compared with that of the entire population in the district of Münster. Farmers were over-represented compared with the general population. Farmers and painters/varnishers showed a significantly higher proportion of reduced sperm counts [odds ratios (OR): 2.13 and 2.17, 95% confidence intervals: 1.18,3.88 and 1.02,4.65] and severely reduced sperm concentrations compared with the entire group of infertile men; in addition, significantly more farmers presented with a history of maldescended testes than other occupational groups (OR: 2.76 and 2.84; CI: 1.12,6.75 and 1.27,6.34). Metal workers/welders formed significantly higher proportions of patients with reduced sperm motility (OR: 5.99; CI: 1.38,26.00). The relatively poor semen parameters of the painters/varnishers could be caused by exposure to toxins. This may also apply to the farmers (fertilizers, herbicides); however, the elevated rate of maldescended testes suggests an effect of exposure during prenatal development or a genetic cause. The findings for metal workers/welders may be because of heat or toxins at the workplace. The study demonstrates that certain occupations are preferentially associated with male infertility. [source]

Y chromosome haplogroups: A correlation with testicular dysgenesis syndrome?

APMIS, Issue 1 2003
KEN McELREAVEY
Testicular dysgenesis syndrome encompasses low sperm quality, hypospadias, cryptorchidism and testicular cancer. Epidemiological studies and genetic data from familial cases suggest that testicular dysgenesis syndrome has a common etiology. The Y chromosome is known to encode genes that are involved in germ cell development or maintenance. We have therefore investigated if different classes of Y chromosomes in the general population (Y chromosome haplogroups) are associated with aspects of the testicular dysgenesis syndrome. We defined the Y chromosome haplogroups in individuals from different European counties who presented with either (i) oligo- or azoospermia associated with a Y chromosome microdeletion, (ii) unexplained reduced sperm counts (<20×106/ml) or (iii) testicular cancer. We failed to find Y chromosome haplotype associations with either microdeletion formation or testicular cancer. However, in a study of the Danish population, we found that a specific Y chromosome haplogroup (hg26) is significantly overrepresented in men with unexplained reduced sperm counts compared with a Danish control population. The factors encoded by genes on this class of Y chromosome may be particularly susceptible to environmental influences that cause testicular dysgenesis syndrome. Our current data highlight the need for further analyses of clinically well-defined patient groups from a wide range of ethnic and geographic origins. [source]