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Male Reproductive Function (male + reproductive_function)

Distribution by Scientific Domains

Medical Sciences	85%

Selected Abstracts

Xenobiotic metabolism, genetic polymorphisms and male infertility

ANDROLOGIA, Issue 4-5 2000
H.-C. Schuppe
Male reproductive function may be impaired by various occupational and environmental chemical agents. The majority of these xenobiotics, however, require metabolic activation in order to exert adverse effects via covalent interactions between intermediate metabolites and cellular macromolecules such as DNA or protein. In addition, metabolization may alter endocrine-disrupting properties of xenobiotics. Thus tissue-specific expression and regulation of multiple xenobiotic-metabolizing enzymes are likely to play an important role in chemically induced disorders of male reproductive organs. Recent studies suggest that genetic polymorphisms underlying inter-individual and inter-ethnic variability of xenobiotic metabolism modulate susceptibility to male reproductive disorders. For cytochrome P450 1A1 (CYP1A1), a key enzyme in extra-hepatic metabolic activation of lipophilic xenobiotics, increased frequencies of two genetically linked polymorphisms have been found among infertile men. [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]

Endocrine disruptors and male reproductive function , a short review

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue S2 2000
Sin-Eng Chia
Semen quality has decline in many countries over the last few decades. There has been an increase in the incidence of testicular cancer world-wide. The incidences of cryptorchidism and hypospadias have also increased in many countries. A biological plausible hypothesis has suggested that man-made chemicals act as endocrine disruptors resulting in altered development of the reproductive tract causing the observed effects. Endocrine disruptors include natural products, pharmaceuticals, industrial products and environmental pollutants. There are limitations in the current in vivo and in vitro assays for the assessment of endocrine disruptors. Epidemiological human studies are necessary to fill in the gap of knowledge. Based on the current knowledge, the impact of endocrine disruptors on the male reproductive function remain to be appreciated. [source]

Mice lacking cyclin-dependent kinase inhibitor p19Ink4d show strain-specific effects on male reproduction

MOLECULAR REPRODUCTION & DEVELOPMENT, Issue 8 2007
Gregory M. Buchold
Abstract p19Ink4d is a member of the INK4 family of cyclin-dependent kinase inhibitors, which are important negative regulators of the G1-phase cyclin-dependent kinases CDK4 and CDK6. On a mixed C57BL/6,×,129P2/OlaHsd background, mice deficient for p19Ink4d exhibited defects in male reproductive function including testicular atrophy, alteration in serum follicle stimulating hormone, qualitative increase in germ cell apoptosis, and delayed kinetics of meiotic prophase markers (Zindy et al., 2001. Mol Cell Biol 21:3244,3255; Zindy et al., 2000. Mol Cell Biol 20:372,378). In this study, a quantitative assessment of these aspects of reproductive capacity demonstrated relatively mild deficits in p19Ink4d,/, males compared to controls. These effects did not dramatically worsen in older males although some seminiferous tubule defects were observed. Following marker-assisted backcrossing into the C57BL/6 background, p19Ink4d,/, males did not display defects in testis weights, sperm numbers, serum FSH, germ cell apoptosis, or kinetics of selected meiotic prophase markers. These studies indicate that a reduction in Ink4 family function by the loss of p19Ink4d is sufficient to induce mild reproductive defects in male mice with a mixed genetic background, but not in the C57BL/6 genetic background. Mol. Reprod. Dev. 74: 1008,1020, 2007. © 2007 Wiley-Liss, Inc. [source]

Reproduction in male rats is vulnerable to treatment with the flavonoid-rich seed extracts of Vitex negundo

PHYTOTHERAPY RESEARCH, Issue 1 2004
Suwagmani Das
Abstract A partially puri,ed ,avonoid-rich extract was prepared from the seed of Vitex negundo. The effect of this extract on the reproductive system of male rats was investigated at four different concentrations. All the major accessory sex organs shed weight when the preparation was administered at doses of ,15 mg/rat/day after 15 days of treatment. The drop in weight was also re,ected in disturbed tissue biochemistry. Secretory products such as citric acid in the prostate, fructose in seminal vesicles and epididymal , -glucosidase activity, indices of accessory sex organ function in males, diminished. Microscopic examination of the sperm derived from the cauda epididymides of treated animals showed only a marginal change in vitality. However, sperm numbers dwindled and slackness in their motility was observed, factors that may impede fertility. Toxicity testing in blood did not point to distress in any of the vital organs. Taken together, it is inferred that the seed extracts of V. negundo interfere with male reproductive function without producing adverse toxicity in other vital organs. Copyright © 2004 John Wiley & Sons, Ltd. [source]