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Chapter 11 - Effects of Environmental Chemicals on Male Reproduction
- from Section 2 - Clinical Evaluation of the Infertile Male
- Edited by Larry I. Lipshultz, Baylor College of Medicine, Texas, Stuart S. Howards, University of Virginia, Craig S. Niederberger, University of Illinois, Chicago, Dolores J. Lamb, Weill Cornell Medical College, New York
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- Book:
- Infertility in the Male
- Published online:
- 08 July 2023
- Print publication:
- 15 June 2023, pp 182-196
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Summary
The potential for chemicals and toxicants to adversely impact health and reproduction is not a new concern; it dates back to biblical times, ancient Egypt, Greece, and the Roman Empire [1, 2]. However, it was not until the middle of the twentieth century that concerns about the effects of chemicals on reproduction were raised. In 1962, Rachel Carlson published her landmark book The Silent Spring, in which she described the harmful effects of pesticides on wildlife reproduction [3]. She is credited with starting the environmental movement, leading to the establishment of the National Institute of Environmental Health Sciences (NIEHS) in 1966 [4] and the National Institute for Occupational Safety and Health (NIOSH) in 1970 [5]. The mission of the NIEHS is to “discover how the environment affects people, in order to promote healthier lives and to provide global leadership for innovative research that improves public health by preventing disease and disability.” The mission of NIOSH is to “generate new knowledge in the field of occupational safety and health and to transfer that knowledge into practice for the betterment of workers.” Through the stewardship of these agencies, as well as those in Europe and the World Health Organization (WHO), research in the fields of occupational and environmental effects on reproduction has dramatically increased [6–8]. Nonetheless, relatively few of the thousands of chemicals used in the workplace or as ingredients in commonly used products, or identified in the environment (air, water, earth, and food), have been examined for their effects on reproductive function. Of those chemicals that have been studied, few have been definitively shown to induce reproductive toxicity.
Chapter 12 - Endocrine evaluation
- Edited by Larry I. Lipshultz, Stuart S. Howards, University of Virginia, Craig S. Niederberger, University of Illinois, Chicago
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- Book:
- Infertility in the Male
- Published online:
- 19 May 2010
- Print publication:
- 24 September 2009, pp 199-214
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Summary
In mammals, spermatogenesis begins with diploid stem cells that resemble other somatic cells; it ends with highly specialized motile haploid cells that are remarkably unique in appearance and function. Continuous production of spermatozoa throughout life requires that spermatogonia replenish themselves. Type B spermatogonia undergo mitosis to give rise to diploid primary spermatocytes. The spermatocytes then cross the blood-testis barrier formed by the Sertoli tight junctions to the adluminal compartment. Spermiogenesis refers to the acquisition by the germ cell of several organelles and accessory structures such as the acrosome and the flagellum. Testosterone and follicle-stimulating hormone (FSH) are the two major regulatory hormones of spermatogenesis. FSH binding to its receptor activates adenylate cyclase, and the resultant rise in cAMP triggers binding of cAMP response element modulator (CREM) to ACT (activator of CREM). The complex then acts as a molecular master-switch for a number of genes involved in spermatogenesis.
Contributors
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- By Ashok Agarwal, Joseph P Alukal, Deborah J Anderson, Linda D Applegarth, Saleh Binsaleh, Elizabeth M Bloom, Karen E Boyle, Nancy L Brackett, Robert E Brannigan, James V Bruckner, Victor M Brugh, Ettore Caroppo, Grace M Centola, Aleksander Chudnovsky, Susan L Crockin, Fnu Deepinder, David M. Fenig, Aaron B Grotas, Matthew P. Hardy, Wayne J. G. Hellstrom, Stanton C Honig, Stuart S Howards, Keith Jarvi, Rajasingam S Jeyendran, William E Kaplan, Edward Karpman, Sanjay S Kasturi, Mohit Khera, Nancy A Klein, Dolores J Lamb, Jane M Lewis, Larry I Lipshultz, Kirk C Lo, Charles M Lynne, R. Dale McClure, Antoine A Makhlouf, Myles Margolis, Clara I. Marín-Briggiler, Randall B Meacham, Jesse N Mills, John P Mulhall, Alexander Müller, Christine Mullin, Harris M Nagler, Craig S Niederberger, Robert D Oates, Dana A Ohl, E. Charles Osterberg, Rodrigo L Pagani, Vassilios Papadopoulos, Joseph A Politch, Gail S Prins, Angela A Reese, Susan A Rothmann, Edmund S Sabanegh, Denny Sakkas, Jay I Sandlow, Richard A Schoor, Paulo C Serafini, Mark Sigman, Suresh C Sikka, Rebecca Z Sokol, Jens Sønksen, Miguel Srougi, James Stelling, Justin Tannir, Anthony J Thomas, Paul J Turek, Terry T Turner, Mónica H. Vazquez-Levin, Moshe Wald, Thomas J Walsh, Thomas M Wheeler, Daniel H Williams, Armand Zini, Barry R Zirkin
- Edited by Larry I. Lipshultz, Stuart S. Howards, University of Virginia, Craig S. Niederberger, University of Illinois, Chicago
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- Book:
- Infertility in the Male
- Published online:
- 19 May 2010
- Print publication:
- 24 September 2009, pp vii-x
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13 - Endocrine assessment and hormone treatment of the infertile male
- Edited by Grace M. Centola, University of Rochester Medical Center, New York, Kenneth A. Ginsburg
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- Book:
- Evaluation and Treatment of the Infertile Male
- Published online:
- 16 September 2009
- Print publication:
- 27 June 1996, pp 194-214
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Summary
Introduction
Male factor infertility is a heterogeneous disorder. The majority of subfertile men do not have an identifiable cause of their infertility (Sokol, 1987, 1992). For example, 74% of 1041 patients seen in Melbourne, Australia, for evaluation of their infertility were diagnosed with idiopathic infertility, even though they presented with azoospermia, oligozoospermia, asthenozoospermia or normozoospermia (Baker et al., 1985). The investigators reported that as semen quality improved there was less of a chance of identifying a cause for the disturbed testicular function (Baker & Burger, 1986). Most treatment regimens for idiopathic male infertility have been unsuccessful. However, a small percentage of men will present with a clearly definable disorder that may lend itself to a therapeutic intervention. The selection of the treatment regimen depends on both the underlying endocrine abnormality and the patient's semen analysis. This chapter will review the endocrine factors leading to disordered sperm function, the evaluation needed to diagnose those conditions, and the available treatment options.
Physiology of the hypothalamic–pituitary–testicular axis
The hypothalamic–pituitary–testicular axis is a closely integrated series of closed loop feedback systems involving the higher centers in the central nervous system, the hypothalamus, the pituitary and the testicular endocrine and germinal compartments.
The hypothalamus produces gonadotropin releasing hormone (GnRH), which is transported to the pituitary gland by a short portal system connecting the two areas. Extrahypothalamic neurotransmitters, norepinephrine and dopamine, regulate GnRH synthesis and its pulsatile release into the hypophyseal portal veins. Norepinephrine facilitates GnRH secretion, while dopamine appears to have both stimulatory and inhibitory effects (Steinberger, 1979; di Zerega & Sherins, 1981).