Reproductive system infertility

Reproductive System. The primary PGs are intimately involved in reproductive physiology (67). PGE2 and PGP2Q, are potent contractors of the pregnant utems and intravenous infusion of either of these compounds to pregnant humans produces a dose-dependent increase in frequency and force of uterine contraction. PGI2 and TXA2 have mild relaxant and stimulatory effects, respectively, on uterine tissue. The primary PGs also play a role in parturition, ovulation, luteolysis, and lactation and have been impHcated in male infertility. 

In some animals, consumption of a phytoestrogen-rich diet can cause temporary infertility and reproductive system disorders (Irvine, 1999). In humans, lower testosterone levels and a decline in human semen quality over the past century have been luiked to increased exposure to environmental endocrine disrupters (EDCs) (Sharpe and Skakkebaek, 1993). Furthermore, cases of sexual impotence have been reported in males exposed to synthetic estrogens in the pharmaceutical industry (Mattison et al., 1990). If this might be the case, the fetal-prepubertal period and Sertoli cell development would be of critical importance (Sharpe and Skakkebaek, 1993). However, an adverse effect of phytoestrogens on male fertility has yet to be proven. Recent work (Mitchell et al., 2001) addressing this point led to the conclusion that up to 40 mg/day of isoflavones over a two-month period had no effects on gonadotrophin and... 

Data on safety have been obtained from in vitro as well as in vivo animal and human studies (see also Section 10.4). About 50 years ago, Australian farmers observed an infertility syndrome in sheep associated with the consumption of clover species (Bennets et al., 1946). The clover compounds shown to cause the infertility (genistein, daidzein, equol, biochanin A, formononetin) were members of the isoflavone family (Bradbury and White, 1951 Shutt and Braden, 1968), raising the question of whether soy might cause infertility in humans (see also Section 10.4.9). A variety of reports further supported adverse effects of isoflavones on animal reproductive systems (Santell et al., 1997 Flynn et al., 2000a,b). 

Two major systems have been identified as toxicity targets for 1,3-DNB the red blood cell and the male reproductive system (see Section 2.2.2). In the red blood cell, 1,3-DNB induces formation of methemoglobin leading to cyanosis (Blackburn et al. 1988 Linder et al. 1988, 1990 Reader et al. 1991). In the male reproductive system, 1,3-DNB causes disruption of spermatogenesis resulting in hypospermia, poor sperm quality, and infertility (Blackburn et al. 1988 Hess et al. 1988 Linder et al. 1988). Whether adverse hematological and reproductive effects are caused by the same mechanism of action remains unresolved. 

Reproductive system Menstrual irregularities decreased fertility increased gonadal steroid metabolism Hypermenorrhea infertility decreased libido impotence oligospermia decreased gonadal steroid metabolism... 

Sexual function and fertility reflect a wide variety of functions that are necessary for reproduction and may be affected by exposure to environmental factors. Any disturbance in the integrity of the reproductive system may affect these functions. Patterns of reported infertility vary around the world, but approximately 10% of all couples experience infertility at some time during their reproductive years. Human studies on altered sexual function/fertility provide the most direct means of assessing risk, but data are often unavailable. For many environmental chemicals, it is still necessary to rely on information derived from experimental animal models and laboratory studies. 

Because of the complexity of the reproductive system, data on age-adjusted infertility rates are sparse. The proportion of US women (age 15-44) who reported some form of fecundity impairment rose from 8% in 1982 and 1988 to 10% in 1995, an increase in absolute numbers from 4.6 to 6.2 million women (Stephen Chandra, 1998). 

Reproductive toxicity Male or female reproductive system Decreased libido and impotence Infertility Interrupted pregnancy (abortion, fetal death, premature delivery) Infant death or childhood morbidity Altered sex ratio and multiple births Chromosome abnormalities and birth defects Childhood cancer... 

Reproductive system Parenteral Testis Infertility Necrosis of germinal epithelium... 

Sikka, S.C., Kendirci, M., Naz, R. (2005). Endocrine dismptors and male infertility. In Endocrine Disruptors Effects on Male and Female Reproductive Systems, 2nd edition (R.K. Naz, ed.), pp. 291-312. CRC Press/Taylor Francis Group, LLC, Boca Raton. 

Female reproduction may be recognized to be complex because it has been studied in greater detail and many more aspects of the female reproductive system are defined than for the male. Certainly the female reproductive system is overtly more dynamic and, perhaps because of this dynamicism, more susceptible to physical, chemical, and emotional stressors. The discrete series of events of the ovarian cycle which requires precise coordination between the central nervous system, hypothalamus, and pituitary in order for gametogenesis and ovulation to take place provides the opportunity for environmental changes to adversely influence normal processes. If these events are delayed or altered appreciably, some form of short-term infertility will most likely result. When this is compared to the male, the relatively monotonous production of hormone and gametes is not as likely to be overtly influenced by short-term events. 

Toxic infertility as used here refers to adverse effects on the reproductive systems of human males and females that result from exposure to xenobiotic single chemicals and chemical mixtures. This infertility may be because of direct toxic effects on the male or female reproductive organs and endocrine systems, or on the developing fetus such that the fetus cannot be either conceived or carried to term after conception. Developmental toxicity, the onset of adverse effects on the developing fetus or child after birth are discussed in Chapter 24. 

Human infertility can result from the action of xenobiotic chemicals on the female reproductive system, the male reproductive system, attack on the fetus, and the induction of effects in utero that are manifest during adulthood, giving rise to a programmed infertility. Spontaneous abortion can ensue when pregnant women are exposed to toxic chemicals such as those in disinfection byproducts produced by the chlorination of drinking water. 

There are a number of abnormalities that can affect the male reproductive system before birth, in childhood, or in adulthood. For the purposes of this chapter, they have been divided into categories of (1) hypogonadotropic hypogonadism, (2) hypergonadotropic hypogonadism, (3) defects in androgen action (Box 53-1), (4) impotence, and (5) gynecomastia. The effects of these abnormalities on infertility are discussed later in this chapter. 

The side effects of anabolic steroids range from acne to deadly liver tumors. Effects on the male reproductive system include testicular atrophy, a decrease in sperm count, and, occasionally, temporary infertility. 

Reproductive hazards — A large number of workplace chemicals, physical and biological, can damage reproductive systems resulting in infertility, spontaneous abortion, developmental impairment or death in an embryo, fetus or child. In the past, OSHA has issued a limited number of rules that acknowledge and provide partial protection from reproductive risks. OSHA is currently developing an action plan to reduce worker exposures to reproductive hazards. 

It has recently been found that kisspeptin can restart the female reproductive system in women who have stopped ovulating due to an imbalance in their sex hormones. Kisspeptin is therefore a potential basis for a new infertility treatment - the kiss of life indeed ... 

Reproductive system Environmental arsenic exposure can impair male fertility. A case-control study in China concluded that elevated inorganic arsenate (Asi(V)) exposure is associated with arsenic-induced male infertility. The mechanism of toxicity by arsenic species may involve oxidative stress and sexual hormone disruption measured by biomarkers including acylcamitines, aspartic acid and hydroxyestrone, which were negatively associated with infertility, and uridine and methylxanthine, which were positively associated [44 ]. Arsenic exposme is also correlated to a decrease in human semen quality as reported in a reproductive-age Chinese cohort. The study demonstrated significant association of dimethyl arsenic species (DMA) concentration with low sperm concentrations [45 -]. 

P4 is a non-saturated a, p cetone, a steroid hormone with vital role in the maintenance of human and animal health. Its imbalance can cause malformations of the reproductive system and also infertility problems (Senger, 1999 Christian, Brent Calda, 2007). 

Toxicology. 2-Methoxyethanol (2ME) affects the central nervous system and depresses the hematopoietic system in animals, it causes adverse reproductive effects, including terato-genesis, testicular atrophy, and infertility. 

Successful reproduction (and sex) involves many complex chemical processes that can be disrupted at various points to reduce fertility and conception. Part of this process is under control of the endocrine system, and chemicals that affect the endocrine system are termed endocrine disruptors. In the 1950s, understanding of the endocrine system led to the development of birth control pills as a way to reduce fertility in humans. This is a desirable and planned use of endocrine disruptors. Subsequently, it was discovered that a number of chemicals released into the environment could disrupt the endocrine system and reduce fertility of wildlife. Some are concerned that exposure to these chemicals, such as DDT and dioxin (TCDD), may also affect human fertility (Table 17.1). Approximately 15% of couples of reproductive age are infertile. Endocrine disruptors may also affect fetal development, causing demasculization and feminization of the offspring, which in turn cause reduced fertility in the next generation. 

---