Effects on Sexual Behavior in .NET

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Effects on Sexual Behavior
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Anabolic steroids, antidepressants and drugs of abuse affect libido, potency, and ejaculatory function. Anabolic steroids are derivatives of testosterone, and have strong genitotropic effects. There is published evidence indicating that anabolic steroids increases sexual desire; however, the frequency of erectile dysfunction is also increased. Treatment with the antidepressant uoxetine has been associated with sexual side effects including delayed or nonexistent ejaculation and hyposexuality. Mice treated in utero with the anitleukemic agent 5-aza-2 -deoxycytidine exhibit abnormal reproductive behavior and low reproductive capacity.
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Effects on Endocrine Function
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Cimetidine (for treatment of peptic ulcers) competes with dihydrotestosterone for receptors in the testis and accessory sex glands. The more common sequelae are low sperm count and gynacomastia. Epidemiological evidence has shown that occupation exposure to oral contraceptives can induce gynacomastia in exposed males. Diethylstilbestrol (DES) antagonizes the activity of fetal testosterone. In the male offspring, testicular hypoplasia, abnormal semen parameters, and infertility result. Ketoconazole has be shown to be transported to the seminal uid and to immobilize the sperm.
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REPRODUCTIVE SYSTEM
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FEMALE REPRODUCTIVE PHYSIOLOGY
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As described previously for the male, the female hormonal signaling is composed of four primary levels: CNS, hypothalamus, anterior pituitary, and gonads. The gonadotropin-releasing hormones of the hypothalamus stimulates the anterior pituitary to release LH and FSH. Subsequently LH and FSHS stimulate the release of estrogen and progesterone from the ovaries (Figure 20.3). Estrogen is secreted in the growing follicle and has effects on the uterus. The oocytes are formed before birth, then develop into the primary oocytes after meiosis. At the time of puberty, the release of gonadotropin stimulates the oocytes to develop into graa an follicles (Figure 20.3).
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Ovarian Cycles. Estrus is the period when the female mammal is most receptive to the male (coincides with high levels of circulating estrogen). Rodents are considered to be polyestrous and have a succession of estrus cycles. Cats are seasonally (spring, early fall) polyestrus, while dogs are monestrous. Humans and higher primates cycle at monthly intervals. Although most mammals ovulate spontaneously, some mammals (cats and minks) undergo provoked or induced ovulation (i.e., stimulated by mating). The estrus cycle and the resulting differences in circulating hormone concentrations at different stages of the cycle are depicted in Figure 20.4. The changes in circulating hormone and the stage of follicle development during an adverse toxicant insult results in a variety of toxicological manifestations.
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Germinal Epithelium
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Primary Follicles
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Corpus Luteum Theca Externa Theca Interna Maturing Follicle
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Figure 20.3 The arrow follows the ovarian follicles (time course) from their maturation from primary follicles to the corpus luteum. (Adapted from Web site of Dr. Steven Scadding and Dr. Sandra K. Ackerley, http://www.uoguelph.ca/zoology/devobio/210labs/ovary4.html.)
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MECHANISMS AND TARGETS OF FEMALE REPRODUCTIVE TOXICANTS
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PITUITARY
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CORPUS LUTEUM
PROGESTERONE
UTERUS
PHASE
22 24
28 days
Menstruation Follicular/Proliferative Lufeel/Secretory
The Hormonal Cycle
Figure 20.4 Women s menstrual cycle. (Courtesy of Women s Health Interactive, http://www. womens-health.com/health center/gynecology/gyn repro menstrual.html.)
20.5 MECHANISMS AND TARGETS OF FEMALE REPRODUCTIVE TOXICANTS
Xenobiotics can adversely affect the normal functions of the cells/organs of the reproductive system. These agents may induce a variety of outcomes, including prevention of ovulation and impairment of ovum transport, fertilization, or implantation. Endocrine disruptors may mimic endogenous hormones as well as directly destroy cellular components, leading to cell death. More indirect effects may include inhibition of key enzymes involved in steroid synthesis.
20.5.1 Tranquilizers, Narcotics, and Social Drugs
Compounds within this class of substances can inhibit hypothalamic pituitary ovarian axis function by inhibiting gonadotropin secretion. Subsequently ovulation and estrus is suppress leading to infertility or reduced fertility.
REPRODUCTIVE SYSTEM
Endocrine Disruptors (EDs)
Endocrine disruptors are compounds (synthetic and naturally occurring) that can alter the normal hormonal balance and function in animals. The historical ED diethylstilbestrol (DES) is a classic example of an endocrine disrupter affecting female reproductive health. In utero exposure of females to DES is associated with the induction of vaginal carcinomas apparent after puberty. In experimental mice, estrogenic substances cause accelerated sexual maturation and irregular estrous cycles and prolonged estrous. In rats, xenoestrogens such as kepone and methoxychlor cause masculinization of the exposed female rats. These rats do not ovulate, lack stimulation of the LH surge, and exhibit male sexual behavior. In humans, estrogen mimicking compounds can alter natural hormonal cycles and have been associated with breast cancer induction. Certain environmental EDs may function as promoters or inducers of carcinogenesis. Polychlorinated biphenyls (PCBs) and a trichloroethane compound (DDT) are persistent in the environment. Serum DDE (a DDT metabolite) levels have been found to correlate with breast cancer incidence.