Organizational versus Activational Effects of Endocrine Toxicants in Visual Studio .NET

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Organizational versus Activational Effects of Endocrine Toxicants
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Effects of receptor agonists or antagonists on endocrine related processes are often described as being either organizational or activational. An organizational effect of an endocrine toxicant is one that typically results from neonatal or prenatal exposure during which time hormones are directing various irreversible aspects of development.
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ENDOCRINE SYSTEM
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Accordingly the disrupting effect of the toxicant also is irreversible. These organizational effects may be evident only later in life during maturation or reproduction. Neonatal exposure to DES resulting in proliferation of epithelial cells of the reproductive tract at reproductive maturity is an example of an organizational effect of an endocrine toxicant. Organizational effects of endocrine toxicants have been of great concern to toxicologists and are the most dif cult type of toxicity to diagnose owing to the temporal separation between exposure and effect. An activational effect of an endocrine toxicant occurs in the same time frame as the exposure and is the consequence of the toxicant disrupting the immediate role of a hormone in some physiological process. Activational effects are reversible following cessation of exposure to the toxicant. For example, androgens contribute to maintenance of the prostate gland in the adult male. Exposure of adult males to an antiandrogen can result in a decrease in prostate size. Cessation of exposure to the antiandrogen then results in restoration of the prostate gland to its normal size.
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Inhibitors of Hormone Synthesis
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Endocrine toxicants can elicit antihormone activity by lowering levels of endogenous hormone in the body. With steroid hormones, chemicals typically elicit this effect by inhibiting enzymes necessary for synthesis of the hormone. For example, the cytochrome P450 enzyme CYP19 is responsible for the aromatization of testosterone to form 17 -estradiol. CYP19 inhibitors such as fadrozol, anastrozole, and letrozole, can lower endogenous 17 -estradiol levels resulting in de-feminization. Cytochrome P450s enzymes also are critical to various hydroxylation reactions that contribute to the synthesis of androgens and other steroid hormones and inhibition of these enzymes can result in a variety of antisteroid hormone effects. For example, the agricultural and medicinal fungicides propiconazole, ketoconazole, and fenarimol are capable of inhibiting P450 enzymes and reducing synthesis and circulating levels of testosterone and other steroid hormones. Toxicological consequences of the lowering of endogenous steroid hormone levels are typically comparable to those effects elicited by antagonists of the hormone s receptor.
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Inducers of Hormone Clearance
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In most species, steroid and thyroid hormones are inactivated and cleared from the body by the same biotransformation processes that are involved in chemical detoxi cation (see 7). Predominant among the hormone biotransformation processes in vertebrates are hydroxylation, glucuronic acid conjugation, and sulfate conjugation. The thyroid hormones T3 and T4 are inactivated and cleared following sulfate and glucuronic acid conjugation, respectively. The glucuronosyl transferase enzymes that are responsible for the elimination of T4 are induced following exposure to phenobarbitaltype inducers and Ah receptor ligands (see 9). Thus exposure to chemicals such as some dioxins and PCBs can result in enhanced clearance of thyroid hormone resulting in low circulating thyroid hormone levels. The resulting hypothyroid state can result in a variety of pathological conditions. In newborn infants, hypothyroidism is associated with cretinism. This organizational syndrome is characterized by mental retardation, short stature, and various neurological abnormalities. In children,
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INCIDENTS OF ENDOCRINE TOXICITY
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hypothyroidism can cause delayed growth and mental development while advancing the onset of puberty in adolescents. Hypothyroidism in adults results in various activational abnormalities including impaired cardiovascular, pulmonary, intestinal, and renal function. Chronic fatigue, lethargy, and dif culty in concentration are also associated with thypothyroidism in adults. Increased clearance of steroid hormones due to induction of hepatic biotransformation enzymes following chemical exposure often has been cited as a possible mechanism by which toxicants could lower circulating testosterone or 17 -estradiol levels. While enhanced clearance of sex steroids has been demonstrated following chemical exposure and induction of hepatic biotransformation enzymes, elegant feedback control mechanisms tend to ensure that more hormone is produced and homeostasis is maintained (Figure 17.2). Enhanced clearance of sex steroids can contribute to endocrine disruption if the toxicity also results in impaired hormone synthesis (i.e., gonadal toxicity or interference with the feedback control of hormone synthesis). 2,3,7,8-Tetrachlorodibenzodioxin appears to lower circulating sex steroid levels via this dual effect.
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