Abstract

Endocrine disruptors are exogenous compounds that pollute the environment and have effects similar to hormones when inside the body. One of the most widespread endocrine disruptors in the wild is the pesticide dichlorodiphenyltrichloroethane (DDT). Toxic doses of DDT are known to cause cell atrophy and degeneration in the adrenal zona fasciculata and zona reticularis. Daily exposure in a developing organism to supposedly non-toxic doses of DDT have been found to impair the morphogenesis of both the cortex and the medulla of the adrenal glands, as well as disturbing the secretion of hormones in cortical and chromaffin cells. Comparison of high and very low levels of DDT exposure revealed drastic differences in the morphological and functional changes in the adrenal cortex. Moreover, the three adrenocortical zones have different levels of sensitivity to the disruptive actions of DDT. The zona glomerulosa and zona reticularis demonstrate sensitivity to both high and very low levels of DDT in prenatal and postnatal periods. In contrast, the zona fasciculata is less damaged by low (supposedly non-toxic) exposure to DDT and its metabolites but is affected by toxic levels of exposure; thus, DDT exerts both toxic and disruptive effects on the adrenal glands, and sensitivity to these two types of action varies in adrenocortical zones. Disruptive low-dose exposure leads to more severe affection of the adrenal function.

Highlights

  • They produce hormone-like effects once they enter the body, even in very low doses, and disrupt the endogenous hormonal homeostatic mechanisms of regulation of the vital processes of living organisms

  • After the Endocrine Society published documents such as the 2012 Statement of Principles titled “Endocrine-Disrupting Chemicals and Public Health Protection”, letters were sent to the European Commission (March 2013) and the Secretariat for the Strategic Approach to International Chemicals Management (June 2013) calling for the introduction of an evidence-based approach to endocrine disruptors, which further contributed to raising awareness of these compounds and improving the understanding of the problem [5]

  • Endocrine disruptors include various classes of anthropogenic chemicals, such as pesticides (DDT and its metabolites), polychlorinated biphenyls [6,7,8,9], bisphenol A [10,11], polybromide diphenyl ethers [12,13,14], phthalates [15]; and other compounds, such as hormone-like substances of plant origin, which are contained in food [16,17]; various compounds used in the production of consumer and plastic goods; and other industrial environmental pollutants [18,19]

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Summary

Studies on the Effects of Low Doses of DDT on the Adrenal Glands

Since endocrine disruptors are agonists and antagonists of natural hormones, studies of the chemical interactions of DDT and the overall effects of DDT and its metabolites on the endocrine organs of animals and humans are of particular relevance. In rats that were developmentally exposed to low doses of DDT, pronounced and prolonged blood overflow and hemorrhages in the zona glomerulosa and outer zona fasciculata were associated with decreased catecholamine blood levels; the redirection of blood to the portal vein through the cortex was an attempt to compensate for the insufficient production of catecholamines by the medulla, aimed at acceleration of gluconeogenesis in hepatocytes [64]. Further studies showed significant suppression of the thyrozine hydroxylase production in chromaffin cells after prolonged exposure to low doses of DDT [66] These investigations clearly demonstrated the ability of low-dose exposure to DDT to change the cytophysiology of chromaffin cells and disruption of the adrenal medulla function

Disruption of Adrenal Cortex Hormone Secretion by Low-Dose Exposure to DDT
Ultrastructural Changes of Zona Glomerulosa Cells
Ultrastructural Changes of Zona Fasciculata Cells
Ultrastructural Changes of Zona Reticularis Cells
Comparison of the Effects of Exposure to Toxic and Disruptive Doses of DDT
Conclusions
24. DDT and Its Derivatives
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