Abstract
Endocrine disruptors (ED) are natural and anthropogenic chemicals that can interfere with hormonal systems at different levels. As such, ED-induced alterations in hormone functions have been implicated in many diseases and pathological conditions, including adverse developmental, reproductive, neurological, cardiovascular, and immunological effects in mammals. The fact that ED may compete with several endogenous hormones for multiple receptors and pathways is not always fully considered. This results in a complex response that depends on the cellular context in terms of receptors and interacting proteins and, thus, may differ between tissues and circumstances. Microglia, neurons, and other immune cells are potential targets and still underappreciated actors in endocrine disruption. Due to the large scale of this topic, this review is not intended to provide a comprehensive review nor a systematic review of chemicals identified as endocrine disruptors. It focuses on the immune-neuro-endocrine network in ED toxicity and research gaps, using atrazine as an example to highlight this complexity and the interrelationship between the immune, endocrine, and nervous systems, and ED.
Highlights
Over the past few decades, industrialized countries have faced a significant increase of diseases, including cancer, allergies, autoimmunity, and neurological disorders, such as cognitive and other neurodevelopmental deficiencies, that can be all linked directly or indirectly to alteration in the immune-neuroendocrine network (Manley et al, 2018)
According to the European Commission, a substance is considered an endocrine disruptor if shows: “(a) an adverse effect in/(non-target organisms), which is a change in the morphology, physiology, growth, development, reproduction or life span of an organism, system orpopulation that results in an impairment of functional capacity, an impairment of the capacity to compensate for additional stress or an increase in susceptibility to other influences; (b) an endocrine mode of action, i.e., it has the potential to alter the function(s) of the endocrine system; (c) the adverse effect is a consequence of the endocrine mode of action.” (Commission Regulation, 2018)
This study provides important clues on the molecular mechanism of action of atrazine
Summary
Over the past few decades, industrialized countries have faced a significant increase of diseases, including cancer, allergies, autoimmunity, and neurological disorders, such as cognitive and other neurodevelopmental deficiencies, that can be all linked directly or indirectly to alteration in the immune-neuroendocrine network (Manley et al, 2018). Related to epigenetic effects (Gely-Pernot et al, 2015), atrazine increases aromatase activity by binding to and inhibiting cyclic nucleotide phosphodiesterase, resulting in elevated cAMP production, sufficient to stimulate prolactin release in pituitary cells and to alter steroidogenesis (Sanderson et al, 2002; Roberge et al, 2004; Kucka et al, 2012).
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