Neuroendocrine actions of organohalogens: thyroid hormones, arginine vasopressin, and neuroplasticity.
Organohalogen compounds are global environmental pollutants. They are highly persistent, bioaccumulative, and cause adverse effects in humans and wildlife. Because of the widespread use of these organohalogens in household items and consumer products, indoor contamination may be a significant source of human exposure, especially for children. One significant concern with regard to health effects associated with exposure to organohalogens is endocrine disruption. This review focuses on PCBs and PBDEs as old and new organohalogens, respectively, and their effects on two neuroendocrine systems; thyroid hormones and the arginine vasopressin system (AVP). Regarding neuroendocrine effects of organohalogens, there is considerable information on the thyroid system as a target and evidence is now accumulating that the AVP system and associated functions are also susceptible to disruption. AVP-mediated functions such as osmoregulation, cardiovascular function as well as social behavior, sexual function and learning/memory are discussed. For both thyroid and AVP systems, the timing of exposure seems to play a major role in the outcome of adverse effects. The mechanism of organohalogen action is well understood for the thyroid system. In comparison, this aspect is understudied in the AVP system but some similarities in neural processes, shown to be targeted by these pollutants, serve as promising possibilities for study. One challenge in understanding modes of action within neuroendocrine systems is their complexity stemming, in part, from interdependent levels of organization. Further, because of the interplay between neuroendocrine and neural functions and behavior, further investigation into organohalogen-mediated effects is warranted and may yield insights with wider scope. Indeed, the current literature provides scattered evidence regarding the role of organohalogen-induced neuroendocrine disruption in the neuroplasticity related to both learning functions and brain structure but future studies are needed to establish the role of endocrine disruption in nervous system function and development.
Kodavanti
Prasada Rao S
PR
Neurotoxicology Branch, Toxicity Assessment Division, B 105-06, National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA. kodavanti.prasada@epa.gov
Curras-Collazo
Margarita C
MC
D000818:Animals; D001127:Arginine Vasopressin / Q000032:analysis / Q000378:metabolism*; D002490:Central Nervous System / Q000187:drug effects / Q000378:metabolism; D052244:Endocrine Disruptors / Q000633:toxicity*; D005260:Female; D006801:Humans; D006846:Hydrocarbons, Halogenated / Q000633:toxicity*; D007858:Learning / Q000187:drug effects; D008297:Male; D051379:Mice; D009473:Neuronal Plasticity / Q000187:drug effects*; D009490:Neurosecretory Systems / Q000187:drug effects*; D020258:Neurotoxicity Syndromes / Q000378:metabolism; D051381:Rats; D012919:Social Behavior; D013961:Thyroid Gland / Q000187:drug effects; D013963:Thyroid Hormones / Q000032:analysis / Q000378:metabolism*
D052244:Endocrine Disruptors; D006846:Hydrocarbons, Halogenated; D013963:Thyroid Hormones; D001127:Arginine Vasopressin