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Perinatal exposure to organohalogen pollutants decreases vasopressin content and its mRNA expression in magnocellular neuroendocrine cells activated by osmotic stress in adult rats
Citation:
Mucio-Ramirez, S., E. Sanchez-Islas, E. Sanchez-Jaramillo, M. Curras-Collazo, V. Juarez-Gonzalez, M. Alvarez-Gonzalez, L. Orser, B. Hou, F. Pellicer, P. Kodavanti, AND M. Leon-Olea. Perinatal exposure to organohalogen pollutants decreases vasopressin content and its mRNA expression in magnocellular neuroendocrine cells activated by osmotic stress in adult rats. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, 329:173-189, (2017).
Impact/Purpose:
This research improves our understanding of the effects of persistent organic chemicals such as polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) on the neuroendocrine system and their role in adverse effects associated with the nervous system. This study demonstrated POCs might interfere with the induction of AVP mRNA transcript levels and resulting protein, causing a central dysfunction of the vasopressinergic system. The results are important to program offices as well as regions in their decision making regarding the endocrine disrupting activity of POCs, which fall in to high production volume (HPV) chemicals. The long term significance is to understand adverse outcome pathways (AOPs) for the effects of these POCs on the nervous system.
Description:
Polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are environmental pollutants that produce neurotoxicity and neuroendocrine disruption. They affect the vasopressinergic system but their disruptive mechanisms are not well understood. Our group reported that rats perinatally exposed to Aroclor-1254 (A1254) and DE-71 (commercial mixtures of PCBs and PBDEs) decrease somatodendritic vasopressin (AVP) release while increasing plasma AVP responses to osmotic activation, potentially emptying AVP reserves required for body-water balance. The aim of this research was to evaluate the effects of perinatal exposure to A1254 or DE-71 (30 mg kg/day) on AVP transcription and protein content in the paraventricular and supraoptic hypothalamic nuclei, of male and female rats, by in situ hybridization and immunohistochemistry. Also cFOS mRNA expression was evaluated in order to determine if the neuroendocrine cells are activated in response to osmotic stimulation. Animals were grouped as: control (vehicle); dehydrated (salt loading), exposed to either A1254 or DE-71; and dehydrated exposed to A1254 or DE-71. The results confirmed a physiological increase in AVP-immunoreactivity (AVP-IR) and gene expression in response to dehydration as reported elsewhere. In contrast the exposed groups did not show this response to osmotic activation, they showed significant reduction in AVP-IR neurons, and AVP mRNA expression as compared to the dehydrated controls. cFOS mRNA expression increased in all the A1254 dehydrated groups, suggesting that the AVP-IR decrease is not due to lack of the response to the osmotic activation. Therefore, A1254 may interfere with the activation of AVP mRNA transcript levels and protein, causing a central dysfunction of the vasopressinergic system.
