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HERO ID
2834884
Reference Type
Journal Article
Title
Permanently compromised NADPH-diaphorase activity within the osmotically activated supraoptic nucleus after in utero but not adult exposure to Aroclor 1254
Author(s)
Coburn, CG; Watson-Siriboe, A; Hou, B; Cheetham, C; Gillard, ER; Lin, L; León-Olea, M; Sánchez-Islas, E; Mucio-Ramírez, S; Currás-Collazo, MC
Year
2015
Is Peer Reviewed?
1
Journal
NeuroToxicology
ISSN:
0161-813X
EISSN:
1872-9711
Volume
47
Page Numbers
37-46
Language
English
PMID
25572879
DOI
10.1016/j.neuro.2014.12.009
Web of Science Id
WOS:000352924800005
Abstract
Stimulated vasopressin (VP) release from magnocellular neuroendocrine cells in the supraoptic nucleus (SON) of hyperosmotic rats is inhibited by treatment with the industrial polychlorinated biphenyl (PCB) mixture, Aroclor 1254. Because VP responses to hyperosmotic stimulation are regulated by nitric oxide (NO) signaling, we studied NO synthase (NOS) activity in the SON of hyperosmotic rats as potential target of PCB-induced disruption of neuroendocrine processes necessary for osmoregulation. To examine PCB-induced changes in NOS activity under normosmotic and hyperosmotic conditions, male Sprague-Dawley rats were exposed to Aroclor 1254 (30mg/kg/day) in utero and NADPH-diaphorase (NADPH-d) activity was assessed in SON sections at three ages: postnatal day 10, early adult (3-5 months) or late adult (14-16 months). Hyperosmotic treatment increased mean NADPH-d staining density of oil hyperosmotic controls by 19.9% in early adults and 58% in late adulthood vs normosmotic controls. In utero exposure to PCBs reduced hyperosmotic-induced upregulation of NADPH-d activity to control levels in early adults and by 28% in late adults. Basal NADPH-d was reduced in postnatal rats. Rats receiving PCB exposure as early adults orally for 14 days displayed normal responses. Our findings show that developmental but not adult exposure to PCBs significantly reduces NOS responses to hyperosmolality in neuroendocrine cells. Moreover, reduced NADPH-d activity produced by in utero exposure persisted in stimulated late adult rats concomitant with reduced osmoregulatory capacity vs oil controls (375±9 vs 349±5mOsm/L). These findings suggest that developmental PCBs permanently compromise NOS signaling in the activated neuroendocrine hypothalamus with potential osmoregulatory consequences.
Keywords
Neurotoxicity; Persistent organic pollutants; Endocrine disrupting chemicals; Nitric oxide; Vasopressin
Tags
IRIS
•
PCBs
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LitSearch August 2015
Pubmed
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