Permanently compromised NADPH-diaphorase activity within the osmotically activated supraoptic nucleus after in utero but not adult exposure to Aroclor 1254

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dc.contributor.affiliationEnvironmental Toxicology Graduate Program, University of California, Riverside 92521, USA.
dc.contributor.emailmcur@ucr.edu (M.C. Currás-Collazo)
dc.creatorGlenn Coburn, Caryes_ES
dc.creatorWatson-Siriboe, Abenaes_ES
dc.creatorHou, Borines_ES
dc.creatorCheetham, Chades_ES
dc.creatorGillard, Elizabeth Racheles_ES
dc.creatorLin, Lisaes_ES
dc.creatorLeón-Olea, Marthaes_ES
dc.creatorSánchez-Islas, Eduardoes_ES
dc.creatorMucio-Ramírez, Samueles_ES
dc.creatorCurrás-Collazo, Margarita Concepciónes_ES
dc.date2015
dc.date.accessioned2025-09-10T16:41:35Z
dc.date.accessioned2026-03-27T15:32:34Z
dc.date.available2025-09-10T16:41:35Z
dc.date.issued2015
dc.date.published2015
dc.descriptionStimulated 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.es_ES
dc.formatPDFes_ES
dc.identifier.doi10.1016/j.neuro.2014.12.009
dc.identifier.eissn1872-9711
dc.identifier.issn0161-813X
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz
dc.identifier.placePaíses Bajos
dc.identifier.urihttps://doi.org/10.1016/j.neuro.2014.12.009
dc.identifier.urihttps://repositorio.inprf.gob.mx/handle/123456789/8405
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.relation47:37-46
dc.relation.jnabreviadoNEUROTOXICOLOGY
dc.relation.journalNeurotoxicology
dc.rightsAcceso Cerradoes_ES
dc.subject.kwNeurotoxicity
dc.subject.kwPersistent organic pollutants
dc.subject.kwEndocrine disrupting chemicals
dc.subject.kwNitric oxide
dc.subject.kwVasopressin
dc.titlePermanently compromised NADPH-diaphorase activity within the osmotically activated supraoptic nucleus after in utero but not adult exposure to Aroclor 1254es_ES
dc.typeArtículoes_ES

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