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Titolo:
PCBs, thyroid hormones, and ototoxicity in rats: Cross-fostering experiments demonstrate the impact of postnatal lactation exposure
Autore:
Crofton, KM; Kodavanti, PRS; Derr-Yellin, EC; Casey, AC; Kehn, LS;
Indirizzi:
US EPA, Div Neurotoxicol, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA US EPA Res Triangle Pk NC USA 27711 es Lab, Res Triangle Pk, NC 27711 USA SUNY Albany, Sch Publ Hlth, Albany, NY 12222 USA SUNY Albany Albany NY USA 12222 bany, Sch Publ Hlth, Albany, NY 12222 USA
Titolo Testata:
TOXICOLOGICAL SCIENCES
fascicolo: 1, volume: 57, anno: 2000,
pagine: 131 - 140
SICI:
1096-6080(200009)57:1<131:PTHAOI>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
POLYCHLORINATED-BIPHENYLS PCBS; EPIDERMAL GROWTH-FACTOR; UDP-GLUCURONOSYLTRANSFERASE INDUCERS; DEVELOPMENTAL EXPOSURE; CONGENITAL HYPOTHYROIDISM; FREQUENCY REPRESENTATION; CHLORINATED DIOXINS; AUDITORY FUNCTION; RISK ASSESSMENT; THYROXINE;
Keywords:
polychlorinated aromatic hydrocarbons; polychlorinated biphenyls; thyroid-axis development; circulating T-4 concentrations; lactation exposure; maternal exposure;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
80
Recensione:
Indirizzi per estratti:
Indirizzo: Crofton, KM US EPA, Div Neurotoxicol, Natl Hlth & Environm Effects Res Lab, MD-74B, Res Triangle Pk, NC 27711 USA US EPA MD-74B Res Triangle Pk NC USA 27711 le Pk, NC 27711 USA
Citazione:
K.M. Crofton et al., "PCBs, thyroid hormones, and ototoxicity in rats: Cross-fostering experiments demonstrate the impact of postnatal lactation exposure", TOXICOL SCI, 57(1), 2000, pp. 131-140

Abstract

Previous research has demonstrated the sensitivity of the developing rat to the hypothyroxinemic and ototoaic effects of perinatal exposure to Aroclor 1254 (A1254). We tested the hypothesis that postnatal exposure via lactation is the major cause of the ototoxicity by cross fostering animals at birth. Primiparous rats (22-24/dose) received 0 or 6 mg/kg A1254 (po in corn oil) from gestation day (GD) 6 to postnatal day (PND) 21. On the day of birth, half of the treated litters and half of the control litters were cross-fostered, resulting in the following groups: Ctrl/Ctrl (controls); A1254/A1254 (perinatal exposure); A1254/Ctrl (prenatal exposure only); and Ctrl/A1254 (postnatal exposure only). We assessed offspring at a number of ages for:serum thyroid hormone concentrations, liver and brain concentrations of PCBs, body weight, mortality, age of eye opening, auditory startle amplitudes, and auditory thresholds for 1 kHz and 40 kHz tones. Circulating thyroxine(T-4) concentrations were sharply reduced at GD 21 in the A1254-exposed group, and on PND 3, 7, 14, and 21 in the A1254/A1254 and the Ctrl/A1254 groups. Smaller decreases in T-4 were observed in the A1254/Ctrl group on PND 3, 7, and 14. PCB concentrations in the liver on PND 21 were sharply elevated in the A1254/A1254 and Ctrl/A1254 groups. Much smaller increases were seen in the A1254/Ctrl group. Age of eye-opening and startle amplitudes were unaffected by treatment. A1254 exposure caused permanent hearing deficits (20 dB increase) at the low frequency (1 kHz) in the A1254/A1254 and Ctrl/A1254 groups. The present findings demonstrated that the critical period for the ototoxicity of developmental A1254 exposure is within the first few postnatal weeks in the rat. This effect is consistent with the greater degree of postnatal hypothyroxinemia resulting from the greater magnitude of exposure that occurs postnatally via lactation.

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Documento generato il 01/12/20 alle ore 07:32:44