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Developmental Triclosan Exposure Decreases Maternal and Offspring Thyroxine in Rats*
Citation:
Paul, K. B., J. M. HEDGE, M. J. DeVito, AND K. M. CROFTON. Developmental Triclosan Exposure Decreases Maternal and Offspring Thyroxine in Rats*. ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY. Society of Environmental Toxicology and Chemistry, Pensacola, FL, 29(12):2840-2844, (2010).
Impact/Purpose:
The current work tested the hypothesis that perinatal triclosan exposure of dams decreases thyroxine in dams and offspring prior to weaning.
Description:
Epidemiological and laboratory data have demonstrated that disruption of maternal thyroid hormones during fetal developmental may result in irreversible neurological consequences in offspring. In a short-term exposure paradigm, triclosan decreased systemic thyroxine (T4) concentrations in female weanling rats via up-regulation of hepatic catabolism. The current work tested the hypothesis that perinatal triclosan exposure of dams decreases thyroxine in dams and offspring prior to weaning. Pregnant Long-Evans rats received triclosan by oral gavage (0-300 mg/kg/day) in com oil from gestational day (GD) 6 through postnatal day (PND) 21. Serum was obtained from pups on PND4, 14, and 21, and from dams on PND22. Maternal weight-gain during the postnatal period decreased approximately 10% in the 300 mg/kg/day treatment group, with no significant effects during the prenatal period (GD6 to parturition). There were no dose-dependent effects on litter weights. Serum T4 was reduced 31% in dams on PND22. In pups, a unique pattern of hypothyroxinemia was observed; serum T4 decreased 27% in PND4 pups with no significant reduction observed on PND14 or PND21. Comparable reductions of approximately 30% in serum T4 at 300 mg/kg/day for dams and PND4 neonates combined with a lack of effect at PND 14 and PND21 suggest that toxicokinetic or toxicodynamic factors may have contributed to a reduced exposure or a reduced toxicological response during the lactation period. Further studies will be necessary to assess a mode of action for the unique pattern of triclosan-induced hypothyroxinemia during early development.
