Gestational and lactational exposure to the polychlorinated biphenyl mixture Aroclor 1254 modulates retinoid homeostasis in rat offspring.

摘要: Polychlorinated biphenyls (PCBs) induce a broad spectrum of biochemical and toxic effects in mammals including alterations the vital retinoid (vitamin A) system. The aim this study was to characterize tissue levels rat offspring their dams following gestational lactational exposure PCB mixture Aroclor 1254 (A1254) assess interrelationship these changes with other established sensitive toxicological endpoints. Sprague-Dawley were exposed orally 0 or 15 mg/kg body weight/day A1254 from day 1 postnatal (PND) 23. Livers, kidneys serum collected on PNDs 35, 77 350. Tissue levels, hepatic cytochrome P450 (CYP) enzymes thyroid hormones analyzed. A multivariate regression between treatment, CYP activities, hormone body/liver weights performed using an orthogonal partial least-squares (PLS) analysis. contribution dioxin-like (DL) components observed also estimated equivalency (TEQ) concept. In both male female short-term occurred at PND35, i.e. decreased retinol retinoic acid (RA) metabolite 9-cis-4-oxo-13,14-dihydro-RA concurrent increases renal all-trans-RA levels. Long-term consisted retinyl palmitate increased that apparent until PND350. Retinoid system associated altered enzyme activities as well liver dams. DL activity within order magnitude theoretical TEQ for different endpoints, indicating significant involvement congeners effects. This shows are affected short- long-term by developmental endpoints concern.