Fundamental Toxicological Sciences

Paper Details

Fundamental Toxicological Sciences
Vol. 5 No. 4 October 16, 2018 p.153-159
Original Article
In utero exposure to 2,2’,4,4’,5,5’-hexachlorobiphenyl accelerates the onset of eye opening in rat offspring
  • Kenichi Kobayashi (National Institute of Occupational Safety and Health /
Kenichi Kobayashi 1) , Muneyuki Miyagawa 1) 2) , Rui-Sheng Wang 1) , Megumi Suda 1) , Soichiro Sekiguchi 1) , Takeshi Honma 1)
1) National Institute of Occupational Safety and Health , 2) Department of Sport and Medical Science, Faculty of Medical Technology, Teikyo University
Keywords: 2,2’,4,4’,5,5’-hexachlorobiphenyl (PCB 153), Postnatal growth, Eye opening, Rat

Prenatal exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) and coplanar polychlorinated biphenyl (PCB) congeners has been reported to accelerate the onset of eye opening of rodents, but the effects of exposure to non-coplanar PCB congeners on the onset of eye opening remain unknown. TCDD binds to the cytosolic ligand-activated transcription factor aryl hydrocarbon receptor (AhR), leading to adverse effects through the alteration of AhR target gene expression. In contrast, non-coplanar PCB congeners show little or no binding to AhR. We examined whether in utero exposure to 2,2’,4,4’,5,5’-hexachlorobiphenyl (PCB 153), a di-ortho-substituted non-coplanar PCB congener, affects the onset of postnatal eye opening of rat offspring. Pregnant rats were given PCB 153 (0, 16, or 64 mg/kg/day) orally from gestational day 10 to 16, and somatic growth and eye opening were assessed in pups. Body weight, body length, and tail length measurements in the PCB 153 groups were lower than the values measured for the control group on postnatal days 1 to 21. However, PCB 153-exposed pups exhibited dose-dependent acceleration of eye opening. These findings suggest that in utero exposure to PCB 153 delays postnatal development but induces unexpected acceleration of eye opening that might not occur through interaction
with AhR.