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© 1990 Oxford University Press

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Developmental Toxicity Evaluation of Acrylamide in Rats and Mice1

ELIZABETH A. FIELD2,*, CATHERINE J. PRICE*, RANDOLPH B. SLEET3,*, MELISSA C. MARR*, BERNARD A. SCHWETZ{dagger} and RICHARD E. MORRISSEY{dagger}

*Chemisiry and Life Sciences, Center for Life Sciences and Toxicology, Research Triangle Institute P.O.Box 12194, Research Triangle Park, North Carolina 27709 {dagger}Developmental and Reproductive Toxicology Group, National Toxicology Program, National Institute of Environmental Health Sciences P.O. Box 12233, Research Triangle Park. North Carolina 27709

Received May 1, 1989; accepted September 26, 1989

Developmental Toxicity Evaluation of Acrylamide in Rats and Mice. FIELD, E. A., PRICE, C. J., SLEET, R. B., MARR, M. C, MORRISSEY, R. E., AND SCHWETZ, B. A. (1990). Fundam. Appl. Toxicol. 14, 502–512. Acrylamide (ACRL), a widely used industrial chemical with neurotoxic effects, was evaluated for developmental toxicity. ACRL in distilled water was administered once daily by gavage on gestational days (gd) 6–17 to mice (0, 3, 15, or 45 mg/kg) and on gd 6–20 to rats (0, 2.5, 7.5, or 15 mg/kg). Following termination (gd 17, mice; gd 20, rats) fetuses were examined for external, visceral, and skeletal malformations. Maternal toxicity during treatment was observed at the highest dose as reduced body weight gain in both species and hindlimb splaying in treated mice only. Weight gain corrected for gravid uterine weight was also reduced in rats at 7.5 and 15 mg/kg/day. Embryo/fetal toxicity was not observed in rats, but fetal weight was reduced in mice administered 45 mg/kg/day. No increase in the incidence of malformations was observed in either species; however, the incidence of variations (predominately extra rib) increased with dose. In summary, administration of ACRL during organogene-sis produced maternal and developmental toxicity at 45 mg/kg/day in mice and maternal, but not developmental, toxicity at doses ≤ 7.5 mg/kg/day in rats.


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