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Evaluation of the Teratogenic Potential of Octyl Acetate in Rats

Wayne C. Daughtrey, Patrick J. Wier, Karl A. Traul, R.W. Biles, Gerard F. Egan

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Abstract

Octyl acetate (CAS RN 108419-32-5) was administered via oral gavage to pregnant Sprague-Dawley rats on Gestation Days 6 through 15 at dose levels of 0,0.1,0.5, and 1.0 g/kg. The dams were weighed and observed for clinical signs of toxicity during pregnancy, and food consumption was measured. On Gestation Day 20 the dams were sacrificed and the fetuses were examined for external, visceral, and skeletal malformations and variations. The mid- and high-dose levels resulted in maternal toxicity as evidenced by reductions in body weight gain and food consumption. There were no statistically significant effects on embryo-fetal lethality or fetal growth for any treatment group. The number of litters with at least one malformed fetus and the mean percentage of the litter malformed were significantly (p < 0.05) elevated in the highdose group only. The results of the present study demonstrate that octyl acetate produced some evidence of developmental toxicity at a dose (1.0 g/kg) that was maternally toxic. Developmental toxicity was not observed at the maternally toxic 0.5 gkg dose level or the maternally nontoxic dose level (0.1 g/kg). Therefore, these data indicate that octyl acetate is not a selective developmental toxicant in the rat.

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What this paper is about

Octyl acetate (CAS RN 108419-32-5) was administered via oral gavage to pregnant Sprague-Dawley rats on Gestation Days 6 through 15 at dose levels of 0,0.1,0.5, and 1.0 g/kg. The dams were weighed and observed for clinical signs of toxicity during pregnancy, and food consumption was measured. On Gestation Day 20 the dams were sacrificed and the fetuses were examined for external, visceral, and skeletal malformations and variations. The mid- and high-dose levels resulted in maternal toxicity as evidenced by reductions in body weight gain and food consumption. There were no statistically significant effects on embryo-fetal lethality or fetal growth for any treatment group. The number of litters with at least one malformed fetus and the mean percentage of the litter malformed were significantly (p < 0.05) elevated in the highdose group only. The results of the present study demonstrate that octyl acetate produced some evidence of developmental toxicity at a dose (1.0 g/kg) that was maternally toxic. Developmental toxicity was not observed at the maternally toxic 0.5 gkg dose level or the maternally nontoxic dose level (0.1 g/kg). Therefore, these data indicate that octyl acetate is not a selective developmental toxicant in the rat.

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Available abstract

Octyl acetate (CAS RN 108419-32-5) was administered via oral gavage to pregnant Sprague-Dawley rats on Gestation Days 6 through 15 at dose levels of 0,0.1,0.5, and 1.0 g/kg. The dams were weighed and observed for clinical signs of toxicity during pregnancy, and food consumption was measured. On Gestation Day 20 the dams were sacrificed and the fetuses were examined for external, visceral, and skeletal malformations and variations. The mid- and high-dose levels resulted in maternal toxicity as evidenced by reductions in body weight gain and food consumption. There were no statistically significant effects on embryo-fetal lethality or fetal growth for any treatment group. The number of litters with at least one malformed fetus and the mean percentage of the litter malformed were significantly (p < 0.05) elevated in the highdose group only. The results of the present study demonstrate that octyl acetate produced some evidence of developmental toxicity at a dose (1.0 g/kg) that was maternally toxic. Developmental toxicity was not observed at the maternally toxic 0.5 gkg dose level or the maternally nontoxic dose level (0.1 g/kg). Therefore, these data indicate that octyl acetate is not a selective developmental toxicant in the rat.

Key concepts: Toxicant, Developmental toxicity, Toxicity, Fetus, Litter, Gestation, Teratology, Pregnancy

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