Effects of lactational administration of acrylamide on rat dams and offspring

We duplicated the study design of Husain et al. (Ind Health 1987; 25:19–28) to determine whether maternal exposure to acrylamide monomer (AM) resulted in offspring neurotoxicity. Wistar rat dams with litters (15/group) were gavaged with AM in saline at 0 or 25.0 mg/kg/d throughout lactation (pnd 0–2...

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Bibliographic Details
Published in:	Reproductive toxicology (Elmsford, N.Y.) Vol. 13; no. 6; pp. 511 - 520
Main Authors:	Friedman, Marvin A, Tylb, Rochelle W, Marr, Melissa C, Myers, Christina B, Gerling, Frieda S, Ross, William P
Format:	Journal Article
Language:	English
Published:	New York, NY Elsevier Inc 01-11-1999 Elsevier
Subjects:	Acrylamide - toxicity Acrylamide monomer Administration, Oral Animals Animals, Suckling Biological and medical sciences Body Weight - drug effects Chemical and industrial products toxicology. Toxic occupational diseases Drinking Behavior - drug effects Feeding Behavior - drug effects Female Fore- and hindlimb grip strength Functional observational battery Lactation - drug effects Male Maternal neurotoxicity Maternal Wistar rats Medical sciences Motor Activity - drug effects Offspring effects during lactation Oral lactational exposure Postwean offspring effects Rats Rats, Wistar Toxicology Various organic compounds Postwean offspring effects Acrylamide monomer Oral lactational exposure Functional observational battery Fore- and hindlimb grip strength Offspring effects during lactation Maternal Wistar rats Maternal neurotoxicity Nervous system diseases Lactation Rat Toxicity Body weight Rodentia Acrylamide Progeny Vertebrata Mammalia Mother Animal Monomer Sciatic nerve
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Summary:	We duplicated the study design of Husain et al. (Ind Health 1987; 25:19–28) to determine whether maternal exposure to acrylamide monomer (AM) resulted in offspring neurotoxicity. Wistar rat dams with litters (15/group) were gavaged with AM in saline at 0 or 25.0 mg/kg/d throughout lactation (pnd 0–21). Maternal feed and water consumption, body weights (BW), and Functional Observational Battery (FOB) were recorded. At weaning (pnd 21), maternal sciatic nerves were examined histologically. Male offspring were retained until pnd 91, with BW and grip strength evaluations. Dosed dams exhibited progressive toxicity, including mortality (two), severely reduced feed and water consumption, BW, and BW gain, and behavioral neurotoxicity (with no sciatic nerve pathology). Nursing offspring at 25.0 mg/kg/d exhibited increased mortality and reduced BW associated with little/no milk in stomachs. Postwean males at 25.0 mg/kg/d exhibited normal BW gain and increasing grip strength over time. Therefore, AM caused maternal toxicity; offspring effects during lactation were consistent with inanition from maternal toxicity. Postwean males exhibited recovery with no signs of AM-mediated toxicity. These results do not support the conclusions of Husain et al.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23
ISSN:	0890-6238 1873-1708
DOI:	10.1016/S0890-6238(99)00043-X