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Benomyl-Induced Craniocerebral Anomalies in Fetuses of Adequately Nourished and Protein-Deprived Rats

机译:苯妥英诱导的充足营养和蛋白质剥夺大鼠的胎儿颅脑异常

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Benomyl, a benzimidazole fungicide, produced craniocerebral and systemic malformations in fetal rats when administered by gavage in doses of 31.2, 62.5, and 125 mg/kg of maternal body weight on days 7-21 of gestation. Malformations increased in incidence and severity with increasing benomyl dosage and nearly doubled when coupled with a protein efficent diet. Protein deficiency alone produced only decreased fetal weight. High benomyl doses produced higher percentages of fetal resorptions and late fetal deaths, and these percentages also increased with protein deficiency. The most common combination of anomalies was hydrocephalus, exencephaly, and periventricular 'overgrowth'. Common systemic malformations included cleft palate, micromelia, hydroureter, and mishapen tails. No fetus was entirely normal at the highest benomyl dose. Thus, it is suggested that benomyl, coupled with a protein-deficient diet, offers a teratogenic model with a spectrum of abnormalities similar to hypervitaminosis A but with a higher yield of specific craniocerebral anomalies. (Copyright (c) 1987 Alan R. Liss, Inc.)

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