Evaluation of teratogenicity and neurotoxicity with maternal inhalation exposure to methyl chloroform.
Evaluation of teratogenicity and neurotoxicity with maternal inhalation exposure to methyl chloroform.
复制标题
母亲吸入暴露于甲基氯仿的致畸性和神经毒性的评价。
DOI：
10.1080/15287398209530159
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Manson,JM
中科院分区：
文献类型：
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作者：
York,RG;Sowry,BM;Hastings,L;Manson,JM
雌性Long-Evans大鼠通过吸入2100 ±暴露。200 ppm甲基氯仿（MC），以确定是否在交配前和怀孕期间的暴露比在交配前或怀孕期间单独暴露对后代更有害。采用2 × 2析因设计，在交配前2 wk至妊娠d20期间暴露4组：（1）妊娠前和妊娠期间暴露MC，（2）单独暴露于交配前MC，（3）单独暴露于妊娠期间MC，（4）妊娠前和妊娠期间暴露于过滤空气。一个t术语，每组的一半被处死，并评估母体毒性，胚胎毒性和致畸性;另一半交付他们的年轻人为以后的行为评价和检查的肉眼nose.No显着差异，发现在测量母体毒性或胚胎毒性，除了胎儿体重下降时，母鼠在怀孕期间单独暴露。在交配前和妊娠期间暴露组的胎仔中观察到骨骼和软组织变异的发生率显著增加。出生后评估包括体重和存活率测量以及旷场活动（21日龄）、转轮活动（40-110日龄）和安非他明激发试验（110-120日龄）的神经行为测试。所有存活的后代在12个月大时进行尸检并检查肉眼病变。这些测量结果均未观察到显著的治疗效应。可以得出结论，雌性大鼠在交配前和/或妊娠期间吸入暴露于2100 ± 200 ppm MC不会对任何测量参数产生持续有害影响。仅在妊娠期暴露的胎仔体重中观察到可逆性发育迟缓，在交配前和妊娠期间暴露的胎仔形态中观察到可逆性发育迟缓，这对产后结局没有影响。
Female Long‐Evans rats were exposed by inhalation of 2100 ±. 200 ppm methyl chlorofrom (MC) to determine whether exposure before mating and during pregnancy was more detrimental to the offspring than exposure either before mating or during pregnancy alone. Four groups were exposed for 2 wk before mating and through d 20 of gestation in a 2 X 2 factorial design: (1) MC exposure before and during pregnancy, (2) MC before mating alone, (3) MC during pregnancy alone, and (4) filtered air before and during pregnancy. A t term, half of each group were sacrificed and assessed for maternal toxicity, embryotoxicity, and teratogenicity; the other half delivered their young for later behavioral evaluation and examination for gross lesions.No significant differences were found in measurements of maternal toxicity or embryotoxicity except for a decrease in fetal body weight when dams were exposed during pregnancy alone. Significantly increased incidences of skeletal and soft tissue variations were seen in fetuses from the group exposed both before mating and during pregnancy. These variations in fetal morphology were indicative of developmental delay rather than true malformations.Postnatal evaluation included body weight and survival measurements and neurobehavioral tests of open‐field activity (21 d of age), running wheel activity (40–110 d of age), and an amphetamine challenge test (110–120 d of age). All surviving offspring were autopsied at 12 mo of age and examined for gross lesions. No significant treatment effects were noted with any of these measurements. It is concluded that inhalation exposure of female rats before mating and/or during pregnancy to 2100 ± 200 ppm MC did not have a persistent detrimental effect on any of the parameters measured. Reversible developmental delays were observed in fetal body weight with pregnancy exposure only, and in fetal morphology with exposure before mating and during pregnancy, which had no influence on postnatal outcome.