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氯化镍对胚胎小鼠的致畸作用及其向胚胎小鼠的转移。

Teratogenic effects of nickel chloride on embryonic mice and its transfer to embryonic mice.

作者信息

Lu C C, Matsumoto N, Iijima S

出版信息

Teratology. 1979 Apr;19(2):137-42. doi: 10.1002/tera.1420190202.

DOI:10.1002/tera.1420190202
PMID:473066
Abstract

Administration of nickel chloride to the pregnant mice on the seventh to eleventh day of their gestational period, resulted in significant embryotoxic effects in terms of an increased resorption rate, a decreased fetal weight, delay in skeletal ossification and high incidence of malformation. Among the cases of fetal malformation, the following malformations were observed to occur at a higher rate of incidence: acephalia, exencephaly, cerebral hernia, open eyelid, cleft palate, micromelia, ankylosis of the extremity, club foot and skeletal anomalies. Most skeletal anomalies were in the form of vertebral and/or rib fusions and were found mostly at thoracic and lumbar levels. The concentration of nickel retained in embryonic tissues was 800 times higher in the exposed compared to control groups and indicated that increased tissue levels of nickel chloride had a toxic influence on the developing embryo.

摘要

在妊娠期第7至11天给怀孕小鼠注射氯化镍,结果显示出显著的胚胎毒性作用,表现为吸收率增加、胎儿体重下降、骨骼骨化延迟以及高畸形发生率。在胎儿畸形病例中,观察到以下畸形的发生率较高:无脑畸形、脑膨出、脑疝、眼睑开放、腭裂、短肢畸形、肢体关节强硬、马蹄内翻足和骨骼异常。大多数骨骼异常表现为椎骨和/或肋骨融合,主要发生在胸段和腰段。与对照组相比,暴露组胚胎组织中保留的镍浓度高800倍,这表明氯化镍组织水平的增加对发育中的胚胎具有毒性影响。

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