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ICR小鼠暴露于甲基汞后生长及腭突发育的特征

Characteristics of growth and palatal shelf development in ICR mice after exposure to methylmercury.

作者信息

Yasuda Y, Datu A R, Hirata S, Fujimoto T

出版信息

Teratology. 1985 Oct;32(2):273-86. doi: 10.1002/tera.1420320216.

DOI:10.1002/tera.1420320216
PMID:4049286
Abstract

A single dose of 25 mg/kg methylmercuric chloride (MeHg) was given orally to gravid ICR mice. Cleft palate was induced in 100% of the offspring, with the critical treatment period ranging from day 10/8 hours (10/8) to 12/16 of gestation. Dose-dependent body weight reduction was observed in day 18 fetuses from both the day 10/8 and 12/16 groups. However, fetal weight reduction was greater in the day 12/16 group for all the MeHg treatments investigated. The relative potency of the induction of cleft palate by MeHg was slightly but significantly higher in the fetuses of the day 12/16 group (1.044-1.197-fold in 95% limits) than in the day 10/8 group. The results showed that when 25 mg/kg of MeHg was given to the fetuses in the day 10/8 group, palatal shelf growth was delayed at a more primitive stage than in the day 12/16 fetuses. Moreover, disharmony of development between the overall fetus and palatal shelf was noticed. Furthermore, in the day 12/16 fetuses, a delay of palatal shelf growth occurred just prior to shelf elevation. Prior to shelf elevation, coordination was probably lost in the development between the fetus and the palatal shelves. Normal palatal closure in ICR fetuses occurs about 1 day and 10 hours earlier (P less than 0.05) than in the A/J fetuses (Biddle, '80). Normal palatal shelves in ICR fetuses moved rapidly, with 3.0 to 5.7 hours (in 95% limits) required for all fetuses to achieve elevation, while, in MeHg-treated groups, palatal shelf elevation did not occur. The results suggest that the cause of the failure in palatal shelf elevation may be understood by examining the disharmonious development of the fetus after exposure to MeHg.

摘要

给妊娠的ICR小鼠口服单剂量25毫克/千克的甲基汞氯化物(MeHg)。100%的后代出现腭裂,关键治疗期为妊娠第10天/8小时(10/8)至12/16天。在第10/8天和12/16天组的第18天胎儿中均观察到剂量依赖性体重减轻。然而,在所有研究的MeHg处理中,第12/16天组的胎儿体重减轻更为明显。与第10/8天组相比,第12/16天组胎儿中MeHg诱导腭裂的相对效力略高但显著更高(95%置信区间为1.044至1.197倍)。结果表明,当给第10/8天组的胎儿给予25毫克/千克的MeHg时,腭突生长在比第12/16天胎儿更原始的阶段延迟。此外,还注意到整个胎儿与腭突之间发育不协调。此外,在第12/16天的胎儿中,腭突生长延迟发生在腭突抬高之前。在腭突抬高之前,胎儿与腭突之间的发育可能失去了协调性。ICR胎儿的正常腭部闭合比A/J胎儿早约1天10小时(P小于0.05)(Biddle,1980年)。ICR胎儿的正常腭突移动迅速,所有胎儿达到抬高所需时间为3.0至5.7小时(95%置信区间),而在MeHg处理组中,腭突未发生抬高。结果表明,通过检查暴露于MeHg后胎儿的不协调发育,可以理解腭突抬高失败的原因。

相似文献

1
Characteristics of growth and palatal shelf development in ICR mice after exposure to methylmercury.ICR小鼠暴露于甲基汞后生长及腭突发育的特征
Teratology. 1985 Oct;32(2):273-86. doi: 10.1002/tera.1420320216.
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Developmental pattern of cAMP, adenyl cyclase, and cAMP phosphodiesterase in the palate, lung, and liver of the fetal mouse: alterations resulting from exposure to methylmercury at levels inhibiting palate closure.胎鼠腭、肺和肝脏中cAMP、腺苷酸环化酶和cAMP磷酸二酯酶的发育模式:暴露于抑制腭闭合水平的甲基汞所导致的改变。
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Prevention by tiopronin (2-mercaptopropionyl glycine) of methylmercuric chloride-induced teratogenic and fetotoxic effects in mice.用硫普罗宁(2-巯基丙酰甘氨酸)预防小鼠甲基氯化汞诱导的致畸和胚胎毒性作用。
Teratology. 1979 Oct;20(2):297-301. doi: 10.1002/tera.1420200213.
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Sensitive stages and dose-response analyses of palatal slit and cleft palate in C57BL/6 mice treated with a glucocorticoid.用糖皮质激素处理的C57BL/6小鼠腭裂和唇腭裂的敏感阶段及剂量反应分析
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Strain differences between C57BL/6 and SWV mice in time of palate closure and induction of palatal slit and cleft palate.C57BL/6小鼠和SWV小鼠在腭部闭合时间以及腭部裂隙和腭裂诱导方面的品系差异。
Teratology. 1985 Apr;31(2):279-83. doi: 10.1002/tera.1420310214.

引用本文的文献

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J Toxicol Environ Health B Crit Rev. 2015;18(5):242-57. doi: 10.1080/10937404.2015.1068719. Epub 2015 Aug 20.
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Inhibition of implantation caused by methylmercury and mercuric chloride in mouse embryos in vivo.
甲基汞和氯化汞对小鼠胚胎体内着床的抑制作用。
Bull Environ Contam Toxicol. 1992 Oct;49(4):541-6. doi: 10.1007/BF00196296.