Diewert V M, Juriloff D M
Teratology. 1983 Dec;28(3):437-47. doi: 10.1002/tera.1420280315.
Maternal treatment with methylmercury (MeHg) has been shown to induce a high frequency of cleft palate and produce growth retardation in rat and mouse fetuses, but the relation between these effects is unknown. The objective of this study was to determine if mandibular growth retardation was a factor that contributed to induction of cleft palate in C57BL/6J mice. Two doses of MeHg (10 mg/kg maternal body weight) were given subcutaneously on days 10 and 11 of gestation, and the fetuses were morphometrically studied on days 14, 15, and 18. Full clefts of the secondary palate were present in approximately half of the treated day 15 and 18 fetuses; therefore, the cleft palate (CP) and noncleft palate (NCP) groups were analyzed separately to facilitate identification of morphologic changes associated with the clefting. The results showed that, compared with controls, the day 14 MeHg-treated fetuses had significantly smaller placental weights, but only half of the fetuses had delayed palatal shelf elevation, reduced body weight, and delayed morphological development. However on day 15, the CP and the NCP groups had similar reductions in body weight and placental weight. A striking downward and forward positioning of the head was present in the MeHg-treated fetuses with the CP group more severely affected than the NCP group. Significant differences between the three groups (control, NCP, and CP) were present with mean head-to-body angles of 67 degrees, 60 degrees and 51 degrees, respectively. The absence of normal head lifting resulted in a relative mandibular retrognathia that when combined with a decrease in mandibular length produced alterations in spatial relations that were most severe in the CP fetuses. The results suggest that after exposure to MeHg, palatal closure is affected by altered tongue posture associated with the abnormal head positioning and shortening of the mandible that develop following placental and embryonic growth retardation.
已表明母体用甲基汞(MeHg)处理会在大鼠和小鼠胎儿中诱发高频率的腭裂并导致生长迟缓,但这些影响之间的关系尚不清楚。本研究的目的是确定下颌生长迟缓是否是导致C57BL/6J小鼠腭裂的一个因素。在妊娠第10天和第11天皮下注射两剂MeHg(10毫克/千克母体体重),并在第14、15和18天对胎儿进行形态测量研究。在大约一半的第15天和18天接受处理的胎儿中出现了继发腭的完全腭裂;因此,分别分析腭裂(CP)组和非腭裂(NCP)组,以便于识别与腭裂相关的形态学变化。结果表明,与对照组相比,第14天用MeHg处理的胎儿胎盘重量明显较小,但只有一半的胎儿出现腭板抬高延迟、体重减轻和形态发育延迟。然而在第15天,CP组和NCP组的体重和胎盘重量有相似程度的降低。在MeHg处理的胎儿中出现了明显的头部向下和向前定位,CP组比NCP组受影响更严重。三组(对照组、NCP组和CP组)之间存在显著差异,平均头身角度分别为67度、60度和51度。正常的头部抬起缺失导致相对的下颌后缩,当与下颌长度减少相结合时,会产生空间关系的改变,这在CP胎儿中最为严重。结果表明,暴露于MeHg后,腭关闭受与异常头部定位相关的舌姿势改变以及胎盘和胚胎生长迟缓后出现的下颌缩短的影响。