Thompson Jennifer, Hipwell Eoin, Loo Hui Voon, Bannigan John
University College Dublin and Conway Institute of Biomolecular and Biomedical Research, Department of Anatomy, Earlsfort Terrace, Dublin, Ireland.
Reprod Toxicol. 2005 Nov-Dec;20(4):539-48. doi: 10.1016/j.reprotox.2005.04.016. Epub 2005 Sep 23.
The aim of this study was to examine cell death and cell proliferation in chick embryos destined to have ventral body wall defects as a result of cadmium (Cd) treatment. Embryos in shell-less culture were treated with 50 microL Cd acetate (8.9x10(-5)M Cd2+) at Hamilton-Hamburger (H.-H.) stage 16-17, or with equimolar sodium acetate. TdT-Mediated dUTP nick end labelling (TUNEL) showed the mode of cell death to be apoptosis commencing 4 h after treatment in somites and neural tube. Desquamation also occurred in the peridermal layer of the ectoderm. Cd caused no changes in the S-phase population of any tissue except ectoderm. The peridermal layer of the latter had a 40% reduction in labeling index (LI) 5.25 h after treatment but increased thereafter, being 30% greater than control values at 25.25 h. The occurrence of gross malformation was strongly correlated with the degree of apoptosis and in turn with the extent of peridermal desquamation. Pre-treatment with zinc acetate (10x the dose of Cd) prevented gross malformation, apoptosis and the effect of Cd on peridermal proliferation. We hypothesize that the ventral body wall defect resulting from Cd treatment in chick embryos is the result of changes in the somites perhaps following interruption of a signalling pathway originating in ectoderm.
本研究的目的是检测因镉（Cd）处理而注定出现腹侧体壁缺陷的鸡胚中的细胞死亡和细胞增殖情况。在汉密尔顿-汉堡（H.-H.）第16 - 17阶段，对无壳培养的胚胎用50微升醋酸镉（8.9×10⁻⁵M Cd²⁺）或等摩尔的醋酸钠进行处理。末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）显示，细胞死亡模式为凋亡，在处理后4小时在体节和神经管中开始。外胚层的周皮层也发生了脱屑。除了外胚层，Cd对任何组织的S期细胞群体均无影响。处理后5.25小时，后者的周皮层标记指数（LI）降低了40%，但此后有所增加，在25.25小时比对照值高30%。严重畸形的发生与凋亡程度密切相关，进而与周皮脱屑程度相关。用醋酸锌（Cd剂量的10倍）预处理可预防严重畸形、凋亡以及Cd对周皮增殖的影响。我们推测，鸡胚中Cd处理导致的腹侧体壁缺陷是体节变化的结果，可能是源于外胚层的信号通路中断之后。
