Effects of cadmium on cell death and cell proliferation in chick embryos

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 μL Cd acetate (8.9 × 10−5 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 (10× 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.