Abstract：
Heavy metals are released into the environment in increasing amounts from different natural and anthropogenic sources. Among them, cadmium contaminates aquatic habitats and represents a threat to Amphibians. To assess the risks of exposure to cadmium in the aquatic environment, we studied the survival rate of early tadpoles of Xenopus laevis under exposure to CdCl2 for 6 days in the concentration range between 0.15 and 150 µM of Cd2+. Tadpoles survived and reached stage 45 before feeding at all concentrations tested except 150 µM Cd2+, which significantly induced death. With an exposure of 15 µM Cd2+, tadpoles\' mean body length decreased, heart rate increased, fastest swimming speed decreased, and distance traveled was greater compared to unexposed controls. Additionally, a witness of neuronal normal development, the neural cell adhesion molecules (NCAM) expression, was decreased. Moreover, this cell-surface glycoprotein exhibited higher polysialylation, a post-translational modification capable to reduce cell adhesion properties and to affect organ development. Our study highlights the effects of Cd2+ on a series of parameters including morphology, physiology, and behavior. They emphasize the deregulation of molecular NCAM suggesting this effector is an interesting biomarker to detect cadmic toxicity in early tadpoles.
摘要：
重金属从不同的自然和人为来源以越来越多的量释放到环境中。其中,镉污染水生栖息地，对两栖动物构成威胁。为了评估水生环境中暴露于镉的风险，我们研究了在0.15至150µM的Cd2浓度范围内暴露于CdCl26天的非洲爪的早期t的存活率。在除150µMCd2+外的所有测试浓度下喂食前，t存活并达到第45阶段。显著诱发死亡。暴露于15µMCd2+，t的平均体长减少，心率增加，最快游泳速度下降，与未暴露的对照组相比，旅行距离更大。此外,神经元正常发育的见证,神经细胞粘附分子（NCAM）的表达，减少了。此外，这种细胞表面糖蛋白表现出更高的聚唾液酸化，能够降低细胞粘附特性并影响器官发育的翻译后修饰。我们的研究强调了Cd2+对一系列参数的影响，包括形态，生理学,和行为。他们强调了分子NCAM的失调，表明这种效应子是一种有趣的生物标志物，可以检测早期t的cadmic毒性。
