Mouchet F, Baudrimont M, Gonzalez P, Cuenot Y, Bourdineaud J P, Boudou A, Gauthier L
Laboratoire d'Ecologie des Hydrosystèmes LEH, UMR CNRS UPS 5177, Université Paul Sabatier, 29 Rue Jeanne Marvig, 31400 Toulouse, France.
Aquat Toxicol. 2006 Jun 15;78(2):157-66. doi: 10.1016/j.aquatox.2006.02.029. Epub 2006 Apr 17.
The present investigation evaluates the toxic potential of Cd in larvae of the frog Xenopus laevis after 12 days of exposure to environmentally relevant contamination levels, close to those measured in the river Lot (France). Several genotoxic and detoxification mechanisms were analyzed in the larvae: clastogenic and/or aneugenic effects in the circulating blood by micronucleus (MN) induction, metallothionein (MT) production in whole larvae, gene analyses and Cd content in the liver and also in the whole larvae. The results show: (i) micronucleus induction at environmental levels of Cd contamination (2, 10, 30 microgL(-1)); (ii) an increased and concentration-dependent quantity of MT in the whole organism after contamination with 10 and 30 microgCdL(-1) (a three- and six-fold increase, respectively) although no significant difference was observed after contamination with 2 microgCdL(-1); (iii) Cd uptake by the whole organism and by the liver as a response to Cd exposure conditions; (4) up-regulation of the genes involved in detoxification processes and response to oxidative stress, while genes involved in DNA repair and apoptosis were repressed. The results confirm the relevance of the amphibian model and highlight the complementarity between a marker of genotoxicity, MT production, bioaccumulation and genetic analysis in the evaluation of the ecotoxicological impact.
本研究评估了非洲爪蟾幼体在暴露于与环境相关的污染水平（接近法国洛特河中测得的水平）12天后镉的潜在毒性。对幼体中的几种遗传毒性和解毒机制进行了分析：通过微核（MN）诱导分析循环血液中的致断裂和/或非整倍体效应、整个幼体中金属硫蛋白（MT）的产生、基因分析以及肝脏和整个幼体中的镉含量。结果表明：（i）在环境镉污染水平（2、10、30微克/升）下诱导微核；（ii）在受到10和30微克/升镉污染后，整个生物体中MT的数量增加且呈浓度依赖性（分别增加了三倍和六倍），而在受到2微克/升镉污染后未观察到显著差异；（iii）作为对镉暴露条件的反应，整个生物体和肝脏对镉的摄取；（4）参与解毒过程和对氧化应激反应的基因上调，而参与DNA修复和细胞凋亡的基因受到抑制。结果证实了两栖动物模型的相关性，并突出了遗传毒性标志物、MT产生、生物累积和遗传分析在评估生态毒理学影响方面的互补性。
