PolyChlorinatedBiphenyls (PCBs) may induce negative effects on the development of many species. Over the last decades, amphibians decline has been reported worldwide and exposure to PCBs has been considered as one of the possible causes. In the present work, we firstly tested the hypothesis that PCBs could induce oxidative stress in young developing amphibians. The results demonstrate that exposure of X. laevis tadpoles to environmental concentrations of Aroclor 1254 interfere with normal growth. They also highlight that very young X. laevis tadpoles express antioxidant systems. PCBs induce deleterious effects on developing amphibians. However, the molecular and cellular mechanisms by which they express their toxicity are still largely unknown, especially at the protein expression level. A proteomics analysis was performed on developing X. laevis tadpoles exposed to Aroclor 1254. Results argue that protein expression is targeted by PCBs in developing amphibians and that proteins reorganization should be taken into account while estimating the toxicological hazard of wild amphibian populations exposed to the toxicants. In amphibians, PCBs are also linked to behavioural abnormalities such as circle swimming in frogs and tadpoles, suggesting a possible neurotoxic action of the toxicants. Once again, there is a lack of informations when considering the neurotoxic effects of PCBs at the protein level. A second proteomics analysis was then performed on the brain of developing X. laevis tadpoles exposed to Aroclor 1254. The results showed that important proteins such as molecular chaperones, mediators of nuclear translocation, components of the Krebs cycle, and proteins implicated in neuronal maturation were induced or repressed in response to PCBs exposure. When considering the work in its globality, it seems that PCBs induce oxidative stress in developing tadpoles. The proteomics approach, even if limited by different technical aspects, allowed the identification of a large group of proteins implicated in an “universal” cellular response to stress. This was true when considering the global response of an organism, or the global response of a specific tissue such as the brain.