Impact of copper in Xenopus laevis liver: Histological damages and atp7b downregulation

Copper is an essential micronutrient but its excess in the dietary can be toxic. Both copper deficiency and abundance can occur in natural conditions and can lead to pathological dysfunctions. Many of the toxic effects of copper, such as increased lipid peroxidation in cell membranes and DNA damage, are due to its role in the generation of oxygen free radicals. Copper is released into the environment by both natural sources and human activities and it can damage organisms and ecosystems. In the present work the effects of copper has been studied on Xenopus laevis, an interesting model organism, after three weeks of exposure at 1 mg/L of CuCl, concentration allowed in the water for human use. The effects of this metal were analysed on the liver at light microscope by Hematoxylin-Eosin, Mallory, Pas and Perls stainings to evaluate the general histology, the glycogen metabolism and presence of hemosiderin. Moreover the number and area of melanomoacrophages, known as inflammation parameters, were assessment. Finally, we investigated the expression of atp7b gene and localization of respective ATP7B protein, the membrane protein involved in Cu detoxication. The achieved results showed that copper, even at a low concentration, causes serious histological alterations of liver. It induces an increase in the size and number of melanomacrophages and higher amount of hemosiderin in the treated than controls. Moreover, it alters the gene expression and localization of ATP7B protein. The data are indicative that an exposition at low and chronic concentration of copper in Xenopus laevis damages seriously the liver. For this reason it's important to consider this metal one of the pollutants involved in the decline of the amphibians and for its possible effects in other vertebrates including humans.