In order to study the accumulation and cytotoxicity of cadmium (Cd) in the brain of zebrafish (Danio rerio), specimens were exposed for 16 days to 1.0 mg · L−1 of CdCl2 and the brains were analysed at 2, 7 and 16 days of treatment. The concentration of Cd in the brains was detected by atomic absorption spectrometry; tissue alterations were revealed under light and electron microscopes. Cadmium concentrations in the brain of treated fish appeared to increase exponentially over time, reaching a peak at 16 days. As regards brain histomorphology, we observed evident tissue disorganisation in treated fish compared with control specimens. This disorganisation appeared particularly at 16 days in the optic tectum, in the ventricle area where the ependymal cells appeared sparsely distributed and in the medulla oblongata. Moderate ultrastructural damage was observed in the fish at 7 days of treatment. In the brain at 16 days of treatment, we observed considerable mitochondrial swelling with a loss of cristae, and several cells showed large autophagic vacuoles. This is indicative of a defence mechanism which occurs over time and in parallel with the accumulation of metal in the organ

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Cadmium is an extremely toxic heavy metal that widely occurs in industrial workplaces with various hazardous effects on brain functions. The cytotoxic effects of cadmium chloride (CdCl ) on the neuroglial components of the zebrafish brain were analysed by detecting the glial fibrillary acidic protein (GFAP) expression and the mRNA levels of myelin genes mbp, mpz and plp1 in adult specimens exposed to cadmium for 2, 7 and 16 days. A significant decrease in the GFAP protein by Western blotting experiments was observed after 2 days of treatment, reaching 55% after 16 days. No change was observed in the mRNA levels. Using immunohistochemistry, a reduction in GFAP-positive structures was revealed with a progressive trend in all the brains at 2, 7 and 16 days of treatment. In particular, a considerable reduction in GFAP-positive fibres, with a different course, was observed in the ventricle areas and at the pial surface and in blood vessels after 16 days. Our experiments also showed a structural and chemical alteration of myelin and upregulation of mpz mRNA levels, the oligodendrocyte gene that is upregulated in experiments of neuronal injury, but not of plp1 and mbp mRNA levels, other myelin structural genes. These data confirm the toxic action of cadmium on the zebrafish brain. This action is time-dependent and involves the glial cells, key components of the protection and function of nerve cells, hence the basis for many neurological diseases. Copyright © 2016 John Wiley & Sons, Ltd.