NEUROTOXICITY INDUCED BY ALCL3 IN ZEBRAFISH BRAIN

The aluminum (Al) is one of the most abundant elements in the Earth's crust, it accumulates in the human body, including the CNS. The exposure to this metal is considered a causative factor for the development of Alzheimer's disease, a disease that affects mainly the cerebral cortex, the amygdala and the hippocampus, structures that find their counterpart in the telencephalon of Zebrafish. The mechanisms by which aluminum interacts with the nervous system, however, are understood only in part. To test the toxicity of Al on the telencephalon of Zebrafish and verify its ability to induce neurodegeneration in this fish, adult individuals were exposed for 7 days at 100 μg/L of aluminum chloride (AlCl3) at ph 5.8. Brains were removed after 2 and 7 days after initiation of treatment. To evaluate the presence of histomorphological alterations were made staining as hematoxylin-eosin and Cresyl Violet and immunohistochemical experiments performed on serialtransverse sections of the forebrain by ABC method using an anti-Aβ42 antibody. The stainings performed on cross sections of the Zebrafish telencephalon have shown tissue alterations already after 2 days of exposure to AlCl3, consisting in dilations of the cerebral parenchyma and vacuoles present in pericellular area at support of possible vascular damage induced. Immunohistochemistry analysis showed in the telencephalon of individuals of control a faint signal at the level of cell bodies of nerve cells that show abundant cytoplasm. The signal was incremented at the intracellular level after 2 and 7 days after start of treatment, a phenomenon that might therefore be associated with an increase in the presence of oligomers of amyloid peptide inside the cells, characteristic of the early stage of Alzheimer’s disease as well as other neurodegenerative diseases. These data confirm the toxic action exerted by Al on the brain and show a correlation between this metal and existing mechanisms at the basis of neurodegenerative diseases even in this fish. The results obtained thus open the way for further analysis aimed at further confirmation of the use of this model for the study of neurodegenerative mechanisms induced by this metal.