NEUROBEHAVIOURAL, HISTOLOGICAL, PHYSIOLOGICAL AND GENE EXPRESSION ALTERATIONS IN ZEBRAFISH BRAIN EXPOSED TO ALUMINIUM

Aluminium (Al), a metal extremely widespread in the world but not essential, is considered dangerous both for the environment and for human health1. It is also indicated as a possible etiological factor in neurodegenerative diseases2 although, its neurotoxic role is still not completely understood. In this study, zebrafish was used like model organism, since useful both for ecotoxicology studies and for exploring neurodegenerative diseases3. Adult zebrafish were exposed to 11 mg/L Al and the swimming ability and the behavioural responses were assessed at 10, 15 and 20 days of exposure. These parameters were correlated with the effects induced by the metal on the brain, evaluating the amount of Al within this organ, the oxidative stress, antioxidant-defences, changes in metabolism and neurotransmission. Furthermore, its neurotoxic role was further investigated evaluating the induced neurodegeneration and the gene-expression of markers involved in the parkinsonism. The behavioural and locomotory responses, suggest an increase in the anxiety state, especially in animals exposed to Al for 15 days, when also the neurodegeneration and accumulation of Al in the brain were evident. According to these data, even the activity of antioxidant enzymes, as superoxide dismutase, glutathione peroxidase and the metallothioneins levels increased after short-term exposures and tended to decrease or stabilize at longer times, though, the reactive oxygen species instead increased in a time-dependent trend. Finally, the expression of genes linked to Parkinsonism also was influenced by exposure to the metal, with an evident greater impact after short time of exposure. Overall, the results contribute to understand the neurotoxic mechanisms activated by Al highlighting correlations between behavioural disorders, oxidative state and neurodegenerative processes.