Aluminium occurs naturally in the environment, but a variety of its compounds are produced and used in different activities of human daily life increasing so the release of this metal in the environment, particularly in water bodies. Our previous studies showed that aluminium chloride (AlCl3) induced phenotypic alterations and damages of the nervous system with decrease of the glial fibrillary acidic protein (GFAP) expression in Danio rerio fish1, optimal model organism for ecotoxicological analysis and for the study of neurodegenerative and neurobehavioral diseases2. In order to assess the toxic effects of this metal, Danio rerio embryos at shield stage were exposed to AlCl3 at the concentrations of 50, 100 and 200 μM respectively for 72 h. We compared the swimming performances of treated larvae with those of the control larvae, assessing different parameters like Distance moved, Velocity mean, Cumulative movement, Meander and Heading using the DanioVision instrument. Collected data showed that AlCl3 significantly affected the behavioural parameters with a trend inversely proportional to the concentrations, in fact the performances worsen at low concentrations compared to higher doses3. In this light, we analysed mRNA expression level by qPCR of different marker genes of neural development and function, including c-fos, appa and appb. C-fos is an immediateearly gene often used as indirect marker of neuronal activity4, while appa and appb are the homolog genes of the mammalian amyloid precursor protein (APP), an essential gene for normal brain development and a key player for the Alzheimer’s disease pathogenesis5. We observed that the expression of these genes was affected by AlCl3. The results confirmed toxic effect of AlCl3 on D. rerio larvae, suggesting the need for further experiments to uncover the mechanisms by which the aluminium exposure affects the normal developmental processes and might be at basis of neurological and behavioural disorders.

ALCL3 INDUCES NEUROBEHAVIOURAL ALTERATIONS IN Danio rerio LARVAE

T. Capriello
Primo
;
A. Donizetti;F. Aniello;I. Ferrandino
Ultimo
2019

Abstract

Aluminium occurs naturally in the environment, but a variety of its compounds are produced and used in different activities of human daily life increasing so the release of this metal in the environment, particularly in water bodies. Our previous studies showed that aluminium chloride (AlCl3) induced phenotypic alterations and damages of the nervous system with decrease of the glial fibrillary acidic protein (GFAP) expression in Danio rerio fish1, optimal model organism for ecotoxicological analysis and for the study of neurodegenerative and neurobehavioral diseases2. In order to assess the toxic effects of this metal, Danio rerio embryos at shield stage were exposed to AlCl3 at the concentrations of 50, 100 and 200 μM respectively for 72 h. We compared the swimming performances of treated larvae with those of the control larvae, assessing different parameters like Distance moved, Velocity mean, Cumulative movement, Meander and Heading using the DanioVision instrument. Collected data showed that AlCl3 significantly affected the behavioural parameters with a trend inversely proportional to the concentrations, in fact the performances worsen at low concentrations compared to higher doses3. In this light, we analysed mRNA expression level by qPCR of different marker genes of neural development and function, including c-fos, appa and appb. C-fos is an immediateearly gene often used as indirect marker of neuronal activity4, while appa and appb are the homolog genes of the mammalian amyloid precursor protein (APP), an essential gene for normal brain development and a key player for the Alzheimer’s disease pathogenesis5. We observed that the expression of these genes was affected by AlCl3. The results confirmed toxic effect of AlCl3 on D. rerio larvae, suggesting the need for further experiments to uncover the mechanisms by which the aluminium exposure affects the normal developmental processes and might be at basis of neurological and behavioural disorders.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/772895
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