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The aim of this study is to evaluate the ameliorative effect of melatonin (MEL) against induced genotoxicity by cobalt (II) chloride (CoCl 2 ) and cobalt nanoparticles (CoNPs) (50 nm). Genotoxicity of CoCl 2 and CoNPs were investigated using single cell gel electrophoresis (COMET) in Drosophila melanogaster hemocytes, which are blood cells of the Drosophila, and the somatic mutation and recombination test (SMART) was used to investigate mutant effects on the Drosophila wings. Three concentrations (0.1, 1, and 10 mM) of CoNPs and CoCl 2 were applied to demonstrate their genotoxic potential. Both CoNPs and CoCl 2 have mutagenic potential for the three concentrations tested in the COMET assay; however, only the 10 mM concentration of the ionic form and two high concentrations (1 and 10 mM) of CoNPs induced genotoxicity in the Drosophila SMART assay. Three different concentrations of MEL (0.1, 0.5 and 2.5 mM) were used against cobalt at highest concentration (10 mM) of both CoCl 2 and CoNPs in both the SMART and COMET assays. MEL ameliorated the genotoxicity induced by CoCl 2 and CoNPs in vivo Drosophila COMET and SMART assays.

Nanogenotoxicology is an emergent area of research, relevant for estimating the potential carcinogenic risk of nanomaterials. Since most of the approaches use in vitro studies, and neglecting the whole organism limits the accuracy of the obtained results, we have used Drosophila melanogaster to study the possible genotoxic potential of cobalt nanoparticles (Co NPs). The wing somatic mutation and recombination test has been the test of choice. This test is based on the principle that the loss of heterozygosis and the corresponding expression of the suitable recessive markers, multiple wing hairs and flare-3 can lead to the formation of mutant clone cells in growing up larvae, which are expressed as mutant spots on the wings of adult flies. Co NPs, as well as the ionic form cobalt chloride, were given to third instar larvae through the food, at concentrations ranging from 0.1 to 10 mM. The results obtained indicate that both cobalt forms are able to induce significant increases in the frequency of mutant clones. Although at low concentrations only Co NPs were genotoxic, the level of genetic damage obtained at the highest dose tested of cobalt chloride (10 mM) showed a significant higher increase in the frequency of total spots than those observed after the treatment with cobalt nanoparticles. As conclusion, our results indicate that Co NPs were able to induce genotoxic activity in the wing-spot assay of D. melanogaster, mainly via the induction of somatic recombination. The differences observed in the behaviour of the two selected cobalt forms may result from differences in the uptake.