Exposure to a sublethal concentration of CdO nanoparticles impairs the vision of the fruit fly (Drosophila melanogaster) by disrupting histamine synthesis and recycling mechanisms.

Abstract

While there is substantial literature on potential risks associated with exposure to emerging nanomaterials, less is known about the potential effects of hazardous metallic nanoparticles on vision, as well as the mechanisms that underpin them. The fruit fly (Drosophila melanogaster) was used as an in vivo model organism to investigate the effects of exposure to a sublethal concentration (0.03mg CdO NPs/mL, which was 20% of the LC50) on fly vision and compound eye ultrastructure. First, we observed a reduction in phototaxis response in treated flies but no change in locomotor activity. Because histamine (HA) has been linked to arthropod vision, we investigated HA synthesis, uptake, and recycling as a possible underlying mechanism for the observed adverse effect of CdO NPs on fly vision. This was accomplished by measuring the expression of the histamine decarboxylase (hdc) gene, which encodes the enzyme that converts the amino acid histidine to histamine (HA), as well as the expression of some genes involved in HA-recycling pathways (tan, ebony, Balat, CarT, and Lovit). The results showed that CdO NPs changed the expression levels of hdc, Lovit, tan, and eboney, indicating that HA synthesis, transport, and recycling were disrupted. Furthermore, less histamine immunolabeling was found in the head tissues of CdO NP-treated flies, particularly in the optic lobes. We also observed and quantified CdO NP bioaccumulation in compound eye tissues, which resulted in a number of cytological changes. Phenotypic effects (undersized eyes) have also been observed in the compound eyes of F1 flies. Considering the significance of vision in an organism's survival, the findings of this study are extremely crucial, as long-term exposure to CdO NPs may result in blindness.