Abstract
Oxidative stress is a critical factor of neurotoxicity and retinal disorders, yet the early cellular mechanisms underlying glial involvement remain poorly understood. In this study, we used Drosophila melanogaster to understand the toxic effects of cobalt chloride (CoCl2)-induced oxidative stress on retinal development, focusing on glial-like cone (semper) cells. CoCl2 exposure resulted in reduced pupal yield, indicating developmental neurotoxicity. Acridine orange and propidium iodide staining of eye-imaginal discs showed reduced fluorescence intensity in treated tissues due to widespread cellular degeneration. Phalloidin and 4',6-diamidino-2-phenylindole staining revealed early cytoskeletal fragmentation in cone cells of pupae and adult CoCl2-trated eye samples, preceding widespread photoreceptor disruption. Functionally, CoCl2-treatment impaired larval crawling, adult climbing, and phototactic behaviour, accompanied by elevated ROS levels at the larval stage, reduced body weight, and decreased adult survival. Biochemical assays showed delayed Superoxide Dismutase and catalase activity, and increased glutathione peroxidase activity. SDS-PAGE and qPCR confirmed heat shock response activation, with significant upregulation of Hsp22, Hsp23, Hsp27, and Hsp70, while Hsp26 remained unchanged. These findings indicate that cone cells as early neurotoxic targets of oxidative stress and establish Drosophila as a valuable oxidative retinopathy model for studying glia-neuron interactions and redox-induced neurodegeneration.
