Early Exposure to Environmental Pollutants: Imidacloprid Potentiates Cadmium Toxicity on Zebrafish Retinal Cells Death

SIMPLE SUMMARY: Simultaneous exposure to several contaminants can create a cross-linkage that leads to increased fish toxicity. Cadmium (Cd), one of the most common metals detected in the environment, can cause concentration-dependent damage in developing fish. Co-exposure of Cd and other contaminants, such as the pesticide imidacloprid (IMI), can cause developmental damage in zebrafish, particularly to eye cells. In fact, co-exposure to concentrations that are in themselves non-toxic can cause morphological damage accompanied by a sharp increase in apoptosis and cell death in retinal cells, with disruption of the antioxidant mechanism. ABSTRACT: In the present study, we analyzed the combination of non-toxic concentrations per se, of Cd and a pesticide the imidacloprid (IMI) (10 and 50 μM for Cd and 195 μM for IMI), to highlight early developmental toxicity and possible damage to retinal cells. Co-exposure to Cd and IMI showed a toxic effect in zebrafish larval development, with lowered degrees of survival and hatching, and in some cases the induction of structural alterations and edema. In addition, co-exposure to 50 and 195 μM, respectively, for Cd and IMI, also showed increased apoptosis in eye cells, accompanied by up regulation of genes associated with antioxidant markers (cat, sod1, nrf2 and ho-1). Thus, the present study aims to highlight how the presence of multiple contaminants, even at low concentrations, can be a risk factor in a model of zebrafish (Danio rerio). The presence of other contaminants, such as IMI, can cause an enhancement of the toxic action of Cd on morphological changes in the early life stage of zebrafish, but more importantly disrupt the normal development of the retina, eventually triggering apoptosis.