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Exposure to microplastics cause gut damage, locomotor dysfunction, epigenetic silencing, and aggravate cadmium (Cd) toxicity in Drosophila
Summary
Researchers used fruit flies as a model to study the effects of microplastics alone and combined with cadmium, a toxic metal commonly used in plastic production. They found that microplastics caused size-dependent gut damage and enhanced cadmium's harmful effects on movement and gene regulation through epigenetic silencing. The study demonstrates that microplastics can amplify the toxicity of co-occurring environmental contaminants and suggests Drosophila as a useful tool for rapid microplastic toxicity screening.
The interactions of microplastics (MPs) with other chemicals and the range of outcomes are of great importance to enhance understanding of their environmental impacts and health risks. Cadmium (Cd) and cadmium compounds are widely used as pigments and stabilizers in plastics, but they readily leach out. Here we addressed the impacts of MPs, Cd, and their joint exposure in a tractable Drosophila melanogaster model. We show that exposure to MPs lead to extensive particle size depended gut damage early in life and an enhancement of Cd-induced inhibition of locomotor-behavioral function in adult flies. In addition, we show that Cd exposure induces epigenetic gene silencing via position-effect variegation (PEV) in somatic tissues that was dramatically enhanced by co-exposure with MPs. The results indicate that MPs can aggravate the toxicity of other environmental contaminants and induce adverse effects across a range of diverse outcomes in a tractable and widely used model organism. These observations raise the prospects of using Drosophila as a tool for the rapid assessment of MP-mediated toxicity.
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