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Hepatic transcriptomic and histopathological responses of common carp, Cyprinus carpio, to copper and microplastic exposure
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Researchers investigated how PVC microplastics interact with copper exposure in common carp over 14 days. They found that the microplastic particles acted as a vector for copper, increasing its accumulation in the liver and worsening tissue damage beyond what either pollutant caused alone. The study suggests that microplastics can amplify the toxic effects of heavy metals in freshwater fish.
The combined effects of copper and polyvinyl chloride (PVC) microparticles were investigated on the metal accumulation, histopathological biomarkers, and targeted transcriptomics in Cyprinus carpio liver. The fish were exposed to 0.25 mg/L copper and/or 0.5 mg/L PVC microparticles over a 14-d period. The results showed that hepatic copper accumulation is facilitated by the PVC microparticles presence in water. All treatments induced significant hepatic stress and inflammation; however, the transcriptional responses involving in detoxification pathways and apoptotic mechanisms were mixed and often down-regulated in the fish exposed to copper and/or PVC microparticles. Exposure to copper and/or PVC microparticles induced hypermeia, leukocyte infiltration and increase in melanomacrophage centers number and area. Generally, the severity of the lesions was in the following order: PVC microparticles < copper < copper+ PVC microparticles. In conclusion, PVC MPs act as a copper vector, facilitating accumulation of copper in the fish liver and increasing the tissue damage.
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Researchers examined the combined effects of copper and PVC microplastics on common carp intestines, finding that co-exposure caused greater histopathological damage and altered stress- and immune-related gene expression compared to either contaminant alone.
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Combined toxicity of polyvinyl chloride microplastics and copper to marine jacopever (Sebastes schlegelii)
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Researchers studied the combined effects of PVC microplastics and copper on a marine fish species and found that the two pollutants together caused significantly more harm than either one alone. The microplastics accelerated copper buildup in the fish's liver, leading to greater oxidative damage and growth problems. This is relevant to human health because fish that accumulate both microplastics and heavy metals may pass those contaminants to people through the food chain.
Pre-Exposure of Common Carp to Ambient Copper and Microplastic Changes the Gill Ionoregulaion-Related Transcripts During Saltwater Exposure
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Common carp were pre-exposed to copper alone or with polyvinyl chloride microplastics for 14 days, then challenged with brackish water to test how microplastic co-exposure alters gill physiology and metal accumulation. Combined exposure changed gill copper concentrations and altered physiological responses to salinity stress, suggesting microplastics modify how fish handle heavy metal toxicity.
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Primary rainbow trout hepatocytes were exposed to copper nanoparticles, microplastics, and their combination for 48 hours, finding that both dissolved copper and copper nanoparticles upregulated antioxidant enzyme transcripts while microplastics alone had minimal effect. Co-exposure to nanoparticles and microplastics did not significantly alter the oxidative stress response beyond nanoparticle effects alone.
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