Cadmium and polyvinyl chloride microplastics induce mitochondrial damage and apoptosis under oxidative stress in duck kidney

Polyvinyl chloride microplastics (PVC-MPs) and Cadmium (Cd) are widely occurring water pollutants that interact with each other to exert toxic effects. As a waterfowl, Muscovy duck is more susceptible to PVC-MPs and Cd than land poultry. In this study, Muscovy duck was used as a research model, and 10 mg/L PVC-MPs and 50 mg/kg Cd were used alone and in combine to explore the effect on the kidney of Muscovy duck. We found that treatment of Cd or PVC-MPs alone changed the kidney weight, increased creatinine and urea nitrogen content, and disrupted oxidative balance and macro/trace element metabolism, while the combination of PVC-MPs+Cd reduced the accumulation of Cd in the kidney. In addition, treatment of Cd and PVC-MPs alone caused mitochondrial damage, increase or decrease of mitochondria-associated proteins (Fis1, Drp1, PGC-1α, Nrf1), and Nrf2 signaling pathway plays a key role in detoxification and alleviation of oxidative stress, and we found that PVC-MPs+Cd treatment recovered related proteins (Nrf2, Keap-1, HO-1, NQO1, AC-SOD₂, SOD₂) compared with the Cd and PVC-MPs alone treatment. Finally, we detected changes in apoptosis-related proteins and genes (Caspase-3, Caspase-9, Bax, Bcl-2, Cytc) and TUNEL staining, and after PVC-MPs+Cd treatment, apoptosis-related proteins/genes recovered and the apoptosis rate decreased compared with the Cd and PVC-MPs alone treatment. These results indicate that renal function is impaired, oxidative stress and trace element metabolism disorder, nuclear factor-E2 related factor 2 (Nrf2) is activated into the nucleus to induce the expression of related antioxidant proteins (such as HO-1, NQO1). These injuries can induce mitochondrial damage and eventually lead to renal cell apoptosis. To sum up, these evidence show that Cd or PVC-MPs can induce kidney oxidative damage, trace element metabolism disorder, mitochondrial damage and apoptosis.