PVC Microplastics and Cadmium Induce Premature Ovarian Insufficiency-like Changes via Glycolipid Metabolism Variation in Duck Ovary

Abstract Emerging as pervasive pollutants, microplastics (MPs) and cadmium (Cd) endanger animals’ health and safety. Currently, there is a lack of evidence about the harm mechanism of coexposure to polyvinyl chloride microplastics (PVC-MPs) and Cd in the avian female reproductive system. In the current study, female Mallard ducks were used to investigate a novel developmental reproductive toxicity strategy related to glycolipid metabolism disorder in duck follicles induced by coexposure to PVC-MPs with Cd, which leads to developmental reproductive toxicity. The findings demonstrated that coexposure to PVC-MPs and Cd enhanced PVC-MP accumulation in ovarian tissue, which impacted granulosa cell (GC) shape and functional activity and hindered folliculogenesis. Coexposure to PVC-MPs with Cd decreased the secretion of glycoprotein of zona pellucida (ZP) secreted by oocytes. Furthermore, coexposure to PVC-MPs with Cd increased oxidative stress (protein carbonyl content (PCC), H2O2) and decreased antioxidative stress (malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT)) enzyme activity in the ovary. Moreover, coexposure to PVC-MPs and Cd markedly enhanced the production of collagen fibers and stimulated the immunosignaling of transforming growth factors-β (TGF-β) and α-smooth muscle actin (α-SMA). Moreover, coexposure to PVC-MPs with Cd induced metabolic disorder of glycolipid proteins glucose transporter 8 (GLUT8), phosphoenolpyruvate carboxykinase (PCK2), triglyceride lipase (ATGL), carnitine palmitoyltransferase 2 (CPT2), and iron overload in the ovary. This work demonstrated that coexposure to PVC-MPs and Cd caused developmental reproductive toxicity in female ducks by triggering oxidative stress and altering glycolipid metabolic proteins. These results provide a novel study avenue for investigating the reproductive harmful mechanisms of PVC-MPs and Cd in bird species.