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PVC Microplastics and Cadmium Induce Premature Ovarian Insufficiency-like Changes via Glycolipid Metabolism Variation in Duck Ovary
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Female ducks exposed to PVC microplastics and cadmium together showed damage to ovarian cells, increased oxidative stress, scarring, and disrupted sugar and fat processing proteins in the ovary. These changes affected egg cell development, suggesting the combined pollutants harm reproductive health in birds.
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.
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Co-exposure of polyvinyl chloride microplastics with cadmium promotes nonalcoholic fatty liver disease in female ducks through oxidative stress and glycolipid accumulation
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Researchers found that female ducks exposed to both PVC microplastics and cadmium together developed nonalcoholic fatty liver disease, with the combination being worse than either pollutant alone. The co-exposure caused oxidative stress and abnormal fat and sugar buildup in the liver. This study is relevant to human health because people are also exposed to microplastics and heavy metals simultaneously, and the combined effects may be more damaging than exposure to either one individually.
Co-exposure to PVC microplastics and cadmium induces oxidative stress and fibrosis in duck pancreas
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Researchers found that exposing ducks to PVC microplastics and cadmium together caused far worse pancreatic damage than either pollutant alone, including severe inflammation, fibrosis, and disrupted organ function. The combined exposure overwhelmed the ducks' antioxidant defenses and caused mitochondrial damage in pancreatic cells. Since waterfowl are highly exposed to both microplastics and heavy metals in contaminated waterways, this study shows how these common pollutants can interact to amplify organ damage.
Cadmium and polyvinyl chloride microplastics induce mitochondrial damage and apoptosis under oxidative stress in duck kidney
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Researchers exposed Muscovy ducks to cadmium and polyvinyl chloride microplastics, both individually and in combination, and found that each pollutant alone caused kidney damage through oxidative stress and mitochondrial dysfunction. Interestingly, the combined exposure actually reduced some markers of damage compared to single exposures, suggesting complex interactions between the two contaminants. The study demonstrates that microplastics and heavy metals can significantly impair kidney function in waterfowl through apoptosis and disrupted cellular defense pathways.
Ferroptosis: First evidence in premature duck ovary induced by polyvinyl chloride microplastics
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Researchers discovered that polyvinyl chloride microplastics caused premature ovarian damage in ducks through a cell death process called ferroptosis, which involves iron-dependent oxidative damage. Higher microplastic concentrations led to iron accumulation, increased oxidative stress, and structural damage to ovarian tissue. This is the first evidence linking microplastic exposure to ferroptosis in the avian reproductive system.
The Effects of Microplastics and Trace Elements on Ovarian Function and Pathology: A Literature Review.
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This review pulls together existing research showing that microplastics and heavy metals like lead and mercury can damage the ovaries, disrupting hormones and speeding up egg reserve loss. Worse, when these pollutants combine, they may cause more harm together than either does alone, raising concerns about everyday environmental exposures and fertility.
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