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Maternal Exposure to Combined Cadmium and Polystyrene Nanoplastics Induces Offspring Testicular Dysplasia via Mitochondrial Reactive Oxygen Species Overactivating the Peroxisome Proliferator-Activated Receptor α-Mediated Autophagy Signaling Pathway
Summary
Researchers investigated the combined effects of maternal exposure to polystyrene nanoplastics and cadmium on offspring in a mouse model. The study found that co-exposure caused testicular developmental abnormalities in offspring through mitochondrial oxidative stress and disrupted autophagy signaling, suggesting that nanoplastics may amplify the reproductive toxicity of co-occurring environmental contaminants.
Nanoplastics (NPs) can carry other environmental contaminants, including heavy metals, such as cadmium, which is one of the most prevalent heavy metals found in polluted soil in China; cadmium has high toxicity and coexists with microplastics in oceans and soils. Therefore, further investigation over the combined toxicity of NPs and cadmium is necessary. Herein, transcriptomics was used to assess the effect of maternal perinatal exposure to polystyrene nanoplastics (PS-NPs) and cadmium on offspring. The results revealed that the sex ratio of offspring drastically changed, the hormone levels in male mouse offspring were affected, testicular mitochondrial dysfunction with mitochondrial reactive oxygen species (mtROS) accumulation occurred, and the peroxisome proliferator-activated receptor α (PPARα)-mediated autophagy signaling pathway was overactivated, thereby leading to uncontrolled apoptosis and proliferation inhibition. Briefly, the potential mechanism is that maternal exposure to combined cadmium and PS-NPs caused mtROS accumulation, thereby inducing excessive autophagy by activating the PPARα-mediated autophagy signaling pathway in offspring testes.