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Nanoplastic PS and cadmium co-exposure accelerates ferroptosis mediated by HIF-1α-related signaling in spermatogonium
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Researchers exposed mouse sperm precursor cells to nanoplastics combined with cadmium and found that co-exposure caused significantly more cell damage than either contaminant alone. The combined treatment triggered a form of cell death called ferroptosis through a specific signaling pathway involving the gene HIF-1a. The study suggests that nanoplastics may worsen the reproductive toxicity of heavy metals commonly found alongside plastic pollution in the environment.
Microplastics (MPs) in the real environment media often adsorbed toxic substances such as heavy metals and this co-exposure may exert various negative effects on human reproduction. In particular, the adsorption capacity of nanoplastics (NPs) is stronger. However, there are few studies focused on the combined toxicity of NPs and heavy metal co-exposure to germ cells. In this study, mouse spermatogonium GC-1 cells were applied as in vitro model to observe the effects of PS-NPs (0.1 μm, 200 mg/L) and cadmium (Cd) chloride (5 μM) on mouse spermatogonia and the underlying mechanism. The results showed that GC-1 cells turned significantly abnormal in morphology, and cell number and survival rate reduced in the co-exposed group. These injuries were restored after the intervention of ferroptosis inhibitor (Fer-1, 1 μM), HIF-1α specific inhibitor (YC-1, 10 μM) and miR-199a-5p mimic (50 nM). Double luciferase gene reporting experiment showed that there existed binding sites of miR-199a-5p to HIF-1α mRNA. Collectively, we found that PS-NPs + Cd co-exposure induced GC-1 cell ferroptosis, which might be mediated by miR-199a-5p/HIF-1α signaling axis. Hopefully, these findings will shed new light on how PS-NPs may impair male reproductive function in real scenario.
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PS-MPs or their co-exposure with cadmium impair male reproductive function through the miR-199a-5p/HIF-1α-mediated ferroptosis pathway
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Researchers found that polystyrene microplastics, especially when combined with cadmium, caused significant reproductive damage in male mice through a cell death pathway called ferroptosis. Smaller microplastic particles were more toxic than larger ones, and the combination of microplastics with cadmium amplified the harm beyond what either caused alone. The study identifies a specific molecular mechanism by which microplastics and heavy metals together may threaten male reproductive health.
Synergistic effect of PS-MPs and Cd on male reproductive toxicity: Ferroptosis via Keap1-Nrf2 pathway
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A mouse study found that microplastics and the heavy metal cadmium work together to cause more severe damage to male reproductive organs than either pollutant alone. The combination triggered a form of cell death called ferroptosis by disrupting a key protective pathway in the body. This is the first study to show this synergistic reproductive harm, suggesting that microplastics can make other environmental toxins more dangerous.
Novel insights into male reproductive toxicity: autophagy-dependent ferroptosis triggered by polylactic acid nanoplastics and copper sulfate
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Researchers exposed mice to polylactic acid nanoplastics combined with copper sulfate and found that the combination caused significant testicular damage through a process linking autophagy to ferroptosis, a form of iron-dependent cell death. The combined exposure was more damaging than either substance alone, disrupting sperm production and testicular tissue structure. The study suggests that nanoplastics from biodegradable plastics may amplify the reproductive toxicity of environmental heavy metals.
Combined exposure of PS-MPs with NaF induces Sertoli cell death and dysfunction via ferroptosis and apoptosis
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This study found that polystyrene microplastics combined with sodium fluoride caused far worse damage to testicular cells in mice than either substance alone. The combination triggered both ferroptosis (iron-dependent cell death) and apoptosis (programmed cell death) in Sertoli cells, which are essential for sperm production. Since both fluoride and microplastics are common environmental contaminants, their combined effect on male reproductive health is a growing concern.
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
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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.
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