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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.
Polylactic acid (PLA) plastics are widely used in packaging for their safety and biocompatibility. However, PLA can generate micro/nanoplastics (MNPs), which infiltrate the food chain and pose health risks by adsorbing heavy metals such as copper (Cu) from the natural environment. This study investigated the role of autophagy-dependent ferroptosis in PLA NPs and Cu-induced testicular injury. C57BL/6J mice were orally exposed to 100 nm PLA NPs and copper sulfate (CuSO) for 4 weeks. The combined exposure caused significant reproductive toxicity, including reduced sperm counts and motility, increased sperm deformation, damaged blood-testis barrier, and disrupted sex hormone levels. Mechanistically, PLA NPs and CuSO triggered oxidative stress and ferritinophagy, leading to iron overload and ferroptosis in testicular tissue. The critical involvement of this pathway was confirmed using ferroptosis and autophagy inhibitors, which mitigated testicular injury. These findings provide the first evidence of reproductive toxicity induced by bio-based PLA NPs and Cu co-exposure, highlighting the vital role of autophagy-dependent ferroptosis in testicular injury and offering new insights into the combined toxicological effects of nanoparticles and environmental pollutants.
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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.
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.
Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte
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Researchers found that polystyrene nanoplastics cause testicular damage in mice through a cell death process called ferroptosis. The nanoplastics triggered the breakdown of iron-storage proteins and reduced levels of a protective mitochondrial protein called CISD1 in sperm cells. The study suggests that nanoplastic exposure may contribute to male reproductive harm by driving excess iron into mitochondria.
Ferroptosis and hepatic fibrosis induced by cooperative exposure to polylactic acid nanoplastics and copper: Emphasis on gut microbiota dysbiosis
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Researchers investigated the combined hepatotoxicity of polylactic acid nanoplastics and copper in mice, focusing on the gut-liver axis. The study found that co-exposure caused synergistic liver damage through ferroptosis, characterized by disrupted glutathione and iron homeostasis, along with gut microbiota dysbiosis and hepatic fibrosis more severe than either pollutant alone.
Co-exposure of cadmium and polystyrene nanoplastics: Induction pyroptosis and autophagy in mice testis
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Researchers investigated the combined effects of cadmium and polystyrene nanoplastics on mouse testicular tissue. The study found that co-exposure produced more severe testicular damage than either substance alone, driven by the interplay between pyroptosis (inflammatory cell death) and autophagy. Inhibiting one of these cellular processes affected the other, suggesting they are closely interconnected in the toxicity response to nanoplastic and heavy metal co-exposure.
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