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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.
The individual toxicity of sodium fluoride (NaF) and microplastics (MPs) has been extensively documented. Owing to their high specific surface area, widespread presence and durability, MPs can adsorb a broad spectrum of environmental contaminants into the organism. However, the combined toxicity of NaF and MPs has not been investigated. This study aimed to assess the effects of combined exposure to NaF and MPs on the function of testicular Sertoli cells (SCs) in male mice, and to investigate the underlying molecular mechanisms. The study revealed that combined exposure to NaF and MPs resulted in a decrease in the negative surface charge of MPs, along with an increase in the number of MPs entering the SCs. Through in vivo observation of the testicular pathological structure, spermatogenesis, and cell apoptosis in 180-day-old male mice, we discovered that combined exposure to NaF (80 mg/L) and MPs (10 mg/L) heightened reproductive toxicity compared to the individual exposure groups. This was evidenced by testicular structural defects, impaired spermatogenesis, and increased testicular cell apoptosis. Our in vitro studies showed that NaF (21 μg/mL) and MPs (100 μg/mL) synergistically induced SCs apoptosis and ferroptosis, leading to a reduction in SCs number and dysfunction. This ultimately resulted in structural and functional damage to the testes. Our findings demonstrate, for the first time, the synergistic effects of NaF and MPs on reproductive toxicity in mammals. These insights may provide valuable contributions to co-toxicity studies involving MPs and other environmental pollutants.
More Papers Like This
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.
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.
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.
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.
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