We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
The mouse model of induced sperm DNA damage caused by polystyrene microplastics exhibited distinct transcriptomic and proteomic features
Summary
Researchers established a mouse model of polystyrene microplastic-induced sperm DNA damage by administering 1 mg/kg/day for 60 days, which significantly elevated the sperm DNA fragmentation index, and characterized the transcriptomic and proteomic profiles associated with this reproductive toxicity.
Polystyrene microplastics (PS-MPs) are extensively utilized in plastic goods worldwide. The ingestion of PS-MPs has resulted in a high rate of DNA fragmentation index (DFI), which can potentially result in infertility and recurrent spontaneous abortion. This study established and characterized a mouse model of polystyrene microplastic (PS-MP)-induced sperm DNA damage (DnaD), and concurrently analyzed the associated transcriptomic and proteomic profiles. Over a period of 60 days, male mice assigned to the PS group were given PS-MPs at a dose of 1 mg/kg/d while the control group was administered an equivalent volume of normal saline. Sperm DNA Fragmentation Index (DFI) was then assessed using the Sperm Chromatin Structure Assay (SCSA).The testis was examined using RNA-seq and data-independent acquisition (DIA) to detect the patterns of mRNA and protein expression. The PS group exhibited an significant increase in the sperm DFI. Compared with the control group, 874 differentially expressed genes (DEGs) and 164 differentially expressed proteins (DEPs) were identified in the PS group. These included Agt, Gstt1, Fetub, Akr1c12, Eln, Gaa, Ppic and Ltbp2. The PI3K/Akt and metabolic pathways exhibited significant enrichment of these genes. After a 60-day period of intragastric injection, our findings indicated that the administration of PS-MPs at a 1 mg/kg/d dosage can lead to DnaD in the sperm of male mice. The metabolic and PI3K/Akt signaling pathways could be associated with the reproductive toxicity of PS-MPs. SUMMARY SENTENCE: The intake of PS-MPs mainly reduces DFI in mice via the metabolic and PI3K/Akt signaling pathways.
Sign in to start a discussion.
More Papers Like This
Whole transcriptome characterization of polystyrene microplastic-induced sperm DNA damage mouse spermatocytes model
Researchers used whole transcriptome sequencing to investigate how polystyrene microplastics cause DNA damage in mouse sperm cells. They found that microplastic exposure significantly increased DNA fragmentation and altered the expression of numerous genes involved in immune response and cellular defense pathways. The study suggests that microplastics may harm sperm DNA integrity primarily by disrupting immune-related and oxidative stress pathways.
Exploring the Biological Effects of Polystyrene Nanoplastics on Spermatogenesis: Insights From Transcriptomic Analysis in Mouse Spermatocytes
Researchers exposed mouse spermatocytes to polystyrene nanoplastics and observed membrane disruption, mitochondrial damage, increased oxidative stress, and DNA damage within 24 hours. Transcriptomic analysis revealed 134 genes with altered expression, many linked to critical reproductive processes like sperm development and mitochondrial organization. The study suggests that nanoplastic exposure may interfere with male reproductive health at the cellular and genetic level.
Transcriptome and proteome analyses reveal the mechanisms involved in polystyrene nanoplastics disrupt spermatogenesis in mice
Using advanced genetic and protein analysis, researchers found that polystyrene nanoplastics disrupted sperm production in male mice after 28 days of exposure. The nanoplastics reduced sperm count and movement, damaged the structure of sperm-producing tubes, triggered cell death, and lowered hormone levels needed for male fertility. This study provides detailed molecular evidence for how nanoplastic exposure could contribute to male reproductive problems.
Integrated transcriptomic and metabolomic analysis reveals the underlying mechanisms for male reproductive toxicity of polystyrene nanoplastics in mouse spermatocyte-derived GC-2spd(ts) cells
Researchers used integrated transcriptomic and metabolomic analysis to investigate how polystyrene nanoplastics affect mouse spermatocyte cells. They found that nanoplastic exposure disrupted lipid metabolism, triggered oxidative stress, and activated cell death pathways in the reproductive cells. The study suggests that nanoplastic exposure may pose risks to male reproductive health by interfering with critical metabolic and gene expression processes in developing sperm cells.
Polystyrene microplastics cause reproductive toxicity in male mice
Male mice exposed to polystyrene microplastics for six weeks showed significant reproductive damage, including reduced sperm count and motility, lower testosterone levels, and visible tissue damage in the testes. The microplastics caused oxidative stress and triggered cell death pathways in the reproductive tissue. These findings add to growing evidence that microplastic exposure could contribute to declining male fertility.