We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
P-075 Microplastic exposure impairs human sperm motility and DNA integrity via oxidative stress
Summary
Researchers exposed 98 human sperm samples to polyvinyl chloride microplastics at various concentrations and found dose-dependent reductions in sperm motility alongside increased oxidative stress and DNA damage. The study suggests that PVC microplastic exposure can significantly impair sperm quality through reactive oxygen species generation, raising concerns about potential reproductive health effects.
Abstract Study question Does exposure to Polyvinyl Chloride (PVC) adversely affect human sperm motility, oxidative stress levels, and DNA integrity? Summary answer PVC exposure significantly reduces sperm motility, increases reactive oxygen species (ROS) levels, and induces sperm DNA damage in a dose-dependent manner. What is known already Microplastics (MPs) have been identified as emerging environmental contaminants with potential adverse effects on human health. Polyvinyl Chloride (PVC), a widely used MP, has been shown to induce damages in biological systems. However, its direct impact on human sperm quality remains poorly understood. Study design, size, duration This in vitro experimental study analyzed 98 sperm samples exposed to different concentrations of PVC (0, 50, 100, 200, 400 μg/ml) for 6 hours at 37 °C, 5% CO2. Sperm motility, oxidative stress levels, and DNA integrity were assessed post-exposure. Participants/materials, setting, methods Human semen samples (n = 98) were collected and sperm samples were subjected to PVC exposure. Sperm motility was evaluated using videomicroscopy, oxidative stress was quantified by measuring ROS levels, and sperm DNA integrity was assessed using a comet assay. Main results and the role of chance Our results demonstrated a significant decrease in sperm motility after PVC exposure, with sperm velocity decreasing by 97.4% (p < 0.001) and total distance traveled declining by 95.8% (p < 0.001) at 400 µg/ml. Additionally, we found that PVC exposure induced a dose-dependent increase in ROS levels, reaching up to a 2-fold increase at 400 µg/ml compared to the control (p < 0.001). Furthermore, PVC significantly increased sperm DNA fragmentation, suggesting potential genotoxic effects. Indeed, the percentage of fragmented DNA rose from 7.15 ± 5.95% (control) to 23.56 ± 17.13%, while tail length increased from 3.43 ± 3.90 μm (control) to 10.17 ± 6.47 μm. These findings confirm PVC’s cytotoxicity to spermatozoa, leading to impaired motility and DNA damage. Limitations, reasons for caution This study was conducted in vitro, and the results may not fully represent in vivo conditions. Further research is required to assess the long-term reproductive consequences of PVC exposure. Wider implications of the findings These results highlight the potential reproductive toxicity of MPs, particularly PVC, and underscore the need for regulatory measures to minimize human exposure. Trial registration number No