We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Co-exposure to polystyrene nanoplastics and triclosan induces synergistic cytotoxicity in human KGN granulosa cells by promoting reactive oxygen species accumulation
AI summary Read the abstract
Researchers found that when human ovarian cells are exposed to both nanoplastics and triclosan (a common antibacterial chemical) at the same time, the toxic effects are worse than either one alone. The combination triggered more cell damage, harmful oxygen molecules, and cell death than individual exposure. This matters because people are typically exposed to multiple pollutants simultaneously, and this synergy could have implications for female reproductive health.
In recent years, nanoplastics (NPs) and triclosan (TCS, a pharmaceutical and personal care product) have emerged as environmental pollution issues, and their combined presence has raised widespread concern regarding potential risks to organisms. However, the combined toxicity and mechanisms of NPs and TCS remain unclear. In this study, we investigated the toxic effects of polystyrene NPs and TCS and their mechanisms on KGN cells, a human ovarian granulosa cell line. We exposed KGN cells to NPs (150 μg/mL) and TCS (15 μM) alone or together for 24 hours. Co-exposure significantly reduced cell viability. Compared with exposure to NPs or TCS alone, co-exposure increased reactive oxygen species (ROS) production. Interestingly, co-exposure to NPs and TCS produced synergistic effects. We examined the activity of superoxide dismutase (SOD) and catalase (CAT), two antioxidant enzymes; it was significantly decreased after co-exposure. We also noted an increase in the lipid oxidation product malondialdehyde (MDA) after co-exposure. Furthermore, co-exposure to NPs and TCS had a more detrimental effect on mitochondrial function than the individual treatments. Co-exposure activated the NRF2-KEAP1-HO-1 antioxidant stress pathway. Surprisingly, the expression of SESTRIN2, an antioxidant protein, was inhibited by co-exposure treatments. Co-exposure to NPs and TCS significantly increased the autophagy-related proteins LC3B-II and LC3B-Ⅰ and decreased P62. Moreover, co-exposure enhanced CASPASE-3 expression and inhibited the BCL-2/BAX ratio. In summary, our study revealed the synergistic toxic effects of NPs and TCS in vitro exposure. Our findings provide insight into the toxic mechanisms associated with co-exposure to NPs and TCS to KGN cells by inducing oxidative stress, activations of the NRF2-KEAP1-HO-1 pathway, autophagy, and apoptosis.
More Papers Like This
Insights into the synergistic toxicity mechanisms caused by nano- and microplastics with triclosan using a dose-dependent functional genomics approach in Saccharomyces cerevisiae
AI summary Read the abstract
Researchers used yeast functional genomics to investigate the combined toxicity of polystyrene nano- and microplastics with the antimicrobial compound triclosan. They found that the combined exposure produced synergistic toxic effects that were more harmful than either contaminant alone, disrupting cellular processes related to membrane integrity and protein function. The study provides molecular-level evidence that microplastics may amplify the toxicity of co-occurring chemical pollutants.
Synergistic toxicity of micro-plastic and micro-pollutants in human cells
AI summary Read the abstract
Researchers tested the synergistic toxicity of polystyrene microplastics and triclosan in Caco-2 human intestinal cells, finding that sorption of triclosan onto oxidized PS bead surfaces was enhanced compared to unmodified beads, and that 48-hour desorption of triclosan from MP surfaces into cell assays resulted in 25% greater cytotoxicity than simultaneous exposure without desorption time.
Polystyrene-microplastics and DEHP co-exposure induced DNA damage, cell cycle arrest and necroptosis of ovarian granulosa cells in mice by promoting ROS production
AI summary Read the abstract
Researchers found that co-exposure to polystyrene microplastics and DEHP (a common plastic additive) caused more damage to mouse ovarian cells than either pollutant alone, triggering excessive oxidative stress that led to DNA damage, cell cycle arrest, and cell death. These findings suggest that microplastics combined with their chemical additives may pose a synergistic threat to female reproductive health.
Interactions of microplastics and organic compounds in aquatic environments: A case study of augmented joint toxicity
AI summary Read the abstract
Researchers investigated how polystyrene microplastics interact with the antimicrobial compound triclosan in simulated environmental and cellular conditions. They found that surface-functionalized microplastics adsorbed significantly more triclosan and released it under cellular conditions, with the combination producing greater toxicity to human intestinal cells than either contaminant alone. The study suggests that microplastics can amplify the harmful effects of co-occurring organic pollutants.
Influence of polystyrene nanoparticles on the toxicity of tetrabromobisphenol A in human intestinal cell lines
AI summary Read the abstract
When human intestinal cells were exposed to both polystyrene nanoparticles and the flame retardant TBBPA together, the chemical pollutant dominated the toxic response, causing oxidative stress, DNA damage, and disruption of mitochondrial function. The study shows that mixing microplastics with other contaminants can produce complex, hard-to-predict health effects in gut cells, which matters because people are routinely exposed to multiple pollutants at once.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.