We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Oxidative stress-activated Nrf2 remitted polystyrene nanoplastic-induced mitochondrial damage and inflammatory response in HepG2 cells
AI summary Read the abstract
Researchers discovered that polystyrene nanoplastics damage human liver cells by causing oxidative stress and mitochondrial damage, but the cells activate a protective pathway called Nrf2 to fight back. When the Nrf2 defense was blocked, the damage from nanoplastics became significantly worse, confirming its protective role. This study helps explain how the liver tries to defend itself against nanoplastic toxicity, and suggests that people with weaker antioxidant defenses may be more vulnerable to liver damage from plastic exposure.
Generated from plastics, microplastics (MPs) and nanoplastics (NPs) are difficult to completely degrade in the natural environment, which can accumulate in almost all lives. Liver is one of the main target organs. In this study, HepG2 and L02 cells were exposed to 0-50 μg/mL polystyrene (PS)-NPs to investigate the mechanism of mitochondrial damage and inflammation. The results showed mitochondria damage and inflammatory caused by NPs, and it can be inhibited by N-acetyl-L-cysteine (NAC). In addition, reactive oxygen species (ROS) activated nuclear factor erythroid-derived factor 2-related factor (Nrf2) pathway. Nrf2 siRNA exacerbated the injury, suggesting Nrf2 plays a protective role. Moreover, p62 siRNA increased ROS and mitochondrial damage by inhibiting Nrf2, but didn't affect the inflammation. In conclusion, Nrf2 was activated by ROS and played a protective role in PS-NPs-mediated hepatotoxicity. This study supplemented the data of liver injury caused by PS-NPs, providing a basis for the safe disposal of plastics.
More Papers Like This
Exposure to polystyrene nanoplastics induces hepatotoxicity involving NRF2-NLRP3 signaling pathway in mice
AI summary Read the abstract
Mice and cultured liver cells were exposed to 20 nanometer polystyrene nanoplastics. The particles raised reactive oxygen species, suppressed the NRF2 antioxidant pathway and increased inflammatory signaling in the liver. Activating NRF2 with the compound tert-butylhydroquinone reduced the oxidative stress.
Adverse effects of pristine and aged polystyrene microplastics in mice and their Nrf2-mediated defense mechanisms with tissue specificity
AI summary Read the abstract
Researchers exposed mice to pristine and UV-aged polystyrene microplastics via intratracheal instillation and found structural damage to the gut, liver, spleen, and testis. Aged microplastics caused greater functional damage than pristine particles, including increased liver enzymes and cholesterol, reduced antioxidant capacity, and tissue-specific activation of the Nrf2 defense pathway.
Didymin protects against polystyrene nanoplastic-induced hepatic damage in male albino rats by modulation of Nrf-2/Keap-1 pathway
AI summary Read the abstract
Researchers tested whether didymin, a natural compound found in citrus fruits, could protect rat livers from damage caused by polystyrene nanoplastics. They found that didymin significantly reduced oxidative stress and inflammation by activating a key protective cellular pathway. The study suggests that certain dietary compounds may help counteract some of the harmful effects of nanoplastic exposure on the liver.
Polystyrene nanoplastics exacerbated Pb-induced liver toxicity in mice
AI summary Read the abstract
Researchers found that polystyrene nanoplastics exacerbated lead-induced liver toxicity in mice, with co-exposure causing higher lead accumulation, more severe inflammation, increased oxidative stress, and greater disruption of protective Nrf2 signaling pathways compared to lead alone.
Rhamnetin abrogates polystyrene microplastics prompted hepatic damage by regulating Nrf-2/Keap-1 pathway
AI summary Read the abstract
Researchers investigated whether rhamnetin, a natural flavonoid, could protect against liver damage induced by polystyrene microplastics in rats administered 0.01 mg/kg PS-MPs for the experimental period. They found that PS-MPs suppressed the Nrf-2/Keap-1 antioxidant pathway, reduced activities of SOD, CAT, GPx, GST, and HO-1 enzymes, elevated ALT, AST, and ALP liver injury markers, and increased apoptotic signaling, while co-administration of 50 mg/kg rhamnetin mitigated all these effects through hepatoprotective, anti-inflammatory, and antioxidant mechanisms.
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.