We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
N-acetyl-L-cysteine alleviated the oxidative stress-induced inflammation and necroptosis caused by excessive NiCl2 in primary spleen lymphocytes
Summary
Researchers found that N-acetyl-L-cysteine (NAC) alleviated oxidative stress-induced inflammation and cell death caused by microplastic exposure, suggesting NAC may protect against microplastic toxicity. The findings point to antioxidant supplementation as a potential mitigation strategy for microplastic-related cellular damage.
Our findings showed that NiCl2 could cause oxidative stress, inflammation, and necroptosis in mice spleen lymphocytes, which could be mitigated in part by NAC. The study provides a point of reference for understanding the toxicological effect of NiCl2. The study suggests that NAC may be useful in reducing the toxicological effect of NiCl2 on the immune system. The research may contribute to the development of effective measures to prevent and mitigate the toxicological effects of NiCl2 on the immune system.
Sign in to start a discussion.
More Papers Like This
N-acetylcysteine suppresses proteasome pathway activation and muscular damage induced by microplastics and chromium nanoparticles
Researchers found chromium nanoparticles and microplastics co-accumulating in human peri-implant muscle tissue from orthopedic patients, and showed in vitro that their combined exposure elevated reactive oxygen species and pro-inflammatory markers, while the antioxidant N-acetylcysteine suppressed the proteasome pathway activation and muscle damage.
Micro-algal astaxanthin ameliorates polystyrene microplastics-triggered necroptosis and inflammation by mediating mitochondrial Ca2+ homeostasis in carp’s head kidney lymphocytes (Cyprinus carpio L.)
Researchers investigated whether astaxanthin, a natural pigment from microalgae, could protect carp immune cells from damage caused by polystyrene microplastics. They found that astaxanthin reduced inflammation and cell death triggered by microplastics by helping maintain calcium balance within the cells' mitochondria. The study suggests that natural antioxidant compounds may help mitigate some of the harmful immune effects of microplastic exposure in fish.
Nano-Selenium Modulates NF-κB/NLRP3 Pathway and Mitochondrial Dynamics to Attenuate Microplastic-Induced Liver Injury
Researchers found that nano-selenium particles could reduce liver inflammation caused by polystyrene microplastics in mice by regulating mitochondrial dynamics and modulating the NF-kB/NLRP3 inflammatory pathway. The study suggests that selenium nanoparticles may help counteract the inflammatory damage that microplastics cause in liver tissue, offering a potential avenue for mitigating microplastic-related organ injury.
Investigation of pulmonary toxicity evaluation on mice exposed to polystyrene nanoplastics: The potential protective role of the antioxidant N-acetylcysteine
Researchers investigated lung damage in mice exposed to inhaled polystyrene nanoplastics and tested whether the antioxidant N-acetylcysteine could offer protection. They found that nanoplastics caused significant lung inflammation, tissue damage, and oxidative stress, but N-acetylcysteine treatment helped reduce these harmful effects. The study suggests that oxidative stress is a key mechanism behind nanoplastic-induced lung injury and points to potential protective strategies.
Preparation and characterization of cysteine-rich collagen peptide and its antagonistic effect on microplastic induced damage to HK-2 cells
Scientists developed a special protein fragment rich in the amino acid cysteine that protected human kidney cells from damage caused by microplastics in lab experiments. The peptide reduced harmful oxidation and inflammation triggered by microplastic exposure. This research points toward potential protective nutrients that could help the body defend against microplastic-related kidney damage.