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Role of Mitochondrial Iron Uptake in Acetaminophen Hepatotoxicity.
Livers
September 2024
Center for Cell Death, Injury & Regeneration, Medical University of South Carolina, Charleston, SC 29425, USA.
Overdose of acetaminophen (APAP) produces fulminant hepatic necrosis. The underlying mechanism of APAP hepatotoxicity involves mitochondrial dysfunction, including mitochondrial oxidant stress and the onset of mitochondrial permeability transition (MPT). Reactive oxygen species (ROS) play an important role in APAP-induced hepatotoxicity, and iron is a critical catalyst for ROS formation.
View Article and Find Full Text PDFUtility of iron concentration two to four hours post ingestion in predicting toxicity.
Am J Emerg Med
January 2025
Froedtert & the Medical College of Wisconsin, 9200 W. Wisconsin Ave, Milwaukee, WI, United States of America; Wisconsin Poison Center, 9000 W Wisconsin Ave, Milwaukee, WI 53226, United States of America.
Introduction: Iron products are widely available over the counter and have the potential to cause serious toxicity. Iron concentrations can be used to prognosticate and guide treatment during acute ingestions. Traditionally, a concentration of 350 μg/dL with symptoms, or 500 μg/dL without symptoms, is considered toxic and will likely need treatment to prevent decompensation.
View Article and Find Full Text PDFIron-MOFs for Biomedical Applications.
Adv Healthc Mater
October 2024
Institut des Matériaux Poreux de Paris, ENS, ESPCI Paris, CNRS, PSL University, Paris, France.
Article Synopsis
- Iron-based metal-organic frameworks (Fe-MOFs) have gained popularity in biomedicine for their low toxicity and versatility, offering potential in drug delivery and various therapies.
- Despite their promise, transitioning Fe-MOFs from lab research to clinical applications is difficult, and the review discusses recent advancements in their synthesis and potential uses in biosensing, antimicrobial, and anticancer therapies.
- Key challenges include developing scalable production methods and gaining a better understanding of their therapeutic mechanisms and risks, which could enhance their integration into clinical practice.
Isoliensinine activated the Nrf2/GPX4 pathway to inhibit glutamate-induced ferroptosis in HT-22 cells.
J Biochem Mol Toxicol
September 2024
Department of Pharmacy, School of Pharmacy, Phase I Clinical Trial Centre, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.
Isoliensinine (ISO), a natural compound, is a bibenzyl isoquinoline alkaloid monomer in lotus seed, which has strong antioxidant and free radical scavenging activities. The oxidative toxicity caused by glutamic acid overdose is one of the important mechanisms of nerve cell injury, and the oxidative toxicity caused by glutamic acid is related to ferroptosis. This study aims to establish a glutamate-induced injury model of mouse hippocampal neurons HT-22 cells, and investigate the protective effect of ISO on the neurotoxicity of glutamate-induced HT-22 cells.
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