Oxidative stress mediates end-organ damage in a novel model of acetaminophen-toxicity in Drosophila.

ABSTRACT: Acetaminophen is the most common cause of acute drug-induced liver injury in the United States. However, research into the mechanisms of acetaminophen toxicity and the development of novel therapeutics is hampered by the lack of robust, reproducible, and cost-effective model systems. Herein, we characterize a novel Drosophila-based model of acetaminophen toxicity. We demonstrate that acetaminophen treatment of Drosophila results in similar pathophysiologic alterations as those observed in mammalian systems, including a robust production of reactive oxygen species, depletion of glutathione, and dose-dependent mortality. Moreover, these effects are concentrated in the Drosophila fat body, an organ analogous to the mammalian liver. Utilizing this system, we interrogated the influence of envir

SUBMITTER: Saeedi BJ 

PROVIDER: S-EPMC9652370 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature