Background and objectives: Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic diseases worldwide. Oxidative stress (OS) is a major contributor toward NAFLD development, while mitochondria play a central role in OS. Our previous study has shown that uric acid (UA), as a dual function metabolite, could alleviate OS. This study examined the impact of UA on mitochondria morphology and function in a model of steatosis using L-02 cells to explore the pathogenesis of NAFLD. Methods: The L‑02 hepatocyte cell line was used to develop a steatosis cell model via 0.3 mM oleic acid (OA) over 24 h, subsequently treated with uric acid (UA) dose of 5, 10, and 20 mg/dL for 24, 48, and 72 h, respectively. The fluorescence intensity of reactive oxygen species (ROS), apoptosis rate, and activity of Succinate dehydrogenase(SDH), cytochrome oxidas(CCO), and adenosine triphosphate(ATP) synthase in electron transport chain (ETC), as well as the content of ATP and 8-OH-dG were examined; ultrastructure was observed under an electron microscope. Results: Treatment with UA at a concentration of 5 and 10 mg/dL decreased the rate of ROS production, apoptosis, and 8-OH-dG concentration, while supporting ATP recovery, and SDH activity in the steatosis model cell. It also promoted lipid droplet metabolism; however, the recovery of mitochondria morphology was not obvious. Conclusions: Treatment with UA dose of 5 and 10 mg/dL could protect mitochondria from OS damage. Future research requires a more stable and effective model. keywords : electron transport chain, oxidative stress, nonalcoholic fatty liver disease
Repositioning of Verrucosidin, a Purported Inhibitor of Chaperone Protein GRP78, as an Inhibitor of Mitochondrial Electron Transport Chain Complex I
