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ALA effectively stabilizes hepatic redox-active iron (Fe 2+ ) expression and depresses the formation of ferroptosis after CSD Considering that overload of the redox-active iron (Fe 2+ ) plays a harmful role in hepatic metabolic function due to its involvement in catalyzing the Fenton reaction, generating ROS, enhancing oxidative stress, exacerbating inflammatory signaling, and leading to the development of ferroptosis, the present study further examined the hepatic Fe 2+ expression, together with the ferroptotic related proteins by the use of TOF-SIMS analysis and immunohistochemistry, respectively

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