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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

(PDF 494 kb) Measured levels of GSH and GSSG in human whole blood by applying different methodological protocols

Olympus, Tokyo, Japan) and analyzed using ImageJ software (Java 1.8.0, National Institutes of Health, Bethesda, MD)

10.1155/2020/3635787 160 QiangW.ShenT.NomanM.GuoJ.JinZ.LinD.et al (2021)

The sections were subjected to dewaxing and rehydration by heating at 60 C, followed by xylene washing and rehydration through a series of graded ethanol solutions and double-distilled water

RNA-Seq was performed in activated T cells, and GSEA plot showed the enriched pathway of oxidative phosphorylation in the combination of both compared with single treatment alone ( A )