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This mechanism plays an important role in host resistance to bacterial infection
This study used only secondary, de-identified data and did not involve the collection, use, or transmittal of individually identifiable data
Cellular GSSG accumulation, as opposed to GSH reduction, rendered hepatocytes susceptible to TNF cytotoxicity Increased GSSG/GSG ratios in response to H 2 O 2 exposure can stem from both GSH reduction and GSSG accumulation (data not shown)
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found that exogenous -KG mimics glutaminase-mediated ferroptosis, while using a transaminase inhibitor, amino-oxyacetate (AOA), reverses ferroptosis [85, 86]
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