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Hepatic IRI is closely linking to the production of reactive oxygen species (ROS) whose augmentation is one of the major initiators in triggering hepatic damage especially in the early stage of IRI [10]

Here are some notable interactions: Chemotherapy Drugs: Glutathione may protect cancer cells from the effects of chemotherapy, potentially reducing the treatment's efficacy

These prodrugs are designed with disulfide bonds or other GSH-reactive moieties that are cleaved in the presence of high GSH concentrations, which are typically 1001,000 times higher in cancer cells compared to normal cells

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The pharmacological effects of S-propargyl-cysteine, a novel endogenous H 2 S-producing compound, in Chemistry, Biochemistry and Pharmacology of Hydrogen Sulfide

IFN- plays a crucial role in the cytotoxicity of NK cells and, in addition, IFN- has been shown to contribute to the activation of CD8 + T cells