gssg

Glutathione oxidized (L(-) -glutathione) is the oxidized form of Glutathione, which is a major antioxidant and antidote in cells. Glutathione oxidized can be used to study sickle cells and red blood cells.

NBDHEX is a potent inhibitor of glutathione S-transferase P1-1 (GSTP1-1) .

4-P-PDOT (4-phenyl-2- propionamidotetralin) is a potent, selective and affinity Melatonin receptor (MT2) antagonist.

Glutathione can occur in reduced (GSH), oxidized (GSSG), or in mixed disulfide forms and is ubiquitous in multiple biological systems serving as the major thiol-disulfide redox buffer of the cell. GSSG is the oxidized form of GSH . It can be reduced back to GSH through the NADPH-dependent enzyme glutathione reductase. GSSG functions as a hydrogen acceptor in the enzymatic determination of NADP+ and NADPH and can be a proximal donor in S-glutathionylation post translational modifications. The ratio of reduced glutathione to oxidized glutathione within cells is often used as an indicator of oxidative stress, with higher concentrations of GSSG predicting increased oxidative stress.

QD-394 is an inducer of reactive oxygen species (ROS) production.1It induces lipid peroxidation, increases in intracellular accumulation of reactive oxygen species (ROS), and decreases in the reduced glutathione (GSH) to oxidized GSH (GSSG) ratio in MIA PaCa-2 pancreatic cancer cells when used at concentrations ranging from 0.5 to 10 μM. QD-394 is cytotoxic to MIA PaCa-2, PANC-1, and BxPC-3 cancer cells (IC50s = 0.64, 0.34, and 0.9 μM, respectively). QD-394 acts synergistically with napabucasin to reduce colony formation in MIA PaCa-2 cells. 1.Hu, S., Sechi, M., Singh, P.K., et al.A novel redox modulator induces a GPX4-mediated cell death that is dependent on iron and reactive oxygen speciesJ. Med. Chem.63(17)9838-9855(2020)

CPT-Se3, a camptothecin (CPT) seleno-derivative, exhibits enhanced anticancer efficacy by effectively killing cancer cells and hindering tumor proliferation. This compound diminishes the GSH/GSSG ratio and total thiols while increasing ROS levels, ultimately triggering apoptosis in Hep G2 cells. Furthermore, CPT-Se3 demonstrates significant cytotoxicity against HeLa, Hep G2, A549, and SMMC-7721 cell lines with IC50 values ranging from 2.19 to 4.7 μM [1].

CPT-Se4, a seleno-derivative of Camptothecin (CPT), exhibits enhanced efficacy in cancer cell eradication and tumor suppression. It reduces the GSH/GSSG balance and total thiol content while increasing ROS concentrations in Hep G2 cells, leading to the induction of cancer cell apoptosis. Furthermore, CPT-Se4 demonstrates cytotoxicity towards a range of cell lines including HeLa, Hep G2, A549, and SMMC-7721, with IC50 values ranging from 2.54 to 6.4 μM [1].

Glutathione Peroxidase (GSH-Px; EC 1.11.1.9), a member of the peroxidase family, catalyzes the oxidation of reduced glutathione (GSH) to oxidized glutathione (GSSG) by forming a disulfide bridge, while concurrently reducing hydrogen peroxide or lipid peroxides to water, serving as a potent antioxidant and protecting against oxidative stress [1].

Glutathione Reductase, Wheat germ (EC 1.6.4.2), is a crucial flavoprotein in the antioxidant defense system. In this process, reduced glutathione (GSH) detoxifies hydrogen peroxide via glutathione peroxidase, becoming oxidized to form oxidized glutathione (GSSG). Glutathione Reductase (GR) then reduces GSSG back to GSH using NADPH, which is converted to NADP+. The regenerated GSH is available for further hydrogen peroxide detoxification. Glutathione Reductase utilizes FAD as a cofactor.

Glutathione Reductase, Wheat germ (EC 1.6.4.2), is an essential flavoprotein in the antioxidant defense system. The reduced glutathione (GSH) is used by glutathione peroxidase to detoxify hydrogen peroxide, during which it is oxidized to form oxidized glutathione (GSSG). The GSSG is then reduced back to GSH by glutathione reductase (GR) using NADPH, which is converted to NADP+ in the process. The regenerated GSH can continue detoxifying hydrogen peroxide. Glutathione Reductase utilizes FAD as a cofactor.

TBE56 is a molecular glue serving as a BACH1 degrader, with an EC50 of 44 nM. It is a weak NRF2 inducer and is the biotinylated form of TBE31. TBE56 interacts with BACH1 via an E3 ligase FBX022-mediated mechanism to promote its degradation. It reduces Fe2+ accumulation, ROS generation, and malondialdehyde (MDA) levels in bone marrow mesenchymal stem cells (BMSCs) overexpressing Prominin-2, while increasing the GSH/GSSG ratio and upregulating GPX4. In a puncture-induced spinal disc degeneration (IVDD) model in SD rats, TBE56 significantly improves disc degeneration, making it useful for studying IVDD.