| Protein Name: | Glutathione reductase (P00390) |
|---|---|
| Gene Name: | GSR |
| Description: | Glutathione reductase, mitochondrial precursor (EC 1 8 1 7) (GR) (GRase) |
| PDB ID: | 1ALG |
| Protein Family: | |
| Protein Category: | Enzyme |
This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs | Toxicity | Mechanism | Reference |
|---|---|---|---|
| Cisplatin | Ototoxicity | Cisplatin ototoxicity is related to depletion of glutathione and glutathione reductase in the cochlea [ ADR Type 2 ] | Application of antioxidants and other agents to prevent cisplatin ototoxicity |
| Cyclophosphamide | Lung Toxicity | Significant reductions (P less than 0 005) in G6PD, GSH-R, and GSH-P activities occurred on days 1-5,indicating that Cyclophosphamide causes lung toxicity [ ADR Type 2 ] | Cyclophosphamide-induced depression of the antioxidant defense mechanisms of the lung |
| Epinephrine | Cytotoxicity | Pretreatment of cells with 100 microM 1,3-bis(2-chloroethyl)-1-nitrosourea which inhibits glutathione reductase,increased the sensitivity of these cells to the epinephrine plasma,which was found to be cytotoxic when incubated with isolated heart cells. [ ADR Type 1 ] | Epinephrine-induced cytotoxicity of rat plasma Its effects on isolated cardiac myocytes Lab |
| Ketoprofen | Intestinal Toxicity | A significant increase of tumor necrosis factor-alpha production and decreases in glutathione levels and glutathione reductase activity after treatment of the racemate and (R)-(-)-ketoprofen,suggesting induced intestinal toxicity could be correlated with a reduced oxidative damage characterized not only by a lack of changes in glutathione reductase activity but also by an absence of up-regulation of tumor necrosis factor-alpha production in intestinal mucosa. [ ADR Type 2 ] | Mechanisms involved in the attenuation of intestinal toxicity induced by (S)-(+)-ketoprofen in re-fed rats |
This panel provides information on drug category
| Toxicity | Source |
|---|