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Literature summary for 1.11.1.12 extracted from

  • Jelinek, A.; Heyder, L.; Daude, M.; Plessner, M.; Krippner, S.; Grosse, R.; Diederich, W.E.; Culmsee, C.
    Mitochondrial rescue prevents glutathione peroxidase-dependent ferroptosis (2018), Free Radic. Biol. Med., 117, 45-57 .
    View publication on PubMed
Search for more literature for 1.11.1.12

Inhibitors

Inhibitors Comment Organism Structure
(1S,3R)-RSL3 disrupts mitochondrial morphology and provokes strong mitochondrial impairment Mus musculus
RSL3 a selective GPx4 inhibitor, mediates concentration-dependent inhibition of GPX4, lipid peroxidation, enhanced mitochondrial fragmentation, loss of mitochondrial membrane potential, and reduced mitochondrial respiration. Ferroptosis inhibitors, such as deferoxamine, ferrostatin-1 and liproxstatin-1, but also CRISPR/Cas9 Bid knockout and the BID inhibitor BI-6c9 protect against RSL3 toxicity. Cell toxicity of the different RSL3 isomers in HT22 wild-type cells, overview Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrial membrane
-
 Mus musculus 31966
-

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
2 glutathione + a hydroperoxy-fatty-acyl-[lipid] Mus musculus
-
 glutathione disulfide + a hydroxy-fatty-acyl-[lipid] + H2O
-
 ?

Organism

Organism UniProt Comment Textmining
Mus musculus O70325
-
-

Source Tissue

Source Tissue Comment Organism Textmining
brain
-
 Mus musculus
-
fibroblast mouse embryonic fibroblasts Mus musculus
-
HT-22 cell
-
 Mus musculus
-
neuron
-
 Mus musculus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
2 glutathione + a hydroperoxy-fatty-acyl-[lipid]
-
 Mus musculus glutathione disulfide + a hydroxy-fatty-acyl-[lipid] + H2O
-
 ?

Synonyms

Synonyms Comment Organism
GPx4
-
 Mus musculus

General Information

General Information Comment Organism
malfunction ferroptosis is an oxidative form of regulated necrotic cell death featuring glutathione (GSH) depletion, disrupted glutathione peroxidase-4 (GPX4) redox defense and detrimental lipid reactive oxygen species (ROS) formation. Mitochondrial damage in models of oxidative glutamate toxicity, glutathione peroxidase depletion, and ferroptosis. (1S,3R)-RSL3, a selective GPx4 inhibitor, mediates concentration-dependent inhibition of GPX4, lipid peroxidation, enhanced mitochondrial fragmentation, loss of mitochondrial membrane potential, and reduced mitochondrial respiration. Ferroptosis inhibitors, such as deferoxamine, ferrostatin-1 and liproxstatin-1, but also CRISPR/Cas9 Bid knockout and the BID inhibitor BI-6c9 protect against RSL3 toxicity. The mitochondria-targeted ROS scavenger mitoquinone (MitoQ) preserves mitochondrial integrity and function, and cell viability despite significant loss of GPX4 expression and associated increases in general lipid peroxidation after exposure to RSL3. BID inhibitor BI-6c9 and ferroptosis inhibitors abrogate 1S, 3R-RSL3 induced cell death, phenotypes, overview Mus musculus
metabolism mitochondrial rescue prevents glutathione peroxidase-dependent ferroptosis Mus musculus