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Literature summary for 6.3.2.2 extracted from

  • Kobayashi, T.; Watanabe, Y.; Saito, Y.; Fujioka, D.; Nakamura, T.; Obata, J.E.; Kitta, Y.; Yano, T.; Kawabata, K.; Watanabe, K.; Mishina, H.; Ito, S.; Kugiyama, K.
    Mice lacking the glutamate-cysteine ligase modifier subunit are susceptible to myocardial ischaemia-reperfusion injury (2010), Cardiovasc. Res., 85, 785-795.
    View publication on PubMed
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Application

Application Comment Organism
medicine mice lacking the glutamate-cysteine ligase modifier subunit are susceptible to myocardial ischaemia-reperfusion injury partly through an increased vulnerability of mitochondria to oxidative damage owing to mitochondrial glutathione reduction Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining

General Information

General Information Comment Organism
physiological function mice lacking the glutamate-cysteine ligase modifier subunit show an increase in myocardial ischaemia-reperfusion injury and apoptosis in ischaemic myocardium. A decrease in mitochondrial glutathione levels in ischaemic myocardium is more pronounced in mice lacking the glutamate-cysteine ligase modifier subunit than in control. The ESR signal intensity of the dimethyl-1-pyrroline-N-oxide-hydroxyl radical adducts in ischaemic myocardium is higher in mice lacking the glutamate-cysteine ligase modifier subunit than in control. Hypoxia-reoxygenation induces greater mitochondrial damage in cultured cardiomyocytes from mice lacking the glutamate-cysteine ligase modifier subunit Mus musculus