A necessary precursor in the biosynthesis of glutathione; contains an isopeptide rather than a eupeptide bond.
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Research article: "Gamma-Glutamylcysteine Ethyl Ester Protects against Cyclophosphamide-Induced Liver Injury and Hematologic Alterations via Upregulation of PPAR[gamma] and Attenuation of Oxidative Stress, Inflammation, and Apoptosis." In this article, S.
Crystal structure of gamma-glutamylcysteine synthetase: insights in to the mechanism of catalysis by a key enzyme for glutathione homeostasis.
Cadmium-mediated oxidative stress in alveolar epithelial cells induces the expression of gamma-glutamylcysteine synthetase catalytic subunit and glutathione S-transferase alpha and pi isoforms: potential role of activator protein-1.
Expression of NQO-1, GST-alpha, gamma-glutamylcysteine synthetase-heavy and -light chains, and microsomal GST was assessed by Northern blot analysis.
Knock down of gamma-glutamylcysteine synthetase in rat causes a cetaminophen-induced hepatotoxicity.
gamma-Glutamylcysteine synthetase and GSH increase in quinone-induced oxidative stress in BPAEC.
Resistance of Leishmania donovani to sodium stibogluconate is related to the expression of host and parasite gamma-glutamylcysteine synthetase.
Gamma-glutamylcysteine ethyl ester (GCEE), a synthetic GSH precursor, has been demonstrated to boost endogenous GSH levels and block oxidative stress in neurons [21, 22] as well as cerebral endothelial cells [23].
Gamma-glutamylcysteine is the limiting substrate in GSH synthesis and thus encourages product formation when present.
Cancer cells produce an enzyme called gamma-glutamylcysteine synthetase (GCS), which metabolizes and inactivates cyclophosphamide.
We have clear evidence that HGF can stimulate the GSH system machinery, particularly the key enzyme in GSH synthesis, the gamma-glutamylcysteine synthetase ([gamma]-GCS), which, in addition, increases GSH content [5, 17]; in the present study we did find the same effect in Chow cells; interestingly, [gamma]-GCS content in HC cells slightly decreased with HGF treatment, but GSH/GSSG ratio presented a different behavior; HGF induced a decrease in the tripeptide ratio at 6 h comparing with Chow cells, and at 12 h GSH ratio exhibited a significant recovery.
To discern the potential mechanisms underlying this differential loss, the levels and the activities of gamma-glutamylcysteine ligase (GCL) and cysteine availability were determined.
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