Showing Metabocard for glutathione (BASm0003064)

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Common NameGlutathione
DescriptionGlutathione is a compound synthesized from cysteine, perhaps the most important member of the body's toxic waste disposal team. Like cysteine, glutathione contains the crucial thiol (-SH) group that makes it an effective antioxidant. There are virtually no living organisms on this planet-animal or plant whose cells don't contain some glutathione. Scientists have speculated that glutathione was essential to the very development of life on earth. glutathione has many roles; in none does it act alone. It is a coenzyme in various enzymatic reactions. The most important of these are redox reactions, in which the thiol grouping on the cysteine portion of cell membranes protects against peroxidation; and conjugation reactions, in which glutathione (especially in the liver) binds with toxic chemicals in order to detoxify them. glutathione is also important in red and white blood cell formation and throughout the immune system. glutathione's clinical uses include the prevention of oxygen toxicity in hyperbaric oxygen therapy, treatment of lead and other heavy metal poisoning, lowering of the toxicity of chemotherapy and radiation in cancer treatments, and reversal of cataracts. (http://www.dcnutrition.com/AminoAcids/) glutathione participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It is also important as a hydrophilic molecule that is added to lipophilic toxins and waste in the liver during biotransformation before they can become part of the bile. glutathione is also needed for the detoxification of methylglyoxal, a toxin produced as a by-product of metabolism. This detoxification reaction is carried out by the glyoxalase system. Glyoxalase I (EC 4.4.1.5) catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II (EC 3.1.2.6) catalyzes the hydrolysis of S-D-Lactoyl-glutathione to glutathione and D-lactate. GSH is known as a substrate in both conjugation reactions and reduction reactions, catalyzed by glutathione S-transferase enzymes in cytosol, microsomes, and mitochondria. However, it is also capable of participating in non-enzymatic conjugation with some chemicals, as in the case of n-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450-reactive metabolite formed by acetaminophen, that becomes toxic when GSH is depleted by an overdose (of acetaminophen). glutathione in this capacity binds to NAPQI as a suicide substrate and in the process detoxifies it, taking the place of cellular protein thiol groups which would otherwise be covalently modified; when all GSH has been spent, NAPQI begins to react with the cellular proteins, killing the cells in the process. The preferred treatment for an overdose of this painkiller is the administration (usually in atomized form) of N-acetylcysteine, which is used by cells to replace spent GSSG and renew the usable GSH pool. (http://en.wikipedia.org/wiki/glutathione).
Structure
Molecular FormulaC10H17N3O6S
Average Mass307.32300
Monoisotopic Mass307.08381
IUPAC Name(2S)-2-amino-4-{[(1R)-1-[(carboxymethyl)carbamoyl]-2-sulfanylethyl]carbamoyl}butanoic acid
Traditional NameGlutathione
CAS Registry Number70-18-8
SMILES[NH3+][C@@H](CCC(=O)N[C@@H](CS)C(=O)NCC(=O)[O-])C(=O)[O-]
InChI IdentifierInChI=1S/C10H17N3O6S/c11-5(10(18)19)1-2-7(14)13-6(4-20)9(17)12-3-8(15)16/h5-6,20H,1-4,11H2,(H,12,17)(H,13,14)(H,15,16)(H,18,19)/t5-,6-/m0/s1
InChI KeyRWSXRVCMGQZWBV-WDSKDSINSA-N
CHEBI IDCHEBI:57925
HMDB IDHMDB0000125
Pathways
NameSMPDB/PathBank
Glutathione metabolism
Pyruvate metabolism
Glutamate Metabolism
Arachidonic Acid Metabolism
Piroxicam Action Pathway
Acetylsalicylic Acid Action Pathway
Etodolac Action Pathway
Ketoprofen Action Pathway
Ibuprofen Action Pathway
Rofecoxib Action Pathway
Diclofenac Action Pathway
Sulindac Action Pathway
Celecoxib Action Pathway
Ketorolac Action Pathway
Suprofen Action Pathway
Bromfenac Action Pathway
Indomethacin Action Pathway
Meloxicam Action Pathway
Mefenamic Acid Action Pathway
Oxaprozin Action Pathway
Nabumetone Action Pathway
Valdecoxib Action Pathway
Naproxen Action Pathway
2-Hydroxyglutric Aciduria (D And L Form)
5-Oxoprolinuria
Gamma-Glutamyltransferase Deficiency
Leigh Syndrome
Pyruvate Dehydrogenase Complex Deficiency
4-Hydroxybutyric Aciduria/Succinic Semialdehyde Dehydrogenase Deficiency
Diflunisal Action Pathway
Pyruvate Decarboxylase E1 Component Deficiency (PDHE1 Deficiency)
Glutathione Synthetase Deficiency
Hyperinsulinism-Hyperammonemia Syndrome
Leukotriene C4 Synthesis Deficiency
Homocarnosinosis
Cyclophosphamide Action Pathway
Pyruvaldehyde Degradation
5-oxoprolinase deficiency
Gamma-glutamyl-transpeptidase deficiency
Primary hyperoxaluria II, PH2
Pyruvate kinase deficiency
Succinic semialdehyde dehydrogenase deficiency
Cyclophosphamide Metabolism Pathway
Acetaminophen Metabolism Pathway
Antipyrine Action Pathway
Antrafenine Action Pathway
Carprofen Action Pathway
Etoricoxib Action Pathway
Fenoprofen Action Pathway
Flurbiprofen Action Pathway
Magnesium salicylate Action Pathway
Lumiracoxib Action Pathway
Lornoxicam Action Pathway
Phenylbutazone Action Pathway
Nepafenac Action Pathway
Trisalicylate-choline Action Pathway
Tolmetin Action Pathway
Tiaprofenic Acid Action Pathway
Tenoxicam Action Pathway
Salsalate Action Pathway
Salicylate-sodium Action Pathway
Salicylic Acid Action Pathway
Acetaminophen Action Pathway
StateSolid
Water SolubilityNot Available
logSNot Available
pKa (Strongest Acidic)1.94
pKa (Strongest Basic)9.22
Hydrogen Acceptor Count7
Hydrogen Donor Count6
Polar Surface Area158.82 Ų
Rotatable Bond Count9
Physiological Charge-1
Formal Charge0
Refractivity69.11 m³·mol⁻¹
Polarizability29.12

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