BRENDA - Ligand view of DL-homocysteic acid (8098

C₄H₉NO₅S

DL-homocysteic acid

AZKJDCFQZVEZJK-FOCLMDBBSA-N

2.6.1.52

homocysteate + 2-oxoglutarate = 4-mercapto-2-oxobutanoate + L-glutamate

640153

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4.4.1.11

DL-homocysteic acid + H2O = ?

701880

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6.3.2.9

ATP + UDP-N-acetylmuramoyl-L-Ala + DL-homocysteic acid = ADP + phosphate + UDP-N-acetylmuramoyl-L-Ala-DL-homocysteic acid

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uncompetitive

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50 mM, 21% inhibition; 50 mM, 23% inhibition

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marked (ca. 64%) decrease of respiratory chain complex I activity in the cerebral cortex of immature rats following seizures induced by bilateral intracerebroventricular infusion of DL-homocysteic acid (600 nanomol/side). Decrease is already evident during the acute phase of seizures (60-90 min after infusion) and persists for at least 20 h after the seizures. Inhibition is selective for complex I since activities of complex II and IV and citrate synthase remain unaffected. Inhibition of complex I activity is not associated with changes in complex I content. Enhanced production of reactive oxygen species by inhibited complex I in mitochondria from DL-homocysteic acid-treated animals. Competitive NMDA receptor antagonist AP7, a selective and potent group II mGluR agonist (2R,4R)-APDC and a highly selective group III mGluR, subtype 8, agonist (S)-3,4-DCPG, significantly reduce the extent of complex I inhibition. The superoxide dismutase mimetic Tempol and a selective peroxynitrite scavenger and decomposition catalyst FeTPPS provide a significant attenuation of complex I inhibition associated with DL-homocysteic acid-induced seizures

692231

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