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Murine Glial Cells Regenerate NAD, After Peroxide‐Induced Depletion, Using Either Nicotinic Acid, Nicotinamide, or Quinolinic Acid as Substrates
Author(s) -
Grant Ross S.,
Kapoor Vimal
Publication year - 1998
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1998.70041759.x
Subject(s) - nad+ kinase , quinolinic acid , nicotinamide , nicotinamide adenine dinucleotide , biochemistry , intracellular , chemistry , nicotinic agonist , nicotinamide phosphoribosyltransferase , niacin , microbiology and biotechnology , biology , enzyme , tryptophan , amino acid , receptor
The potential for regeneration of intracellular pyridine nucleotide levels from different precursors, after peroxide‐induced NAD depletion, in cultured glial cells was investigated. Cultured murine glial cells showed a decrease in intracellular NAD levels of >40% after treatment with H 2 O 2 (100 µ M ). Removal of the H 2 O 2 followed by a 2‐h incubation did not result in NAD recovery in the absence of precursors. However, NAD levels increased significantly in these cells after the following substrate additions, at minimum effective concentrations of 1 m M for quinolinic acid (QUIN), 500 µ M for nicotinamide, and 2 µ M for nicotinic acid. The regeneration of significant amounts of NAD from nicotinic acid at doses 250 and 500 times lower than either nicotinamide or QUIN indicates a preferred route for NAD biosynthesis in glial cells in vitro, probably via nicotinic acid phosphoribosylation.