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Glucose deprivation decreases nitric oxide production via NADPH depletion in immunostimulated rat primary astrocytes
Author(s) -
Shin Chan Young,
Choi Ji Woong,
Ryu Jae Ryun,
Ko Kwang Ho,
Choi JungJin,
Kim HyunSoo,
Kim HeeSun,
Lee JaeChul,
Lee Sun Jung,
Kim Hyoung Chun,
Kim WonKi
Publication year - 2002
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.10032
Subject(s) - nitric oxide , astrocyte , biology , nitric oxide synthase , intracellular , cofactor , endocrinology , neuroglia , medicine , biochemistry , enzyme , central nervous system
We have previously reported that the production of nitric oxide (NO) in immunostimulated astrocytes was markedly decreased under glucose‐deprived conditions. The present study was undertaken to find the contributing factor(s) for the decreased NO production in glucose‐deprived immunostimulated astrocytes. NO production in rat primary astrocytes was stimulated for 24–48 h by cotreatment with lipopolysaccharides (1 μg/ml) and interferon‐γ (100 U/ml). Decreased NO production in immunostimulated astrocytes by glucose deprivation was mimicked by the glycolytic inhibitor 2‐deoxyglucose and reversed by addition of pyruvate and lactate. Glucose deprivation did not alter the expression of inducible nitric oxide synthase (iNOS) in immunostimulated astrocytes. Addition of β‐NADPH, but not tetrahydrobiopterine, both of which are essential cofactors for NOS function, completely restored the NO production that was decreased in glucose‐deprived immunostimulated astrocytes. Glucose deprivation and immunostimulation synergistically reduced intracellular NADPH level in astrocytes. The results indicate that glucose deprivation decreases NO production in immunostimulated astrocytes by depleting intracellular NADPH, a cofactor of iNOS. GLIA 37:268–274, 2002. © 2002 Wiley‐Liss, Inc.