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NITRIC OXIDE MODIFIES GLYCOLYTIC PATHWAYS IN CULTURED HUMAN SYNOVIOCYTES
Author(s) -
Borderie D.,
Marechal H.,
Ekindjian O. G.,
Hernvann A.
Publication year - 2000
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1006/cbir.2000.0498
Subject(s) - sodium nitroprusside , glyceraldehyde 3 phosphate dehydrogenase , nitric oxide , glycolysis , chemistry , lactate dehydrogenase , nitric oxide synthase , inflammation , dehydrogenase , snap , biochemistry , enzyme , biology , immunology , computer graphics (images) , organic chemistry , computer science
Nitric oxide (NO) is a free radical produced during inflammation following activation of an inducible NO synthase by pro‐inflammatory cytokines such as IL‐1β. Since both NO and IL‐1β are involved in the physiopathology of inflammatory arthropathies, we investigated the effects of exogenous NO on glycolytic pathways in cultured human osteoarthritic synovial cells. NO generated from S‐nitroso‐N‐acetyl penicillamine (SNAP) or sodium nitroprusside (SNP) inhibited glucose uptake (by 50% after 1h of incubation) and lactate production by 16% (SNAP) and 8.5% (SNP) after 3h. Both NO donors also reduced production of glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH), an enzyme of the glycolytic pathway. This effect was reversed by haemoglobin, a NO scavenger with higher affinity for the radical. In contrast, the effect on glucose uptake appeared to be irreversible.