Inhibition of NADPH supply by 6-aminonicotinamide: Effect on glutathione, nitric oxide and superoxide in J774 cells

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Abstract

We have examined the integrity of J774 cell nitric oxide (NO) production and glutathione maintenance, whilst NADPH supply was compromised by inhibition of the pentose pathway with 6-aminonicotinamide. In resting cells 6-phosphogluconate accumulation began after 4 h and glutathione depletion after 24 h of 6-aminonicotinamide treatment. Cellular activation by lipopolysaccharide/interferon-λ decreased glutathione by ~50% and synchronous 6-aminonicotinamide treatment exacerbated this to 31.2% of control (P<0.05). In activated cells NO-2 production was inhibited by 60% with 6-aminonicotinamide (P<0.01), and superoxide production by 50% (P<0.01) in zymosan-activated cells. NADPH production via the pentose pathway is therefore important to sustain macrophage NO production whilst maintaining protective levels of glutathione. Copyright (C) 1998 Federation of European Biochemical Societies.

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Hothersall, J. S., Gordge, M., & Noronha-Dutra, A. A. (1998). Inhibition of NADPH supply by 6-aminonicotinamide: Effect on glutathione, nitric oxide and superoxide in J774 cells. FEBS Letters, 434(1–2), 97–100. https://doi.org/10.1016/S0014-5793(98)00959-4

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