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Influence of neopterin on the generation of reactive oxygen species in human neutrophils
Author(s) -
Razumovitch Julia A,
Semenkova Gali,
Fuchs Dietmar,
Cherenkevich Sergey N
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00796-8
Subject(s) - neopterin , chemistry , lucigenin , reactive oxygen species , chemiluminescence , superoxide , singlet oxygen , superoxide dismutase , granulocyte , biopterin , nitric oxide , luminol , monocyte , biochemistry , microbiology and biotechnology , oxidative stress , oxygen , nitric oxide synthase , immunology , biology , enzyme , chromatography , organic chemistry , tetrahydrobiopterin
Neopterin is synthesized by human monocyte‐derived macrophages primarily upon stimulation with the cytokine interferon‐γ. We studied the influence of neopterin on the generation of reactive oxygen species (ROS) in human peripheral blood neutrophils. Radical formation was measured using a biochemiluminometer. Neutrophils were isolated from peripheral blood of healthy donors. The generation of ROS by neutrophils suspended in Earl's solution (pH=7.4) at 37°C was investigated by monitoring of chemiluminescence using luminol and lucigenin as light emitters. Neopterin induced chemiluminescence in suspensions of neutrophils in the presence of luminol, but not of lucigenin. Neopterin affected only adhesive cells. Addition of neopterin into the suspension of the cells involving D ‐mannitol, L ‐histidine and diazabicyclo[2.2.2]octane (DABCO) decreased luminol‐dependent chemiluminescence (LDCL) of the neutrophils. The action of superoxide dismutase (SOD) and 2‐phenyl‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl‐3‐oxide (PTIO) reduced neopterin‐induced LDCL of neutrophils. Data suggest that neutrophils respond on exposure to neopterin with additional generation of singlet oxygen, hydroxyl radical and nitric oxide by nicotinamide adenine dinucleotide phosphate (NADPH)‐independent pathways.