Stimulation of the respiratory burst in human neutrophils by crystal phagocytosis

Abstract
Exposure to monosodium urate crystals (MSU) stimulated the respiratory burst of human neutrophils as measured by increased O2 consumption and the generation of superoxide radicals (O2\documentclass{article}\pagestyle{empty}\begin{document}$ \[\bar .\] $\end{document}). From the comparison of data derived from nitroblue tetrazolium and cytochrome C reduction (two methods of detecting O2\documentclass{article}\pagestyle{empty}\begin{document}$ \[\bar .\] $\end{document} release), it appears that O2\documentclass{article}\pagestyle{empty}\begin{document}$ \[\bar .\] $\end{document} production in response to MSU may be compartmentalized, i.e., occur predominantly in the intracellular space. After exposure to MSU, neutrophils from patients with chronic granulomatous disease lost viability at the normal rate; thus products of the respiratory burst are not likely to be responsible for cell death.