Zinc Inhibition of Respiratory Burst in Zymosan-Stimulated Neutrophils : A Possible Membrane Action of Zinc

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The effect of Zn²⁺ on the respiratory burst of rat pleural neutrophils was studiesd. Serum treated zymosan (STZ)-stimulated O₂ consumption was inhibited by Zn²⁺ depending on hte Zn²⁺ concentration and time of cell incubation. Addition of Zn²⁺ after the stimulation of cells with STZ did not inhibit the O₂ consumption Zn²⁺ failed to affect the cell viability or the opsonizing process of STZ, indicating that the inhibition of O₂ consumption was not due to te direct cytotoxic action of Zn²⁺ or to the interaction of Zn²⁺ with STZ. In addition, the activity of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, an enzyme responsile for the respiratory burst of neutrophils, was not inhibited by Zn²⁺. These results suggested that Zn²⁺ may inhibit some process of the activation of NADPH oxidase.Equimolar Zn²⁺ 8-hydroxyquinoline complex (Zn-8HQ), which is known to be unable to penetrate the cell membrane, inhibited the O₂ consumption more drastically than did Zn²⁺ alone. 8-Hydroxyquinoline alone did not cause significant inhibition of O₂ consumption, indicating that the inhibitory effect of Zn²⁺ is potentiated by complexing with 8-hydrozyquinoline. The inhibition of O₂ consumption Zn²⁺ was almost completely restored by washing and reincubating the Zn²⁺-treated cells in Zn²⁺-free medium. On the other hand, in the cells treated with Zn-8HQ, the same treatment of cell washing and reincubation only partially restored the O₂ consumption. These results suggested that Zn²⁺ may be acting on the cell membrane of neutrophils.