Macrophages and neutrophils play an important role in natural host defence system. When these phagocytes recognize foreign particles, such as bacterium and fungi, they escape the vascular system, migrate towards the site of infection, followed by phagocytosis and intracellular killing of the invading microorganisms by bactericidal reactive oxygen species derived from the superoxide anion. Superoxide anion production and hydrogen peroxide production were measured spectrophotometrically by a superoxide dismutase-inhibitable reduction of ferricytochrome c and by a catalase-inhibitable oxidation of phenol red, respectively. Phagocytosis was quantified by fluorescence quenching assay using fluorescein conjugated Escherichia coli (E. coli). In vitro treatment of the new quinolones was effective in markedly potentiating the production of superoxide anion in macrophages. The potentiation is prolonged with tosufloxacin (TFLX) but transient for ofloxacin (OFLX), lomefloxacin (LFLX), fleroxacin (FLRX), sparfloxacin (SPFX), and levofloxacin (LVFX). A similar potentiation by TFLX was seen with the production of superoxide anion in neutrophils, while the other five new quinolones were effective in markedly reducing that production in neutrophils. Moreover, all of the new quinolones significantly inhibited phagocytosis of E. coli in macrophages By contrast, OFLX, LFLX, FLRX and LVFX caused an increase of phagocytosis of E. coli in neutrophils. However, TFLX and SPFX failed to significantly affect phagocytosis in neutrophils. Therefore, the new quinolones may differentially affect the function of macrophages and neutrophils.