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The purpose of this study was aimed at the investigation of the
possible action mechanisms of Pb accetate on the superoxide
generation of mouse peritoneal neutrophils (PMN). The in-vitro
study, Pb at low concentration (1μM) significantly enhanced
PMA-induced superoxide generation but at high concentration
(10-250μM) inhibited fMLP-action. Although phosphatase
inhibitors (Okadaic acid and microcystine) as well as
cytochalesin B augmented superoxide generation, Pb (3.5μM) did
not show any interaction with them. The in-vivo study, Pb
acetate (1500 ppm in drinking water) admini- stration for a
short period of either 2 weeks or 6 weeks, significantly
enhanced superoxide generation, coupled with increased PKC and
decreased phosphatase activities of the treated mouse
peritoneal PMN. This result agrees with the current working
hypothesis of the important role of protein phosphorylation in
the activation of NADPH oxidase. The reduced harvest of
peritoneal PMN from the Pb treated mice was evidently related
to the decreased chemotactic and migration ability of PMN which
was suspected to be due to the release of tumor necrosis factor
from PMN induced by Pb. Zn acetate was proofed in this study as
an antidote fo Pb acetate in vivo.
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