Abstract

Abstract The finding that the accumulation of K+ by rabbit peritoneal neutrophils is inhibited by p-nitrophenyl ethyl phosphonate esters is confirmed. This inhibition does not increase with time. Moreover, phenyl ethyl phosphonates, which are very poor inactivators of known serine esterases, inhibit K+ accumulation as efficiently as do the corresponding p-nitrophenyl ethyl phosphonates. These findings support the previous conclusion that organophosphorus inhibitors of serine esterases do not inhibit K+ accumulation of rabbit leukocytes by inactivating a serine esterase. The cell-dependent inhibition of chemotaxis of rabbit neutrophils by p-nitrophenyl ethyl phosphonates increases with time. Phenyl ethyl phosphonates do not inhibit chemotaxis but may actually enhance it. These findings indicate that the cell-dependent inhibition of chemotaxis by p-nitrophenyl ethyl phosphonates does not depend on the inhibition of K+ accumulation. They provide further support for the hypothesis that the cell-dependent inhibition of chemotaxis depends on the inhibition of an “activated esterase.” The inhibition by p-nitrophenyl ethyl phosphonates of K+ retention by rabbit neutrophils increases with time. The phenyl ethyl phosphonates are much less active in this regard. Evidence is presented that the inhibition of K+ retention probably cannot account for the cell-dependent inhibition of chemotaxis.

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