Abstract
We show that a purified preparation of the prominent tartrate-resistant acid phosphatase (E.C.3.1.3.2), isolated from the external surface of the intracellular parasite Leishmania donovani (promastigote form), inhibits toxic oxidative metabolite production of neutrophils. Preincubation of a neutrophil suspension (2.5 × 10 6 cells/ml) for 15 min at 37 C with 250 units (1 unit equals 1 nmole of 4-methylumbelliferyl phosphate cleaved per hr at pH 5.5) of the acid phosphatase in Krebs-Ringer phosphate buffer (pH 7.4) decreased O 2 consumption, O 2 − production, and H 2O 2 production of N-formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe)-stimulated neutrophils to 15–25% of control values. The acid phosphatase also affected concanavalin A-stimulated O 2-production by neutrophils, but had no effect on the rate of phorbol myristic acetate-stimulated O 2 − production, chemotactic peptide binding, degranulation, or membrane depolarization. Addition of an acid phosphatase inhibitor (Complex E; (NH 4) 6[P 2Mo 18O 62]·9H 2O) to suspensions of opsonized promastigotes and neutrophils resulted in a threefold or greater enhancement of O 2 − production. These results suggest a possible pathophysiologic role for the acid phosphatase of L. donovani promastigotes.
Published Version
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