Respiratory burst activity in rat alveolar macrophages: particle-stimulated oxygen consumption independent of superoxide anion release.
Van Scott MR; Miles PR; Castranova V
Cellular chemiluminescence. Van Dyke K, Castranova V, eds. Boca Raton, FL: CRC Press, 1987 Jul; :21-37
Respiratory burst activity during stimulation of alveolar macrophages was studied in-vitro. The purpose of the study was to test the assumption that oxygen consumption stimulated by exposing alveolar macrophages to xenobiotics was used in releasing superoxide- anion (O2-). Suspensions of alveolar macrophages obtained from male Sprague-Dawley-rats were stimulated with 0 to 3000 micrograms per milliliter (microg/ml) concanavalin-A (11028710) (conA) or 0 to 6.0mg/ml zymosan (9010724) particles. Oxygen consumption and release of hydrogen-peroxide and O2- by the suspensions was monitored. The time course and dose response curves for zymosan and conA stimulated oxygen consumption did not match those for hydrogen- peroxide and O2- production. The maximum rate of oxygen consumption induced by zymosan occurred at a lower concentration than was required to release O2- or hydrogen-peroxide. ConA at concentrations above 600microg/ml decreased oxygen consumption and hydrogen-peroxide release. O2- release increased over the entire range of conA concentrations. Additionally rat alveolar macrophages were preincubated with 0 or 0.12 millimolar cytochrome-c (9007436), followed by 0.1 to 2.0mg/ml zymosan. The effects on oxygen consumption were monitored. Rat alveolar macrophages were treated with 0 or 0.1mg/ml zymosan and 0 or 5microg/ml cytochalasin-B (14930962). The effects on oxygen consumption and O2- and hydrogen- peroxide formation were monitored. Cytochrome-c inhibited zymosan induced oxygen consumption by 40 percent. Cytochalasin-B stimulated zymosan induced oxygen consumption and hydrogen-peroxide release by 98.5 and 44 percent, respectively, but had no effect on O2- production. The authors conclude that all of the stimulated increase in oxygen consumption in alveolar macrophages is not used in generating O2-. Some of the increase may be consumed by mechanical processes involving microfilament activation.
In-vitro-studies; Alveolar-cells; Dose-response; Physiological-chemistry; Oxidative-processes; Phagocytic-activity; Oxygen-uptake
11028-71-0; 9010-72-4; 9007-43-6; 14930-96-2
Van Dyke K; Castranova V