Abstract
Sendai virus (150 haemagglutinating units/10(6) cells) stimulates rat thymocytes incubated in medium containing 5 mM-glucose at 37 degrees C to produce luminol-dependent chemiluminescence and a simultaneous increase in O2 consumption of 40%. Stimulation of thymocytes with Sendai virus is accompanied by reduction of exogenous acetylated ferricytochrome c, which is inhibited by superoxide dismutase, and the quantitative conversion of ferricyanide to ferrocyanide, which is not. Replacement of air in the gas space with N2 inhibits the chemiluminescent response by 97% but does not prevent the virus-stimulated reduction of ferricyanide. The non-permeant ferricyanide anion (2 mM) also inhibits the chemiluminescent response to Sendai virus, its accompanying 'extra' O2 uptake and the reduction of acetylated ferricytochrome c without affecting the basal respiration of the cells. Thymocytes in which the basal O2 consumption has been stimulated maximally with dinitrophenol (10 microM) or inhibited completely with antimycin A (0.1 microM) respond to Sendai virus with an additional increment of ferricyanide-inhibitable O2 consumption. The chemiluminescent response to virus is not inhibited by concentrations of antimycin A that block the basal respiration completely. We suggest that a portion of the increased O2 uptake induced by Sendai virus is involved in the non-mitochondrial reduction of O2 to O2- at the cell surface where the non-permeant ferricyanide anion inhibits O2-. formation by acting as an alternative high-affinity electron acceptor to O2.