Concanavalin A-induced chemiluminescence in rat thymus lymphocytes. Its origin and role in mitogenesis

Abstract

1. The luminol-dependent chemiluminescence of rat thymocytes responding to concanavalin A can be resolved into glucose-dependent and glucose-independent portions. 2. The glucose-dependent portion, supported by D-glucose and D-mannose oxidation, is inhibited by catalase (200 microgram/ml), amobarbital (1 mM) and hexose analogues that block D-glucose uptake. Thus concanavalin A may activate, transiently, an NAD(P)H oxidase that utilizes reducing equivalents derived from the oxidation of exogenous glucose to give dismutation products of O2- (including H2O2) as its major products. 3. The glucose-independent portion is inhibited by eicosa-5,8,11,14-tetraynoic acid but not by indomethacin. It may therefore be associated with the conversion of hydroperoxy intermediates of arachidonic acid metabolism to hydroxy products by the lipoxygenase pathway. 4. Preincubation of thymocytes for 18 h in serum-free medium enhances the subsequent chemiluminescent response to concanavalin A severalfold and evokes the response at a lower threshold concentration. The incorporation of [3H]thymidine by preincubated cells is similarly enhanced at low doses of concanavalin A, whereas the response to optimal doses is unaltered. 5. Catalase does not inhibit the enhanced incorporation of [3H]thymidine obtained in response to concanavalin A, but instead amplifies the response to low doses in the same manner as preincubation.

Three‐peaked chemilluminescent response of human peripheral blood leukocytes following stimulation with phytohaemagglutinin (PHA)

“…The synergistic interaction between monocytes and lymphocytes to produce enhanced chemiluminescence has been observed previously (Clement and Lehmeyer, 1983;Hume et al, 1981), and it has also shown that it is the binding of lectins to the cell surface which is the most important initiator of CL (Mookerjee et al, 1980). Two distinct mechanisms are involved in the generation and handling of the excited oxygen species in monocytes and polymorphonuclear leukocytes and this may account for the different response times to PHA-C (Nguyen et al, 1983).…”

Regulation of reactive oxygen species (ROS) production by C18 fatty acids in Jurkat and Raji cells

“…Generation of moderate amounts of ROS (reactive oxygen species) by several non-phagocytic leucocytes, including B-lymphocyte cell lines [1][2][3][4], human tonsillar B-lymphocytes [5], thymocytes [6,7], human NK (natural killer) cells [8,9], human peripheral T-lymphocytes [10] and T-lymphocyte cell lines [11], has been described.…”

Chemiluminescence in the assessment of polymorphonuclear leukocyte function in chronic inflammatory periodontal disease

“…Cheson et al (53) reported that reactive oxygen species alone are not enough in the production of CL and suggested that the oxidation of particle components was necessary for CL to occur. Recently, two modes of CL have been distinguished: a glucose-dependent component and a glueose-independent component; the latter associated with formation of intermediates of arachidonic acid mctabolistn via tlic lipoxygenasc pathway (54,55,56). Cheung et al (56) suggest that glucosedependent CL Is elosely related to the activation of NADPH oxidase and is inhibited by scavengers and inhibitors of reactive oxygen speeies.…”