Abstract
To assess the site of bilirubin toxicity to cells, we have studied O2− production of PMN by two different stimulators; con-canavalin A(ConA)+cytochalasin D(CytD) which acts on the cell surface, and phorbor myristate acetate(PMA) which acts intracellularly. PMNs separated from cord blood using LymphoprepR were incubated in the buffered solution(pH 7.4) with different molar ratios of bil/alb for 30 min. at 37°C. Using a special double beam photodetector, O2− was measured by an increase in the difference in the absorbance(550-540)nm, due to the reduction of ferri-cytochrome C. Unbound bilirubin(UB) was determined by automated peroxidase method(UB Analyzer). More than 96% viability of PMNs was maintained in each solutions. O2− production by ConA+CytD was inhibited more than that by PMA which directly activates intra-cellular protein kinase C as UB levels rose. These results suggest that the critical site at which bilirubin exerts its toxicity is mainly on cell surface receptor rather than on intracellular functions. The inhibitory action increased as UB rose.
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Nakamura, H., Uetani, Y., Takada, S. et al. 1465 INHIBITORY ACTION OF BILIRUBIN ON O2 PRODUCTION BY POLYMORPHONUCLEAR LEUCOCYTES(PMN). Pediatr Res 19, 355 (1985). https://doi.org/10.1203/00006450-198504000-01489
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DOI: https://doi.org/10.1203/00006450-198504000-01489