Abstract
In order to determine the role of the glutathione cycle in granulocyte (PMN) oxidative metabolism, rats were made glutathione peroxidase (GSH-Px) deficient(def), by feeding them a selenium def diet. After 12-15 weeks def rat PMN GSH-Px was 23 U/mg protein compared to 155 U/mg protein for controls. We studied the effect of GSH-Px deficiency on phorbol myristate acetate (PMA) stimulated PMN hexose monophosphate shunt (HMPS) activity and O2− production. HMPS activity was similar for def and control rats for the first 5 min. of incubation with PMA. However, over 20 min., def PMN produce 480 cpm/2.5×106 cells and control 920 cpm/2.5×106 cells. When stimulated with L-amino acid oxidase and L-leucine HMPS was 220 in def and 570 cpm/20 min/2.5×106 cells in control PMN. Initial rates of PMA stimulated O2− production were the same in def and control (2.8, 2.78 nmol O2−/min/106 PMN). However, at 5, 10, and 20 min. the rates of O2− production in the def were 44%, 14%, and 3% of O2− produced at 2 min. This is compared to 52%, 36%, and 23% O2− produced at 2 min. in the control. Incubation of PMN with L-amino acid oxidase and L-leucine for 20 min. resulted in a loss of 85% of PMA stimulatable O2− production in def compared with 43% in controls. This effect was abolished with the concomittant addition of catalase. We conclude that H2O2 in the rat PMN is metabolized through the glutathione cycle and GSH-Px protects PMN against H2O2 mediated destruction of their O2− generating system.
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Baker, S., Cohen, H. & Orkin, S. 785 PREMATURE TERMINATION OF OXIDATIVE BURST IN GLUTATHI-ONE PEROXIDASE DEFICIENT RAT NEUTROPHILS. Pediatr Res 15 (Suppl 4), 573 (1981). https://doi.org/10.1203/00006450-198104001-00809
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DOI: https://doi.org/10.1203/00006450-198104001-00809