Showing papers by "Henry Jay Forman published in 1990"

Protection of alveolar macrophages from hyperoxia by gamma-glutamyl transpeptidase

Abstract: Exposure to hyperoxia causes loss of alveolar macrophage cell function Toxicity was measured as suppression of the respiratory burst stimulated by phorbol myristate acetate subsequent to exposure (435% depression by 2-h exposure to 5 atm absolute O2 vs controls) The presence of extracellular glutathione significantly protected these cells (7% loss) gamma-Glutamyl transpeptidase, a membrane enzyme with its active site directed outward, was necessary for use of extracellular glutathione This was demonstrated using the gamma-glutamyl transpeptidase inhibitor, serine-borate complex, which significantly blocked both protection of cells by extracellular glutathione and extracellular glutathione-dependent synthesis of glutathione The principal use of glutathione in antioxidant defense is as a substrate for glutathione peroxidase The apparent Km for glutathione of glutathione peroxidase of rat alveolar macrophages was determined to be 2 mM; however, rat alveolar macrophages have approximately 13 mM intracellular glutathione, which is insufficient for maximal enzymatic activity During hyperoxic exposure, this deficit would probably be more significant Thus the ability of extracellular glutathione along with gamma-glutamyl transpeptidase activity to provide amino acids for de novo glutathione synthesis appears to be a potentially important component of antioxidant defense

Chemoattractant and Leukotriene B4 Production from Rat Alveolar Macrophages Exposed to Nitrogen Dioxide

Abstract: The present study examined the hypothesis that exposure of alveolar macrophages to nitrogen dioxide (NO2) resulted in enhanced production of a lipophilic chemotactic agent for neutrophils, possibly leukotriene B4 (LTB4). Neutrophil migration was significantly increased in response to the reconstituted ethyl acetate extract of the medium surrounding macrophages exposed for 1 h to 5 or 20 ppm NO2. Compared with air-treated macrophages, production of LTB4 was found to be significantly increased by exposure to 5 ppm NO2, but unchanged by exposure to 20 ppm NO2. Treatment of macrophages with the calcium ionophore A23187 at a concentration of 2 µM for 15 min following a 1-h exposure to 5 ppm NO2 led to a significant increase in the production of LTB4 compared with A23187-treated air controls; however, LTB4 production in response to the calcium ionophore was unchanged following exposure to 20 ppm NO2. Thus, while increased neutrophil migration in response to products from macrophages exposed to 5 ppm NO2 correla...