GLUCOSE MODULATES CELL-DEATH DUE TO NORMOBARIC HYPEROXIA BY MAINTAINING CELLULAR ATP

To determine whether glucose depletion is a principal determinant of h yperoxic cell. death in vitro, human lung epithelial-like cells (A549) were exposed to hyperoxia (95% O-2) in either 10, 30, or 50 mi of med ium (Ham's F-12K). Glucose was depleted in the medium after 36, 60, or 96 h, respectively. Medium lactate dehydrogenase (LDH) activity incre ased only after glucose was depleted. To confirm that glucose depletio n was critical to cell death, cells exposed to 95% O-2 were supplement ed with glucose at regular intervals to reestablish initial medium glu cose concentrations. Other cells received no supplements. Without supp lementation, glucose was depleted within 48 h, followed within 12 h by an almost complete loss of cell ATP and elevated medium LDH activity. Glucose-supplemented cells appeared normal microscopically and did no t release LDK activity despite an extracellular pH of 6.5 due to ferme ntation. Additional experiments at sea-level pressure confirmed that g lucose supplementation prevents extensive cell death in hyperoxia in c ultured A549 cells.