Oxygen radical scavengers protect alveolar macrophages from hyperoxic injury in vitro.
Damage to alveolar macrophages (AM) from hyperoxia (95% O2) is associated with release of factors that recruit and activate neutrophils, but the mechanisms underlying injury to AM from hyperoxia are unknown. We hypothesized that damage to AM from hyperoxia involves generation of highly reactive toxic oxygen derivatives, and we tested this premise by exposing cultured rabbit AM to hyperoxia in the presence of scavengers that inactivate various reactive oxygen species. We found that either dimethyl thiourea, a scavenger of hydroxyl radical, or catalase, a scavenger of H2O2, protected cultured rabbit AM against hyperoxic damage, which suggests that H2O2 or an H2O2-derived product, such as hydroxyl radical, contribute to damage to AM from hyperoxia.
D000818:Animals; D002374:Catalase / Q000494:pharmacology*; D002478:Cells, Cultured; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D008264:Macrophages / Q000187:drug effects* / Q000648:ultrastructure; D010100:Oxygen / Q000633:toxicity*; D011650:Pulmonary Alveoli / Q000187:drug effects* / Q000648:ultrastructure; D011817:Rabbits; D013890:Thiourea / Q000031:analogs & derivatives* / Q000494:pharmacology
C038983:1,3-dimethylthiourea; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D013890:Thiourea; D010100:Oxygen