Harada R N, Vatter A E, Repine J E
Am Rev Respir Dis. 1983 Oct;128(4):761-2. doi: 10.1164/arrd.1983.128.4.761.
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.
高氧(95%氧气)对肺泡巨噬细胞(AM)的损伤与招募和激活中性粒细胞的因子释放有关,但高氧损伤AM的潜在机制尚不清楚。我们推测高氧对AM的损伤涉及高反应性有毒氧衍生物的产生,我们通过在使各种活性氧失活的清除剂存在下,将培养的兔AM暴露于高氧环境来验证这一假设。我们发现,作为羟基自由基清除剂的二甲基硫脲或作为H2O2清除剂的过氧化氢酶,均可保护培养的兔AM免受高氧损伤,这表明H2O2或H2O2衍生的产物(如羟基自由基)会导致高氧对AM的损伤。