Dedhia H V, Ma J Y, Vallyathan V, Dalal N S, Banks D, Flink E B, Billie M, Barger M W, Castranova V
Department of Medicine, West Virginia University, Morgantown 26506.
J Toxicol Environ Health. 1993 Sep;40(1):1-13. doi: 10.1080/15287399309531772.
Exposure of rats to hyperoxia (100% oxygen for 64 h) resulted in striking alterations in the properties of samples obtained by bronchoalveolar lavage. The yield of neutrophils, lymphocytes, and red blood cells was increased, while the number of harvested alveolar macrophages decreased. The acellular lavage fluid level of protein was elevated, indicating lung damage. However, acellular phospholipid levels were unchanged. The ability of alveolar macrophages to produce reactive forms of oxygen in response to zymosan was significantly decreased by oxygen exposure. This impaired function was not fully explained by a decrease in viability of these phagocytes. In contrast, stimulant-induced chemiluminescence was elevated after hyperoxia. This rise was not due to a change in cellular antioxidant levels or to a discernible increase in arachidonic acid metabolites. However, it was associated with increased cellular lipid peroxidation.
将大鼠暴露于高氧环境（100%氧气，持续64小时）会导致支气管肺泡灌洗所获样本的特性发生显著改变。中性粒细胞、淋巴细胞和红细胞的产量增加，而收获的肺泡巨噬细胞数量减少。无细胞灌洗液中的蛋白质水平升高，表明肺受到损伤。然而，无细胞磷脂水平未发生变化。氧气暴露显著降低了肺泡巨噬细胞对酵母聚糖产生活性氧形式的能力。这些吞噬细胞活力的降低并不能完全解释这种功能受损。相反，高氧暴露后刺激物诱导的化学发光增强。这种升高并非由于细胞抗氧化剂水平的变化或花生四烯酸代谢产物的明显增加。然而，它与细胞脂质过氧化增加有关。
