Simon L M, Raffin T A, Douglas W H, Theodore J, Robin E D
J Appl Physiol Respir Environ Exerc Physiol. 1979 Jul;47(1):98-103. doi: 10.1152/jappl.1979.47.1.98.
O2-mediated alterations in cell energy metabolism may play a role in structural and functional abnormalities described in type II pneumocytes (T-II-P) following in vivo hyperoxia. Bioenergetic alterations produced by hyperoxia (95% O2) were therefore examined in a culture-maintained cell line derived from T-II-P. Exposure of cell monolayers to 95% O2 for 96 h results in a significant decrease in O2 consumption (from 0.52 +/- 0.07 to 0.30 +/- 0.08, P less than 0.01), suggesting impaired mitochondrial energy provision. In addition, there are increased rates of aerobic lactate production (from 2.89 +/- 0.52 to 3.84 +/-0.80, P less than 0.05) with loss of Pasteur effect, indicating a shift to glycolytic metabolism at relatively high PO2's. These metabolic changes are not accompanied by altered activities of critical mitochondrial (cytochrome oxidase) or glycolytic (pyruvate kinase, phosphofructokinase) enzymes. Altered cell bioenergetics following hyperoxia may this represent an important secondary mechanism leading to functional abnormalities in T-II-P.
体内高氧环境下，氧介导的细胞能量代谢改变可能在II型肺细胞（T-II-P）的结构和功能异常中发挥作用。因此，我们在一种源自T-II-P的培养细胞系中研究了高氧（95%氧气）引起的生物能量变化。将细胞单层暴露于95%氧气中96小时，导致氧气消耗显著降低（从0.52±0.07降至0.30±0.08，P<0.01），提示线粒体能量供应受损。此外，有氧乳酸生成速率增加（从2.89±0.52增至3.84±0.80，P<0.05），同时巴斯德效应丧失，表明在相对较高的氧分压下代谢转向糖酵解。这些代谢变化并未伴随关键线粒体酶（细胞色素氧化酶）或糖酵解酶（丙酮酸激酶、磷酸果糖激酶）活性的改变。高氧后细胞生物能量的改变可能是导致T-II-P功能异常的重要继发机制。
