Bassett D J, Rabinowitz J L
Am J Physiol. 1985 May;248(5 Pt 1):E553-9. doi: 10.1152/ajpendo.1985.248.5.E553.
Continuous exposure to low concentrations of ozone has previously been associated with proliferation of lung alveolar type II epithelial cells. In this study, 14C incorporation into tissue lipids was determined in isolated rat lungs by perfusion with [U-14C]glucose, at a time of maximal hyperplasia brought about by 3 days continuous exposure to 0.6 ppm ozone. Ozone exposed lungs exhibited increased rates of glycolytic energy production, indicated by an 89% increase in 3H2O generation on perfusion with [5-3H]glucose, from a control value of 17.5 +/- 2.1 mumol X h-1 X g-1 X dry wt-1 (+/- SE, n = 4). Ozone exposure resulted in enhanced 14C incorporations into glyceride-glycerol and fatty acid moieties of lung lipids of 95 and 180%, respectively, with a greater proportion of label being recovered in shorter chain fatty acids. Although increased labeling was observed in both neutral and phospholipids, the pattern of 14C recovery suggested a relative increased glucose carbon incorporation into lung free fatty acids, phosphatidic acid, and such membrane associated lipids as phosphatidylinositol and those containing sphingosine. These results are consistent with the needs of a dividing cell population for enhanced energy production and synthesis of new lipids.
先前已有研究表明,持续暴露于低浓度臭氧环境会导致肺泡II型上皮细胞增殖。在本研究中,通过向分离的大鼠肺脏灌注[U-¹⁴C]葡萄糖,在连续3天暴露于0.6 ppm臭氧导致的最大增生期,测定了¹⁴C掺入组织脂质的情况。暴露于臭氧的肺脏表现出糖酵解能量产生速率增加,用[5-³H]葡萄糖灌注时,³H₂O生成量增加了89%,对照值为17.5±2.1 μmol·h⁻¹·g⁻¹·干重⁻¹(±标准误,n = 4)。臭氧暴露导致肺脂质甘油酯甘油和脂肪酸部分的¹⁴C掺入分别增加了95%和180%,且在较短链脂肪酸中回收的标记比例更高。尽管在中性脂质和磷脂中均观察到标记增加,但¹⁴C回收模式表明,葡萄糖碳相对更多地掺入肺游离脂肪酸、磷脂酸以及诸如磷脂酰肌醇和含鞘氨醇的膜相关脂质中。这些结果与分裂细胞群体对增强能量产生和合成新脂质的需求一致。