Effect of Hyperoxia on the Viability and Proliferation of the Primary Type II Alveolar Epithelial Cells

• Published in: Cell biochemistry and biophysics 2013-12, Vol.67 (3), p.1539-1546
• Main Authors: Liu, Xiu-xiang, Yu, Xiu-rong, Jia, Xiu-hong, Wang, Ke-xuan, Yu, Zheng-yan, Lv, Chang-jun
• Format: Article
• Language: English
• Subjects: Animals; Biochemistry; Biological and Medical Physics; Biomedical and Life Sciences; Biophysics; Biotechnology; Cell Biology; Cell Hypoxia; Cell Proliferation; Cell Survival; Cells, Cultured; Epithelial Cells - cytology; G1 Phase; Life Sciences; Pharmacology/Toxicology; Rats; Rats, Sprague-Dawley; S Phase; Time Factors; Translational Biomedical Research
• ISSN: 1085-9195; 1559-0283
• DOI: 10.1007/s12013-013-9658-9

To observe the effect of hyperoxia on the growth of type II alveolar epithelial cells (AEC II). The lungs of 19-day gestation fetal rats were primary cultured and the AEC II were purified by differential adhesion method. The cells were divided into control (normoxia) group and hyperoxia group. The cell growth, cell viability, cell apoptosis, and cell cycle were examined at 2, 4, 6, and 8 days of normoxia or hyperoxia exposure. The number of cells in hyperoxia-exposed group significantly decreased as compared to those of air control group. Number of cells in hyperoxia group was the highest at day 2 of exposure and gradually decreased with time. The viability of cells exposed to hyperoxia was substantially reduced compared with cells exposed to air. Percentage of cells in G1 phase and S phase in hyperoxia group increased gradually with increase in exposure duration and significant differences were seen at day 4 and day 6 compared with either the preceding time points and also with corresponding air-exposed cells. The percentage of both early apoptotic cells (Annexin-V + /PI − ) and late apoptotic cells and necrotic cells (Annexin-V + /PI + ) increased significantly in cells exposed to hyperoxia compared with cells exposed to air. Hyperoxia inhibits proliferation, viability and growth of AEC II and promotes apoptosis.