Oxygen-Dependent-Regulation of Ehrlich Ascites Tumor Cell Respiration by Nitric Oxide

Cell Structure and Function

Jitsuo Akiyama¹  Tatsuji Yasuda⁵  Yoko Inai⁵  Alan A. Horton⁴  Kozo Utsumi²  Yoshiki Takehara²  Munehisa Yabuki⁵  Eisuke F. Sato³  Masayasu Inoue³ 

[1] Donan Institute of Medical Science;Institute of Medical Science, Center for Adult Diseases;Department of Biochemistry, School of Medicine, Osaka City University Medical School;School of Biochemistry, The University of Birmingham;Department of Cell Chemistry, Institute of Molecular and Cell Biology, Okayama University Medical School

关键词: nitric oxide;    mitochondrial respiration;    glycolysis;    energy metabolism;    Ehrlich ascites tumor cells;   

DOI  :  10.1247/csf.21.151

学科分类：分子生物学，细胞生物学和基因

来源: Japan Society for Cell Biology

【 摘 要 】

References(31)Cited-By(10)Effects of nitric oxide (NO) on oxygen uptake of Ehrlich ascites tumor cells (EATC) were examined in a study of the biological actions of NO on respiration and energy metabolism at the cellular level. Endogenous respiration of EATC was inhibited reversibly by NO in a dose dependent manner. Oxyhemoglobin, an NO trapping agent, restored the respiration promptly. The inhibitory action of NO also depended on oxygenconcentration, and the duration of suppression was prolonged remarkably at low oxygen tension. Similar inhibition was also observed in the presence of glucose. In this case, both lactate production and glucose consumption were promoted by NOC 18, an NO generating agent, and the activation was enhanced by lowering the oxygenconcentration. Furthermore, the membrane potential of EATC was depolarized transiently by adding NO, and the degree of depolarization was decreased in the presence of glucose. These results suggest that at physiologically low oxygen tension in ascites fluid, NO acts not only as a cytotoxic respiratory inhibitor but also as a regulatory factor in the energy metabolism of EATC.

【 授权许可】

Unknown