Mitochondrial ATP hydrolysis and ATP depletion in thymocytes and Ehrlich ascites carcinoma cells

FEBS Letters

Dedov, V.N.²  Chernyak, B.V.²  Gabai, V.L.¹ 

[1] Medical Radiology Research Center, Russian Academy of Medical Sciences, 240920 Obninsk, Kaluga Region, Russian Federation;A.N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, 119899 Moscow, Russian Federation

关键词: ATP depletion;    Glycolysis;    Mitochondrial ATPase;    ATPase inhibitor protein (IF1);    EAC cell;    Thymocyte;    EAC;    Ehrlich ascites carcinoma;    CCCP;    carbonylcyanide m-chlorophenylhydrazone;   

DOI  :  10.1016/0014-5793(94)80629-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

When Ehrlich ascites carcinoma (EAC) cells and thymocytes were treated with uncoupler or rotenone in glucose-free medium, rapid ATP depletion was observed in both types of the cells. Oligomycin slowed down ATP loss in thymocytes, but not in EAC cells. Thus, mitochondrial ATP hydrolysis appears to be significant in deenergized thymocytes in contrast to EAC cells, in which other ATP consuming reactions were prevailing. Complete deenergization of mitochondria by uncoupler or rotenone in these cells resulted in inactivation of mitochondrial ATPase by 65–75%. The effect was observed after complete and rapid (20–30 s) disruption of the cells with detergent, Lubrol WX. ATPase was blocked by the specific inhibitor protein (IF₁) as it was shown by the studies on reactivation of this enzyme. When respiration is blocked but ATP content is supported by glycolysis, mitochondrial ATPase is not suppressed by IF₁, and maintains the energization of mitochondria. It is concluded that under complete de-energization of mitochondria IF₁, significantly inhibits mitochondrial ATP hydrolysis and may slow down ATP loss in thymocytes and EAC cells.

【 授权许可】

Unknown