ACELL August 46/2
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چکیده
Tonkonogi, M., and K. Sahlin. Actively phosphorylating mitochondria are more resistant to lactic acidosis than inactive mitochondria. Am. J. Physiol. 277 (Cell Physiol. 46): C288–C293, 1999.—Oxidative phosphorylation of isolated rat skeletal muscle mitochondria after exposure to lactic acidosis in either phosphorylating or nonphosphorylating states has been evaluated. Mitochondrial respiration and transmembrane potential (DCm) were measured with pyruvate and malate as the substrates. The addition of lactic acid decreased the pH of the reaction medium from 7.5 to 6.4. When lactic acid was added to nonphosphorylating mitochondria, the subsequent maximal ADP-stimulated respiration decreased by 27% compared with that under control conditions (P , 0.05), and the apparent Michaelis-Menten constant (Km) for ADP decreased to 10 μM vs. 20 μM (P , 0.05) in controls. In contrast, maximal respiration and ADP sensitivity were not affected when mitochondria were exposed to acidosis during active phosphorylation in state 3. Acidosis significantly increased mitochondrial oxygen consumption in state 4 (post-state 3), irrespective of when acidosis was induced. This effect of acidosis was attenuated in the presence of oligomycin. The addition of lactic acid during state 4 respiration decreased DCm by 19%. The ratio between added ADP and consumed oxygen (P/O) was close to the theoretical value of 3 in all conditions. The addition of potassium lactate during state 3 (i.e., medium pH unchanged) had no effect on the parameters measured. It is concluded that lactic acidosis has different effects when induced on nonphosphorylating vs. actively phosphorylating mitochondria. On the basis of these results, we suggest that the influence of lactic acidosis on muscle aerobic energy production depends on the physiological conditions at the onset of acidity.
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ACELL August 46/2
JOHN M. PARK,1 ROSALYN M. ADAM,1 CRAIG A. PETERS,1 PAUL D. GUTHRIE,1 ZIJIE SUN,2 MICHAEL KLAGSBRUN,3 AND MICHAEL R. FREEMAN3 1Urologic Laboratory, Department of Urology, 3Laboratory for Surgical Research, Children’s Hospital, and Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115; and 2Departments of Surgery and Genetics, Stanford University School of Medicine, Stanford,...
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متن کاملACELL October 46/4
NABENDU S. CHATTERJEE,1 CHANDIRA K. KUMAR,1 ALVARO ORTIZ,1 STANLEY A. RUBIN,2 AND HAMID M. SAID1 1Medical Research Service, Veterans Affairs Medical Center, Long Beach 90822, and Department of Medicine and Physiology/Biophysics, University of California School of Medicine, Irvine 92697; and 2Veterans Affairs West Los Angeles, Los Angeles 90073, and Department of Medicine, University of Californ...
متن کاملACELL August 46/2
Golovina, Vera A. Cell proliferation is associated with enhanced capacitative Ca21 entry in human arterial myocytes. Am. J. Physiol. 277 (Cell Physiol. 46): C343–C349, 1999.—Depletion of Ca21 stores in the sarcoplasmic reticulum (SR) activates extracellular Ca21 influx via capacitative Ca21 entry (CCE). Here, CCE levels in proliferating and growth-arrested human pulmonary artery smooth muscle c...
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