scholarly journals Dextran strongly increases the Michaelis constants of oxidative phosphorylation and of mitochondrial creatine kinase in heart mitochondria

1998 ◽  
Vol 254 (1) ◽  
pp. 172-180 ◽  
Author(s):  
Frank Norbert Gellerich ◽  
Fanny Dorine Laterveer ◽  
Bernard Korzeniewski ◽  
Stephan Zierz ◽  
Klaas Nicolay
Keyword(s):  
Creatine Kinase ◽  
Oxidative Phosphorylation ◽  
Heart Mitochondria ◽  
Mitochondrial Creatine Kinase ◽  
Michaelis Constants

Thyroid control over membrane processes in rat heart

1991 ◽  
Vol 261 (4) ◽  
pp. L66-L71
Author(s):  
Enn K. Seppet ◽  
Lumme Y. Kadaya ◽  
Tomoji Hata ◽  
Ants P. Kallikorm ◽  
Valdur A. Saks ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Oxidative Phosphorylation ◽  
Atpase Activity ◽  
Rat Heart ◽  
Transport Processes ◽  
Functional Coupling ◽  
Mitochondrial Creatine Kinase ◽  
Thyroid State ◽  
Hyperthyroid Heart ◽  
Pumping Activity

We have studied the effects of hypo- and hyperthyroidism on sarcolemmal (SL) and sarcoplasmic reticular (SR) ion transport processes and mitochondrial energy production in rat heart. The following conclusions were derived. 1) Compared with euthyroid state, hyperthyroidism led to increased SR Ca+-accumulation. In SL, the activities of Ca2+-stimulated adenosine triphosphatase (ATPase), ATP-dependent Ca+ pumping, and Na+-Ca2+ exchanger were not affected; but ouabain-sensitive Na+-K+-ATPase activity was enhanced. 2) Hypothyroidism resulted in depressed activities of Ca2+ pumps both in SL and SR. In SL, the Na+-K+-ATPase activity was decreased, but Na+-Ca2+ exchange was unaltered. 3) Thus slower relaxation of the hypothyroid myocardium may be attributed to depressed functioning of Ca2+ pumps in SR and SL, whereas faster relaxation of the hyperthyroid heart may be based on increased Ca2+-pumping activity of SR. 4) Hyperthyroidism and hypothyroidism, respectively, led to enhanced and decreased rates of mitochondrial phosphocreatine synthesis. The thyroid state appears to control the functional coupling between mitochondrial creatine kinase and ATP-ADP translocase: the energy of oxidative phosphorylation was transformed into phosphocreatine more effectively in mitochondria from hypothyroid hearts than in those from hyperthyroid hearts. euthyroid; hyperthyroid; hypothyroid; mitochondrial creatine kinase; myocardium; oxidative phosphorylation; phosphocreatine synthesis; sarcolemma; sarcoplasmic reticulum

ADP-regenerating enzyme systems in mitochondria of guinea pig myometrium and heart

1997 ◽  
Vol 272 (2) ◽  
pp. C399-C404 ◽  
Author(s):  
J. F. Clark ◽  
A. V. Kuznetsov ◽  
G. K. Radda
Keyword(s):  
Creatine Kinase ◽  
Oxidative Phosphorylation ◽  
Guinea Pig ◽  
Adenylate Kinase ◽  
Enzyme System ◽  
Nucleotide Metabolism ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Mitochondrial Creatine Kinase ◽  
Michaelis Constant ◽  
Enzyme Systems

Any enzyme or enzyme system that produces ADP in proximity to the mitochondria may be capable of stimulating respiration. Hexokinase (HK), adenylate kinase (AK), and mitochondrial creatine kinase (Mi-CK) all catalyze reactions that produce ADP and thus may play a role in cellular nucleotide metabolism or control of mitochondrial oxidative phosphorylation. Respiratory characteristics and enzyme activities of mitochondria simultaneously isolated from heart and uterus of the gravid guinea pig were compared. The abilities of AMP, glucose, and creatine to stimulate mitochondrial respiration via AK, HK, and Mi-CK systems, respectively, were examined. Although the uterine Mi-CK activity is low compared with the values found in heart, the activities of HK and AK were significantly greater. Furthermore, the abilities of HK and AK to stimulate respiration (functional activity) were greater in the uterine mitochondria. Indeed, the activity of AK was sufficient to generate maximal (state 3) respiration. The apparent Michaelis constant (Km) for ADP to stimulate respiration in the isolated uterine mitochondria was significantly different from that of the heart mitochondria (9.6 +/- 0.9 and 5.1 +/- 1 microM ADP, respectively). It is concluded that uterine mitochondria can use HK and AK systems in addition to the CK system in enhancing local ADP concentration, which may aid in the mitochondrial responses to energetic demands.

Phosphocreatine pathway for energy transport: ADP diffusion and cardiomyopathy

1991 ◽  
Vol 261 (4) ◽  
pp. 30-38
Author(s):  
V. A. Saks ◽  
Y. O. Belikova ◽  
A. V. Kuznetsov ◽  
Z. A. Khuchua ◽  
T. H. Branishte ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Oxidative Phosphorylation ◽  
Energy Transport ◽  
Isolated Heart ◽  
Cellular Respiration ◽  
Regulation Of Respiration ◽  
Mitochondrial Creatine Kinase ◽  
Kinase Reaction ◽  
Cardiomyopathic Hamsters ◽  
Creatine Kinase Reaction

Chemically skinned (by treatment with saponin, 40 μg/ml) isolated cardiomyocytes were used to study the intracellular diffusion of ADP and creatine (Cr). Stimulation of respiration was studied in these cardiomyocytes without intact sarcolemma and in isolated heart mitochondrial by addition of ADP and Cr in the presence of 0.2 mM ATP (via mitochondrial creatine kinase reaction: Cr + MgATP = MgADP + PCr). The Michaelis constant (Km) for Cr was similar in both cases, 5.67 ± 0.11 (SD) mM in skinned myocytes and 6.9 ± 0.2 mM in mitochondria, showing that there is no significant restriction to the diffusion of this substrate. However, the apparent Km for external ADP increased from 17.6 ± 1.0 μM for mitochondria to 250 ± 38 μM for skinned cardiomyocytes, showing decreased diffusivity of ADP as a result of binding to cellular structures. In the presence of 25 mM Cr, the Km for ADP for myocytes decreased to 35.6 ± 5.6 μM due to the coupling of the creatine kinase and oxidative phosphorylation reactions. Provision of substrate for the creatine kinase reaction amplified the weak ADP signal in the regulation of respiration. The activity of the mitochondrial creatine kinase was decreased by a factor of two in cardiomyopathic hamsters and human hearts and was associated with a twofold decrease in creatine-stimulated respiration. These data show a potentially key role of mitochondrial creatine kinase in the regulation of cellular respiration and the possible importance of changes in its activity for the functional disturbances of the cardiomyopathic heart. cellular respiration; creatine kinase; oxidative phosphorylation

Thyroid control over membrane processes in rat heart

1991 ◽  
Vol 261 (4) ◽  
pp. 66-71
Author(s):  
Enn K. Seppet ◽  
Lumme Y. Kadaya ◽  
Tomoji Hata ◽  
Ants P. Kallikorm ◽  
Valdur A. Saks ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Oxidative Phosphorylation ◽  
Atpase Activity ◽  
Rat Heart ◽  
Transport Processes ◽  
Functional Coupling ◽  
Mitochondrial Creatine Kinase ◽  
Thyroid State ◽  
Hyperthyroid Heart ◽  
Pumping Activity

We have studied the effects of hypo- and hyperthyroidism on sarcolemmal (SL) and sarcoplasmic reticular (SR) ion transport processes and mitochondrial energy production in rat heart. The following conclusions were derived. 1) Compared with euthyroid state, hyperthyroidism led to increased SR Ca2+-accumulation. In SL, the activities of Ca2+-stimulated adenosine triphosphatase (ATPase), ATP-dependent Ca2+ pumping, and Na+-Ca2+ exchanger were not affected; but ouabain-sensitive Na+-K+-ATPase activity was enhanced. 2) Hypothyroidism resulted in depressed activities of Ca2+ pumps both in SL and SR. In SL, the Na+-K+-ATPase activity was decreased, but Na+-Ca2+ exchange was unaltered. 3) Thus slower relaxation of the hypothyroid myocardium may be attributed to depressed functioning of Ca2+ pumps in SR and SL, whereas faster relaxation of the hyperthyroid heart may be based on increased Ca2+-pumping activity of SR. 4) Hyperthyroidism and hypothyroidism, respectively, led to enhanced and decreased rates of mitochondrial phosphocreatine synthesis. The thyroid state appears to control the functional coupling between mitochondrial creatine kinase and ATP-ADP translocase: the energy of oxidative phosphorylation was transformed into phosphocreatine more effectively in mitochondria from hypothyroid hearts than in those from hyperthyroid hearts. euthyroid; hyperthyroid; hypothyroid; mitochondrial creatine kinase; myocardium; oxidative phosphorylation; phosphocreatine synthesis; sarcolemma; sarcoplasmic reticulum

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