scholarly journals Activation of sea-urchin sperm motility is accompanied by an increase in the creatine kinase exchange flux

1997 ◽  
Vol 325 (2) ◽  
pp. 411-416 ◽  
Author(s):  
Ferdi A. van DORSTEN ◽  
Markus WYSS ◽  
Theo WALLIMANN ◽  
Klaas NICOLAY
Keyword(s):  
Creatine Kinase ◽  
Sea Urchin ◽  
Magnetization Transfer ◽  
Order Rate Constant ◽  
Phosphate Transport ◽  
High Energy ◽  
Sperm Activation ◽  
Kinetics Of ◽  
Sea Urchin Sperm ◽  
Exchange Flux

The kinetics of the creatine kinase (CK) reaction were studied in suspensions of quiescent and active, intact sea-urchin spermatozoa in artificial seawater, using 31P-NMR magnetization transfer. In inactive sperm, no CK-mediated exchange flux was detected, whereas in activated motile sperm, the forward pseudo-first-order rate constant was 0.13±0.04 s-1 at 10 °C, corresponding to a steady-state CK flux of 3.1±0.5 mM·s-1. Intracellular pH shifted from 6.6±0.1 to 7.6±0.1 upon activation. The phosphocreatine (PCr)/ATP and PCr/Pi ratios were only marginally reduced in activated sperm, whereas the estimated cytosolic free ADP concentration increased remarkably from 9 μM in quiescent, to 114 μM in activated spermatozoa. The elevation of CK flux upon sperm activation is discussed in the light of the proposition that in sea-urchin spermatozoa, which are fuelled entirely by oxidative phosphorylation, high-energy phosphate transport is mediated by a ‘CK/PCr shuttle‘.

31P-NMR analysis of sea urchin sperm activation

1983 ◽  
Vol 149 (1) ◽  
pp. 289-294 ◽  
Author(s):  
R. Christen ◽  
R.W. Schackmann ◽  
F.W. Dahlquist ◽  
B.M. Shapiro
Keyword(s):  
Sea Urchin ◽  
31P Nmr ◽  
Nmr Analysis ◽  
Sperm Activation ◽  
Sea Urchin Sperm

Sea urchin sperm creatine kinase: The flagellar isozyme is a microtubule-associated protein

1988 ◽  
Vol 178 (2) ◽  
pp. 307-317 ◽  
Author(s):  
Robert M. Tombes ◽  
A. Farr ◽  
Bennett M. Shapiro
Keyword(s):  
Creatine Kinase ◽  
Sea Urchin ◽  
Sea Urchin Sperm

scholarly journals Diaphragm and cardiac mitochondrial creatine kinases are impaired in sepsis

2007 ◽  
Vol 102 (1) ◽  
pp. 44-53 ◽  
Author(s):  
Leigh A. Callahan ◽  
Gerald S. Supinski
Keyword(s):  
Creatine Kinase ◽  
Oxygen Consumption ◽  
Transport System ◽  
Phosphate Transport ◽  
High Energy ◽  
Creatine Kinase Activity ◽  
Functional Coupling ◽  
Mitochondrial Creatine Kinase ◽  
Western Blots ◽  
Protein Levels

Previous studies indicate that ATP formation by the electron transport chain is impaired in sepsis. However, it is not known whether sepsis affects the mitochondrial ATP transport system. We hypothesized that sepsis inactivates the mitochondrial creatine kinase (MtCK)-high energy phosphate transport system. To examine this issue, we assessed the effects of endotoxin administration on mitochondrial membrane-bound creatine kinase, an important trans-mitochondrial ATP transport system. Diaphragms and hearts were isolated from control ( n = 12) and endotoxin-treated (8 mg·kg−1·day−1; n = 13) rats after pentobarbital anesthesia. We isolated mitochondria using techniques that allow evaluation of the functional coupling of mitochondrial creatine kinase MtCK activity to oxidative phosphorylation. MtCK functional activity was established by 1) determining ATP/creatine-stimulated oxygen consumption and 2) assessing total creatine kinase activity in mitochondria using an enzyme-linked assay. We examined MtCK protein content using Western blots. Endotoxin markedly reduced diaphragm and cardiac MtCK activity, as determined both by ATP/creatine-stimulated oxygen consumption and by the enzyme-linked assay (e.g., ATP/creatine-stimulated mitochondrial respiration was 173.8 ± 7.3, 60.5 ± 9.3, 210.7 ± 18.9, was 67.9 ± 7.3 natoms O·min−1·mg−1 in diaphragm control, diaphragm septic, cardiac control, and cardiac septic samples, respectively; P < 0.001 for each tissue comparison). Endotoxin also reduced diaphragm and cardiac MtCK protein levels (e.g., protein levels declined by 39.5% in diaphragm mitochondria and by 44.2% in cardiac mitochondria; P < 0.001 and P = 0.009, respectively, comparing sepsis to control conditions). Our data indicate that endotoxin markedly impairs the MtCK-ATP transporter system; this phenomenon may have significant effects on diaphragm and cardiac function.

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