robin082006 Forum Hero

Topics: 471 Posts: 5,125
| | 06/11/06 - 07:32 PM  
 
   
 
|   #2 |
B decrease in ATP causes decrease in ATPase, which transport 3 Na+ out and 2K+ in, resulting in swelling of cells.
___________________ The Key to Succeed is Patience.
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| star1 Forum Guru

Topics: 93 Posts: 826
| | 06/11/06 - 07:38 PM  
 
   
 
|   #3 |
B
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| nadiabarati
| | 06/11/06 - 08:29 PM  
 
   
 
|   #4 |
thanks robin for the explanation. But why A is wrong?
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| hlab27 Forum Newbie
Topics: 0 Posts: 16
| | 06/12/06 - 06:04 AM  
 
   
 
|   #5 |
I thought A was wrong since the FFA are being used up by the mitochondria to keep up the ATP reserves. Agreed with B
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| Jlcalisto Forum Newbie

Topics: 6 Posts: 22
| | 10/12/07 - 03:56 PM  
 
   
 
|   #6 |
You are right ATP is needed for efflux of Na, but at a mitochondrial level the disruption of its membrane causes the sweeling.
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| Jlcalisto Forum Newbie

Topics: 6 Posts: 22
| | 10/12/07 - 04:02 PM  
 
   
 
|   #7 |
Cell. 1997 Nov 28;91 (5):627-37 9393856 [Cited: 60] Bcl-xL regulates the membrane potential and volume homeostasis of mitochondria. [My paper] M G Vander Heiden , N S Chandel , E K Williamson , P T Schumacker , C B Thompson Mitochondrial physiology is disrupted in either apoptosis or necrosis. Here, we report that a wide variety of apoptotic and necrotic stimuli induce progressive mitochondrial swelling and outer mitochondrial membrane rupture. Discontinuity of the outer mitochondrial membrane results in cytochrome c redistribution from the intermembrane space to the cytosol followed by subsequent inner mitochondrial membrane depolarization. The mitochondrial membrane protein Bcl-xL can inhibit these changes in cells treated with apoptotic stimuli. In addition, Bcl-xL-expressing cells adapt to growth factor withdrawal or staurosporine treatment by maintaining a decreased mitochondrial membrane potential. Bcl-xL expression also prevents mitochondrial swelling in response to agents that inhibit oxidative phosphorylation. These data suggest that Bcl-xL promotes cell survival by regulating the electrical and osmotic homeostasis of mitochondria. Mesh-terms: Anti-Bacterial Agents, pharmacology; Antimycin A, pharmacology; Apoptosis, physiology; B-Lymphocytes, chemistry; B-Lymphocytes, cytology; B-Lymphocytes, ultrastructure; Cytochrome c Group, metabolism; Flow Cytometry; Gene Expression, physiology; Homeostasis, physiology; Human; Intracellular Membranes, metabolism; Intracellular Membranes, pathology; Jurkat Cells, chemistry; Jurkat Cells, cytology; Jurkat Cells, ultrastructure; Membrane Potentials, physiology; Microscopy, Electron; Mitochondria, pathology; Mitochondria, physiology; Mitochondria, ultrastructure; Mitochondrial Swelling; Oxidative Phosphorylation, drug effects; Proto-Oncogene Proteins c-bcl-2, genetics; Support, U.S. Gov't, P.H.S.; Transfection;
___________________ JL
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| SmokyWaters Forum Elite
Topics: 6 Posts: 458
| | 10/20/07 - 11:02 AM  
 
   
 
|   #8 |
I AM SORRY BUT WHY WUD FFA ACCUMULATE? think about it n u will know that its not the answer... when there is ISCHEMIA the anareobic glycolysis takes over...FFA oxidation REQUIRES oxygen which doesnt occur ...secondly this switch takes time...I dun want to go into details of this but simply put... Na/K pump needs IMMEDIATE energy which is possible through anaerobic glycolysis and for that GLYCOGEN stores deplete...secondly when thats gone...mito swells up...needs Ca homeostatsis as well as sodium homeo to maintain the state...
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