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ETC inhibitors;acetate in glycogen;ischemia;melonate;HELP

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ETC inhibitors;acetate in glycogen;ischemia;melonate;HELP

Postby psychic_pizza » Sun Mar 23, 2008 7:30 am

I have an assignment to do, and Im stuck on a few questions.. any help would be appreciated

1)Oligomycin B and cyanide both inhibit oxidative phosphorylation when the substrate is either pyruvate or succinate. Dinitrophenol can distinguish between these inhibitors. Explain.

I know that Cyanide inhibits ETC, while oligomycin and 2,4-dinitrophenol inhibit ATP synthesis, but how does DNP influence both? why does it have to distinguish between the two?

2)Although animals cannot synthesize glucose from acetyl CoA if a rat is fed 14C-labelled acetate some of the label will end up in the liver glycogen. Explain.

I know that it has to do with incorporation into fatty acid synthesis? but havnt been able to find anything on how it occurs

3)During an ischemic attack the blood supply to a tissue is dramatically reduced causing the cells to undergo severe oxygen deprivation. It seems obvious that this should cause a cessation of cellular activity but why would it cause cell death?

4)Krebs found that the citric acid cycle could be inhibited by malonate and that this inhibition could be overcome by raising the oxaloacetate concentration. Explain how this could occur.
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Postby MrMistery » Sun Mar 23, 2008 5:37 pm

well, dinitrophenol permeabilizes the inner mitochondrial membrane for protons. If cyanide was used, dinitrophenol would have no effect, because protons had not been pumped in the first place. If oligomycin had been used the protons would have been stuck on the outer side of the membrane, because oligomycin inhibits the F0F1 ATP Synthase, and would therefore pass through the membrane producing heat when dinitrophenol was added.

2 - no idea. I think i'm missing something.

3 - it should be obvious that a straving cell will die, just like a starving human will eventually die. ATP is needed to preserve the functioning of the cell, cell life cannot pause.

4. It has to do with synthesis of fatty acids, I think - malonic acid is an important player in the synthesis of fatty acids. When malonate concentration is high, fatty acid synthesis is high, and therefore the carbon skeletons need to be directed that way, calling for a reduction of the krebs cycle. However, oxaloacetate is the last intermediate in the Krebs cycle, which forms citrate when it receives an acetyl group. I'm guessing there is some mechanism that prevents accumulation of excess oxaloacetate, but I can't think of anything now. I'll let you know if I figure it out.
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