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Respiration helppp

what's the importance of decarboxylation,
dehydrogenation, the reduction of NAD and FAD,
and substrate level phosphorylation during the Krebs cycle
thankss

Reply 1

Callicious

You can easily find the answers via Google :P

I'll try to help nonetheless.

Decarboxylation removes carbon dioxide from a molecule, i.e. via the enzyme decarboxylase. Another example of an enzyme that does his is succinyl CoA synthase, which substitutes a CO2 for a CoA molecule, which by definition is decarboxylation. The importance is that it makes the molecule capable of continuing along a metabolic pathway: enzymes work specific to substrates, and if we didn't decarboxylate a molecule it might not be able to continue along the metabolic pathway it was travelling along. Take pyruvic acid for example, it must be decarboxylated and dehydrogenated before it can form acetyl CoA via a binding of acetate and CoA, and this itself is for the purpose of another metabolic pathway, the TCA cycle.

Dehydrogenation does the same, however there is another significance: it reduces electron carrier coenzymes. Dehydrogenation happens through countless enzymes in the entire metabolic pathway that glucose follows to finishing up at its common products, i.e. water. It removes a H2 group from a molecule, reducing an electron carrier such as NAD or FAD with one hydrogen for the former and two the latter (albeit a finicky part, the hydrogen extra comes from the fluid surrounding it, not the second hydrogen from dehydrogenation) and subsequently these electron carriers can flow through to the electron transport chain to be regenerated, in the process providing electrons for the electron transport system. Fun trivia, the carrier NAD in the cytosol must be shuttled in to the mitochondria, and so in the average scenario yields less than an NAD within the matrix from TCA: the best case is identical. The ETS yields the most ATP by far compared to TCA/Glycolysis, and hence without dehydrogenation to reduce these electron carriers such as NAD and FAD, well, good luck xD

Substrate level phosphorylation is phosphorylation through a donor molecule rather than through a chain of redox reactions, i.e. oxidative phosphorylation, which is powered through the electrons travelling down a reduction gradient (or something along those lines, I'm a little shady on how to phrase it. Point is they progressively travel down an energy gradient in the inner membrane, triggering pumping of protons in to the intermembrane space, etc, proton motive force/chemiosmosis, that's not the question) ... the significance here is that it uses a donor molecule to phosphorylate, i.e. a highly energetic molecule of bisphosphoglyceric acid in glycolysis is capable of phosphorylating an ATP molecule to form a still-energetic phosphoglyceric acid, which you guessed it goes forward to do it again (after a dehydration.. etc)

Specifically for Krebs huh... well, when succinyl CoA synthase removes a CoA group from succinyl CoA a molecule of GDP (guanosine diphosphate) is phosphorylated through a free inorganic phosphate ion, and this newly formed GTP (guanosine triphosphate) can phosphorylate an ADP molecule, forming GDP and ATP, and this by definition is substrate level phosphorylation. That's all I have for specificity regarding TCA and substrate level phosphorylation.

Hope I helped! I'd recommend going on Physicsandmathstutor and finding the WJEC datasheets for respiration, they're quite intuitive.