Kreb Cycle Help!

[Oohhlala]

Hi!

 

For my biochemistry class we have an assignment to explain how a hypothetical defect of an enzyme in the Kreb cycle could decrease the overall ATP production. We get to choose which enzyme has the defect and explain how it could decrease ATP.

 

I wanted to use aconitase and explain how it could set off a chain reaction of defects causing enzymes to not work properly. Meaning, if there is no isocitrate dehydrogenase, then oxidative decarboxylation cannot take place. Without this process that produces alpha-ketoglutarate and CO2, NAD cannot be converted to NADH. Ultimately without NADH, reoxidation of NADH and FADH2 cannot occur which is necessary to create ATP.

 

Does this make any sense? Is there a better way of explaining it? I am lost.

 

Thank you!

 

[irfuzzbucket]

Sounds like you have a decent explanation

 

Things to remember:

 

A defect in one enzyme does not change the other enzymes. It prevents a product from being formed which means that the krebs cycle would no longer cycle.

A->B->C doesn't work if B never gets created.

 

I would change the word "reoxidation" to something better, or describe it better (ETC).

 

does this impact anaerobic respiration?

[Function]

I'm not aware of the steps in the cycle anymore (for about 2 years lol), but a small intermezzo:

 

I find the statement "A -> B -> C doesn't work if B never gets created" a bit blunt; in medicine, people with high blood pressure may be administered (although there are many other preferential drugs) ACE-inhibitors: ACE, or angiotensin converting enzyme, converts angiotensin-I to angiotensin-II, which, through several steps and processes, does accomplish a raise in blood pressure.

 

Angiotensinogen (an alpha-2-globulin, a precursor of angiotensin-I) gets converted to angiotensin-I via renin

Angiotensin-I -> angiotensin-II via ACE

 

Blocking ACE will indeed block the formation of AT-II out of AT-I.

However, and that is why specific angiotensin receptor-antagonists (called sartans) are more effective in case of hyptertension, AT-II may also be formed by other enzymes than only ACE (which then can still bind to, and activate, angiotensin receptors).

 

My point here: A -> B -> C is not necessarily as linear as depicted here, but B and C may be formed with other enzymes/products/coenzymes, and this should be looked up. But then again, I no longer have any knowledge on the Krebs cycle and do not wish to make (possibly false) statements on the formation of its products. Just keep this in mind.

Edited July 8, 2016 by Function

[CharonY]

On a broader scale one has to remember that the TCA cycle is the central of metabolism, i.e. a lot of conversion from one class of metabolites passes through the cycle. As a corollary there are many bypasses that flow in and out of the TCA cycle. Hence changes withing the cycle can have quite broad effects on many metabolite pools and, as already mentioned, the cycle is not, well, linear. There are single-step reactions which can have similar effects as OP outlines, but there are various branches that can be used to bypass a defective enzyme (to a certain degree).

Finally, one should add that it is also dependent on the organisms, as especially prokaryotes have massive variability when it comes to how the TCA cycle is formed and what bypasses it can use under varying conditions.