Question about pyruvate decarboxylation

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uvaGirL07

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Pyruvate decarboxylation occurs in the mitochondrial matrix, correct?
That's what I thought and that's what my notes are saying, but one of the Kaplan practice exam solutions said that pyruvate decarboxylation occurs in the cytoplasm...................... it's an error, right? Just looking for some confirmation. Thanks! :D
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uvaGirL07 said:
Pyruvate decarboxylation occurs in the mitochondrial matrix, correct?
That's what I thought and that's what my notes are saying, but one of the Kaplan practice exam solutions said that pyruvate decarboxylation occurs in the cytoplasm...................... it's an error, right? Just looking for some confirmation. Thanks! :D
Click to expand...


Yeap...pyruvate is formed by Glycolysis in cytoplasm and then it is transported inside mitochondria via active trasnport where is it broken down by Citric acid cycle.

P.S. i checked it with Campbell and Reece
 
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Thanks! Just FYI for other people taking Kaplan's tests, this error was in the Kaplan Practice Exam #2 question #11. :D
 
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uvaGirL07 said:
Pyruvate decarboxylation occurs in the mitochondrial matrix, correct?
That's what I thought and that's what my notes are saying, but one of the Kaplan practice exam solutions said that pyruvate decarboxylation occurs in the cytoplasm...................... it's an error, right? Just looking for some confirmation. Thanks! :D
Click to expand...
If it is a prokaryote then pyruvate decarboxylation occurs in the cytosol.
 
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uvaGirL07 said:
Thanks! Didn't know that...

but Kaplan's question definitely did not specify haha :D
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Prokaryotes don't have membrane bound organelles so how could it have mitochondria?

You have to learn how to make inferences like that on the DAT. It can save your butt!
 
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uvaGirL07 said:
Thanks! Just FYI for other people taking Kaplan's tests, this error was in the Kaplan Practice Exam #2 question #11. :D
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I'm glad you said that. I've been saving my exams but want to know, are Kaplan's tests generally error free?
 
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I'm not done taking all the practice exams yet, but yes, they're pretty much error free. I don't really like some questions on the PAT section though. I don't agree with some of their answers... I think some of the aperture diagrams could've been drawn better... hehe :D
 
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uvaGirL07 said:
I'm not done taking all the practice exams yet, but yes, they're pretty much error free. I don't really like some questions on the PAT section though. I don't agree with some of their answers... I think some of the aperture diagrams could've been drawn better... hehe :D
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Yeah, the pat questions could use something more. I'm gonna do those first, then move on practicing on with other stuff.

So have we reached a consensus on your problem? Was it the cytosol or matrix?
 
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in eukaryotes: mitochondrial matrix
in prokaryotes: cytosol :D

I have my test on the 22nd... this Saturday................ *sigh* :(
 
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TheWiredNerv said:
Stay confident. That is huge!
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yes sir! hehe I'll try to stay confident... my kaplan scores have been ranging from 20-22 AA, and my dat achiever 18-19... achiever definitely killed my confidence... haha

I'll be taking my last practice exam either tomorrow or friday... thank God it's a Kaplan one and not an achiever one... lol :laugh:

I'm hoping that my real scores will reflect my Kaplan scores..... :scared:

btw you have a sexy chem score :D
 
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uvaGirL07 said:
yes sir! hehe I'll try to stay confident... my kaplan scores have been ranging from 20-22 AA, and my dat achiever 18-19... achiever definitely killed my confidence... haha

I'll be taking my last practice exam either tomorrow or friday... thank God it's a Kaplan one and not an achiever one... lol :laugh:

I'm hoping that my real scores will reflect my Kaplan scores..... :scared:

btw you have a sexy chem score :D
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Hey! That is almost identical to what I got on my practice! You probably will do better than me!
 
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jigabodo said:
Hey! That is almost identical to what I got on my practice! You probably will do better than me!
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You must be kidding... lol :laugh:
I would kill for your scores.... *drool*
but thanks for giving me hope... I would be happy with a 21 though. hehe :D
 
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How I remembered it fundamentally, was by knowing that the eukaryotic cytosol is a reducing environment, and the mitochondrial matrix is an oxidative microenvironment. Since pyruvate is oxidatively decarboxlyated, it cannot occur in the eukaryotic cytosol.

Also, just a little brainteaser for your preparation.

Assuming that each NADH yields 2.5 ATP, and each FADH yields 1.5 ATP, how much ATP is generated per molecule of glucose in a eukaryote vs. a prokaryote.
 
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in prokaryotes...

2 + (2*2.5) + (2*2.5) + 2 + (6*2.5) + (2*1.5) = 32 atp

but normally it is 3 atp/nadh, so it should be 38 atp

is that right? :confused:

what about eukaryotes?

is there still a difference in the atp yield per nadh during glycolysis when it's going into the mitochondria? or still assuming 2.5?
 
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Montserrat said:
How I remembered it fundamentally, was by knowing that the eukaryotic cytosol is a reducing environment, and the mitochondrial matrix is an oxidative microenvironment. Since pyruvate is oxidatively decarboxlyated, it cannot occur in the eukaryotic cytosol.

Also, just a little brainteaser for your preparation.

Assuming that each NADH yields 2.5 ATP, and each FADH yields 1.5 ATP, how much ATP is generated per molecule of glucose in a eukaryote vs. a prokaryote.
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Wow. This is a pretty difficult question. A 2 point difference in AA actually means quite a big gap between us 2.

http://www.plantsciences.ucdavis.ed...3/2005/Carbohydrate Catabolism (Web 2005).pdf

That is a pretty nice illustration of metabolism from my biochem class. Page 108 shows that there should be 38 ATP total produced per Glucose (Assuming 1 NADH = 3 ATP, 1 FADH2 = 2 ATP). If we were to use Monster's assumption, then it would be 32 ATP produced total per glucose molecule in eukaryotes.

Because 10 NADH = 25 ATP, 2 FADH2 = 3 ATP, and another 4 ATP from Glycolysis and TCA.

I am gonna need some time for prokaryote, though...
 
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I didn't really intend it to be that difficult a question. There's just one detail among prokaryotes that makes their process slightly different. And actually... TheWiredNerv hit on it earlier ;).
 
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Montserrat said:
How I remembered it fundamentally, was by knowing that the eukaryotic cytosol is a reducing environment, and the mitochondrial matrix is an oxidative microenvironment. Since pyruvate is oxidatively decarboxlyated, it cannot occur in the eukaryotic cytosol.

Also, just a little brainteaser for your preparation.

Assuming that each NADH yields 2.5 ATP, and each FADH yields 1.5 ATP, how much ATP is generated per molecule of glucose in a eukaryote vs. a prokaryote.
Click to expand...
2.5 and 1.5 are the correct and current accepted values in most literature. 2 and 3 are old and not correct anymore haha.

You get 2 NADH net from glycolysis and 2 net ATP = 7 ATP total. However, the 2 NADH are unable to be transported into the mitochondria for oxidative phosphorylation. They must be shipped in as FADH2 and thus only count as 1.5 ATP each = 5 ATP total for glycolysis.

The PDH complex (pyruvate decarboxylation in the mitochondria) yields 2 NADH = 5 ATP.

The TCA cycle yields 3 NADH and 1 FADH2 per turn, plus 1 GTP per turn x 2 turns = 6 NADH (15 ATP), 2 FADH2 (3 ATP), and 2 GTP (2 ATP) = 20 ATP.

Total = 5 + 5 + 20 = 30 ATP in eukaryotes.

In prokaryotes it would be 32 ATP because they do not lose the 2 ATP it takes to shuttle NADH from glycolysis into the mitochondria. Of course this is because they don't have mitochondria.
 
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Spoiler warning due to the

arrow-up.jpg
 
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All that crap was on our midterm in October.

Earlier today (9am) was the final on genetics, protein synthesis, and cell receptors, etc. Oh my GOD I am soooooo happy to be done with biochem FOREVER!!! :D
 
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Should we know how to do all of these ATP calculations? I've just been learning the molecules and the NET ATP. Good enough? :confused:
 
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I remember my biology section of the DAT having more analytical questions than the Kaplan practice and the Topscore exams. Part of how I studied, was reading over something mechanistic, and devising questions to mimic what might be asked.

If it's helpful to people currently studying, I can post a question every now and then.

----

Take cyanide - not something good to feed the dog. Cyanide is an effective poison, because it binds irreversibly to the cytochrome C oxidase heme group within the active site of the protein. So when someone is exposed to cyanide:

1) difference in pH outside and inside the mitochondrial matrix is as big as it's going to get, so no more electrons can be pumped against the gradient
2) anaerobic glycolysis depletes the pyruvate stores, and subsequently slows the Krebs Cycle, and electron transport chain, slowing down the rate that protons are pumped
3) the electron transport chain stops transporting electrons and stops pumping protons
4) NADH becomes fully oxidized to NAD+ by the Krebs Cycle, and thus cannot reduce NADH dehydrogenase. Therefore, no protons are pumped.


PS. I won't regurgitate questions from the actual DAT examination, so please don't ask.
 
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rose786 said:
Should we know how to do all of these ATP calculations? I've just been learning the molecules and the NET ATP. Good enough? :confused:
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Not specifically, no. But if I recall, even the Kaplan blue book listed the net products from glycolysis, PDC, and Krebs (both in net and generated ATP, NADH, and FADH2).

I didn't ask the questions specifically for number crunching, but just to highlight a point thewirednerv made about the lack of mitochondria in prokaryotes - something that I think DAT takers should definitely know and be able to apply in veiled questions.
 
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Montserrat said:
Not specifically, no. But if I recall, even the Kaplan blue book listed the net products from glycolysis, PDC, and Krebs (both in net and generated ATP, NADH, and FADH2).

I didn't ask the questions specifically for number crunching, but just to highlight a point thewirednerv made about the lack of mitochondria in prokaryotes - something that I think DAT takers should definitely know and be able to apply in veiled questions.
Click to expand...

Ok :thumbup:

You can now resume your nerd speak. :laugh:
 
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Montserrat said:
Take cyanide - not something good to feed the dog. Cyanide is an effective poison, because it binds irreversibly to the cytochrome C oxidase heme group within the active site of the protein. So when someone is exposed to cyanide:

1) difference in pH outside and inside the mitochondrial matrix is as big as it's going to get, so no more electrons can be pumped against the gradient
2) anaerobic glycolysis depletes the pyruvate stores, and subsequently slows the Krebs Cycle, and electron transport chain, slowing down the rate that protons are pumped
3) the electron transport chain stops transporting electrons and stops pumping protons
4) NADH becomes fully oxidized to NAD+ by the Krebs Cycle, and thus cannot reduce NADH dehydrogenase. Therefore, no protons are pumped.


PS. I won't regurgitate questions from the actual DAT examination, so please don't ask.
Click to expand...


1) Nope. No protons being pumped = not ETC
2) Nope. Nothing wrong with a lot of the statement. However, the causality is off. Initially, the ETC will stop functioning, leading to no protons being pumped and no reconstitution of NAD+. The TCA would then stop b/c of the lack of NAD+, causing a pyruvate buildup and initiation of anaerobic fermentation.
3) Ding Ding ! Oxygen won't be able to bind Cyt C oxidase, so Cyt C oxidase will remain in it's reduced form. Cyt C will then not be able to oxidize Cyt C Reductase, and etc etc. End result = cessation of ETC function.
4) Nope. In the TCA, NAD+ is reduced to NADH.

Correction Answer: What is #3, Alex.
 
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Montserrat said:
, causing a pyruvate buildup and initiation of anaerobic fermentation.
3) Ding Ding ! Oxygen won't be able to bind Cyt C oxidase, so Cyt C oxidase will remain in it's reduced form. Cyt C will then not be able to oxidize Cyt C Reductase, and etc etc. End result = cessation of ETC function.


Correction Answer: What is #3, Alex.
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Prokaryotes can still carry out the electron transport chain because some use Sulfur based compounds instead of oxygen!
 
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TheWiredNerv said:
Prokaryotes can still carry out the electron transport chain because some use Sulfur based compounds instead of oxygen!
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So when someone is exposed to cyanide:
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Prokaryotes are people too ? ..... you must be part of the liberal agenda to anthropomorphize everything !


I don't know if I was the Alex you were referring to loll.
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alex-trebek-31167.jpg


Alex Trebek. There can only be one.
 
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And brought back by popular demand !
-------------------------------------


The alpha ketoglutarate dehydrogenase (AKDC) is responsible for catalyzing the third step in the TCA. It has a thiamine pyrophosphate (TPP) prosthetic group that is non covalently bound to the enzyme as part of the active site. It's vital in the function of the enzyme.

A disease in thiamine deficiency, which can be brought about by diets high in polished white rice (in underdeveloped nations) leads to the development of Beriberi. Which best describes the thiamine deficiency's effect on metabolic events in humans ?

A. Glycolysis would continue anaerobically to uphold ATP levels at normal levels
B. Glycolysis rate would increase
C. Acetyl-CoA would be provided via fatty acid metabolism in order that the Krebs cycle proceed as normal
D. Glucose metabolic rate would decrease, with ATP production increasing.
 
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Montserrat said:
And brought back by popular demand !
-------------------------------------


The alpha ketoglutarate dehydrogenase (AKDC) is responsible for catalyzing the third step in the TCA. It has a thiamine pyrophosphate (TPP) prosthetic group that is non covalently bound to the enzyme as part of the active site. It's vital in the function of the enzyme.

A disease in thiamine deficiency, which can be brought about by diets high in polished white rice (in underdeveloped nations) leads to the development of Beriberi. Which best describes the thiamine deficiency's effect on metabolic events in humans ?

A. Glycolysis would continue anaerobically to uphold ATP levels at normal levels
B. Glycolysis rate would increase
C. Acetyl-CoA would be provided via fatty acid metabolism in order that the Krebs cycle proceed as normal
D. Glucose metabolic rate would decrease, with ATP production increasing.
Click to expand...


bon merde :thumbup:
 
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rose786 said:
What's The Answer?!!!!!!
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This question isn't that bad. I think the wrong answers are more informative for the sake of DAT knowledge, but think simple before thinking complicated...Well, either that, or let Streetwolf beat this question up :rolleyes:.
 
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Montserrat said:
This question isn't that bad. I think the wrong answers are more informative for the sake of DAT knowledge, but think simple before thinking complicated...Well, either that, or let Streetwolf beat this question up :rolleyes:.
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Would it kill you to say I was right? Even Alex would say I was right.
 
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Patience grasshopper.

For choice (C), acetyl CoA enter's the Krebs cycle in which step ? Which step is inhibited with the deficiency ?
 
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Montserrat said:
Patience grasshopper.

For choice (C), acetyl CoA enter's the Krebs cycle in which step ? Which step is inhibited with the deficiency ?
Click to expand...

Not more questions!

Hokay...Pyruvate is converted to AcetylCoA, which starts Krebs. So it inhibits Oxoloacetate --> Citrate, and Krebs wouldn't occur.

But the question says the third step of Krebs wouldn't occur. So it's not C. (?)

I don't get why it would be D. Why would ATP increase with glucose metabolism decreasing?
 
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