My personal USMLE Problem( yes I think i am queen :p)- Biochem Thread

[HarveyR]

---

Members do not see this ad.

Hey guys,

So i have stated a biochem thread please bear out with me.

I came across this note:
In all, translation uses 4 high-energy phosphate bonds per amino acid:

• 2 during aminoacylation (tRNA charging): ATP → AMP (A for Activation)
• 1 during tRNA "loading" into the A-site: GTP → GDP (G for Gripping)
• 1 during translocation: GTP → GDP (G for Going places)

I just wanna know why 2 during amionoacylation. Isn't it just one bond bcs ATP is broken to AMP and PPi?
I am confused please explain me.

 

[Reperfused]

Hey guys,

So i have stated a biochem thread please bear out with me.

I came across this note:
In all, translation uses 4 high-energy phosphate bonds per amino acid:

• 2 during aminoacylation (tRNA charging): ATP → AMP (A for Activation)
• 1 during tRNA "loading" into the A-site: GTP → GDP (G for Gripping)
• 1 during translocation: GTP → GDP (G for Going places)

I just wanna know why 2 during amionoacylation. Isn't it just one bond bcs ATP is broken to AMP and PPi?
I am confused please explain me.

ATP has 3 Phosphates.
First, ATP is broken down to ADP. That's one bond broken.
Next, ADP is broken down to AMP. That's the second bond broken.
Hence, breakage of two P-bonds give you AMP + PPi

 

[HarveyR]

ATP has 3 Phosphates.
First, ATP is broken down to ADP. That's one bond broken.
Next, ADP is broken down to AMP. That's the second bond broken.
Hence, breakage of two P-bonds give you AMP + PPi

Hey thank you very much for you reply 🙂

But where i find difficulty in understanding is that breaking of ATP to AMP and PP is like a single reaction where only the bond between AMP and PP is broken. The way you described seems like ATP is broken to AMP + Pi + Pi not necessarily resuting in Pyrophosphate (PPi) where the bond between the phosphate groups are intact.

Please do kindly help me clear my confusion.

May God bless You 😀

 

[Reperfused]

It's not a 2 step process. That was only for clarification. It all happens spontaneously. But my point is, that two bonds are broken, not one. Because 2 phosphates have been removed. And yes in the end those 2 phosphates remain combined as PPi.

 

[HarveyR]

It's not a 2 step process. That was only for clarification. It all happens spontaneously. But my point is, that two bonds are broken, not one. Because 2 phosphates have been removed. And yes in the end those 2 phosphates remain combined as PPi.

How is two bonds are broken when its not a two step process? What makes sense is that after the two step process the two inorganic phosphate groups just reattach with themselves...ami I missing something here? :'(

 

[FindMeOnTheLinks]

Aminoacylation is considered to use 2 ATP equivalents because the reaction is ATP --> AMP, where PPi is released. It's one step. This is because ATP --> ADP and ADP --> AMP is energetically equivalent to ATP --> AMP. And technically ADP --> AMP is hydrolysis of a high energy phosphate bond. Therefore aminoacylation is considered the use of two ATP equivalents, though it is only one step. Look up the mechanism with arrows and you will understand.

 

[HarveyR]

Aminoacylation is considered to use 2 ATP equivalents because the reaction is ATP --> AMP, where PPi is released. It's one step. This is because ATP --> ADP and ADP --> AMP is energetically equivalent to ATP --> AMP. And technically ADP --> AMP is hydrolysis of a high energy phosphate bond. Therefore aminoacylation is considered the use of two ATP equivalents, though it is only one step. Look up the mechanism with arrows and you will understand.

Oh do you have any link? Can you please post it here? I will definitely look up into that 😀 !!!! Thank you so much in advance <3

 

[HarveyR]

I have another question you lovely bunch.
I have read that toxins can disrupt the Electron Transport Chain and they can increase/ decrease the Proton gradient and oxygen consumption. My question is how does it inroad or decrease the proton gradient and how does it affecthte oxygen consumption? Can anyone please explain or provide any helpful link?

 

[HarveyR]

Hey guys!
I am really confused. Can anyone please help me understand what does this sentence mean?
"ApoB-48 lacks the C terminal LDL receptor"
Me is so confused :'(

 

[worldbeater]

I have another question you lovely bunch.
I have read that toxins can disrupt the Electron Transport Chain and they can increase/ decrease the Proton gradient and oxygen consumption. My question is how does it inroad or decrease the proton gradient and how does it affecthte oxygen consumption? Can anyone please explain or provide any helpful link?

The electron chain is made up of 5 components in order to generate ATP. FADH (worth 1.5 ATP) and NADH (worth 2.5 ATP) are dropped off at specific spots to create energy. Energy is created by a H+ ion diving downwards from the 1st component to reach the 2nd component, then the third, etc. If the H+ ion is blocked by a poison, instead of moving downwards, it generates excess heat, causing the ETC to stop. With oxygen consumption, I don't know if it would go up or down, but I would guess since the ETC is not working and your generating more heat, consumption would go up.

I don't know all the poisons off the top of my head in the correct order, but from what I can recollect (there might be some spelling errors):
Components:
1) Amytal, Rotenone
2) Malonate
3) Antimycin
4) Carbon Monoxide (competitive inhibitor of oxygen [World Q], has 200x more affinity), Chloramphenicol (disrupts 50s ribosomal subunit in bacteria [World Q], "blasts bone marrow" [World Q])
5) Oligomycin

"ApoB-48 lacks the C terminal LDL receptor"

More LDL receptors allow all bad cholesterol to be "soaked up" and delivered to the liver for processing and not be present in the blood. So if you have a problem with LDL receptors, your cholesterol level will go up. ApoB48 is transport system, for one of the 5 types of hyperlipidemia problems. If you are missing it, you have a problem with normal physiology, I think it's a Type II hyperlipidemia deficiency problem.

 

[HarveyR]

More LDL receptors allow all bad cholesterol to be "soaked up" and delivered to the liver for processing and not be present in the blood. So if you have a problem with LDL receptors, your cholesterol level will go up. ApoB48 is transport system, for one of the 5 types of hyperlipidemia problems. If you are missing it, you have a problem with normal physiology, I think it's a Type II hyperlipidemia deficiency problem.

Hey thanks a lot! I must have specified the question better. I wanted to write how do you compare the structure of ApoB-100 both ApoB-48. This sentence was written in relation to the comparison between ApoB-48 and ApoB-100.

And thank you so much for the clarification about ECT chain as well. Lots of LOVE.

 

[worldbeater]

Hey thanks a lot! I must have specified the question better. I wanted to write how do you compare the structure of ApoB-100 both ApoB-48. This sentence was written in relation to the comparison between ApoB-48 and ApoB-100.

The exact structure? I have no idea, I just know different components act on different areas for transport of VLDL from the liver, to IDL (breakdown product of VLDL), etc. I haven't seen any practice questions getting that specific. I'll have to look at the full diagram again to figure out on what areas they act on.

And thank you so much for the clarification about ECT chain as well. Lots of LOVE.

No problem, gives me a chance to rehearse the information.