Tricarboxylic acid cycle (Kreb’s Cycle)

AIM : Oxidation of Acetyl CoA to CO2 and H20. Also connectiong almost all individual metabolic pathways.

LOCATION:Mitochondrial matrix

 

FUNCTION: Generates high amount of NADH/FADH2 that act as fuel for ATP synthesis in ETC.

 

REQUIREMENT: Aerobic conditions only (NADH and FADH2 can be regenerated in ETC only in presence of oxygen)

REACTIONS IN KREB’S CYCLE

(Citrate is Kreb’sStarting Substrate ForMaking Oxaloacetate)

Enzymes Mnemonics

So — citrateSynthetase                   

At —Aconitase

Another —Aconitase

Dance —isocitrate Dehydrogenase

Devon — alpha-ketoglutarate Dehydrogenase

Sipped — Succinyl-CoASynthetase

Down — Succinate Dehydrogenase

Five —fumarase

Drinks — malate dehydrogenase

Regulation of TCA:

Sr. No.

Regulating Enzyme

Inhibitred by

Activated by

1.       

Citrate Synthase

ATP

NADH

Acetyl CoA

SuccinylCoa

 

———–

2.       

Isocitrate dehydrogenase

ATP

NADH

ADP

3.       

Alpha-Ketoglutarate

Succinyl CoA

NADH

 

———–

Availability of ADP is also one of the regulating factors.

Krebs cycle is both catabolic and anabolic in nature , hence regarded as amphibolic

Reactions associated are:

  1. Oxaloacetate →Synthesis of Aspartate
  2. Alpha-Ketoglutarate → Synthesis of Glutamate
  3. Succinyl CoA → Synthesis of Porphyrins and Heme
  4. Mitochondrial Citrate →cytoplasm → cleaved to get acetyl CoA → Synthesis of fatty acids , sterols , etc..

 

Ox — Oxaloacetate

Such As — Aspartate

Keto — alpha-Ketoglutatrate

And

Gluta — Glutamate

Succeded —Succinyl CoA

Merrily — Mitochondrial

In

Proper — Porphyrin

Blood shed — Heme

In

Canada — Citrate

 

           -Shivani Indrekar (MIMER Medical College)

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