Abstract
The citric acid cycle, also known as the Krebs cycle or tricarboxylic acid cycle, is central to the formation of usable energy forms in cells. This essay will give detail on how this is achieved and the cycle’s links to other metabolic pathways such as oxidative phosphorylation. It will also explore how the cycle functions in anabolic and catabolic forms while replenishing used intermediates before examining how the cycle is regulated.
Introduction
The citric acid cycle being named “the hub of the metabolic wheel” is testament to its importance within the cell and within the organism. Andreas (1) described the fact that because its of such importance that it is logical to assume that it was one of the first components of the cell …show more content…
This is done through a series of reactions which aims to regenerate oxaloacetate for the prolonged continuation of the cycle. Acetyl coenzyme A (acetyl coA) is the input to start the cycle and is derived from glycolysis but first has to go through an intermediate stage, sometimes called the ‘link reaction’ which uses the pyruvate dehydrogenase complex. Pyruvate, the product of glycolysis, releases CO2 and 2 electrons to form acetyl coA which can then enter the cycle. Glycolysis takes place in the cytoplasm of the cell while the citric acid cycle occurs in the mitochondria, specifically the mitochondrial …show more content…
This means that the cycle has roles in both catabolic and anabolic reactions. A catabolic reaction is one that releases energy by breaking a compound down where as an anabolic reaction uses energy to ‘build’ compounds. This means that the cycle is known as an amphibolic pathway (3).
The cycle previously described of regenerating oxaloacetate is one which contains several stages involving the breakdown of certain compounds forming catabolic reactions. The breakdown of the six carbon compound, citrate, formed by oxaloacetate and coA is an example of this. The reduction of NAD and FAD (to NADH and FADH2) is coupled by the reduction of the six carbon compound and intermediates. The citrate and its intermediates are also decarboxylated to release two molecules of CO2. This is eventually exhaled from the body as waste
The citric acid cycle, also known as the Krebs cycle or tricarboxylic acid cycle, is central to the formation of usable energy forms in cells. This essay will give detail on how this is achieved and the cycle’s links to other metabolic pathways such as oxidative phosphorylation. It will also explore how the cycle functions in anabolic and catabolic forms while replenishing used intermediates before examining how the cycle is regulated.
Introduction
The citric acid cycle being named “the hub of the metabolic wheel” is testament to its importance within the cell and within the organism. Andreas (1) described the fact that because its of such importance that it is logical to assume that it was one of the first components of the cell …show more content…
This is done through a series of reactions which aims to regenerate oxaloacetate for the prolonged continuation of the cycle. Acetyl coenzyme A (acetyl coA) is the input to start the cycle and is derived from glycolysis but first has to go through an intermediate stage, sometimes called the ‘link reaction’ which uses the pyruvate dehydrogenase complex. Pyruvate, the product of glycolysis, releases CO2 and 2 electrons to form acetyl coA which can then enter the cycle. Glycolysis takes place in the cytoplasm of the cell while the citric acid cycle occurs in the mitochondria, specifically the mitochondrial …show more content…
This means that the cycle has roles in both catabolic and anabolic reactions. A catabolic reaction is one that releases energy by breaking a compound down where as an anabolic reaction uses energy to ‘build’ compounds. This means that the cycle is known as an amphibolic pathway (3).
The cycle previously described of regenerating oxaloacetate is one which contains several stages involving the breakdown of certain compounds forming catabolic reactions. The breakdown of the six carbon compound, citrate, formed by oxaloacetate and coA is an example of this. The reduction of NAD and FAD (to NADH and FADH2) is coupled by the reduction of the six carbon compound and intermediates. The citrate and its intermediates are also decarboxylated to release two molecules of CO2. This is eventually exhaled from the body as waste