Enzymes are proteins that act as catalysts during a biochemical process. Catalysts are non-changing enzymes that can increase or decrease activation energy to accelerate or slow down a biochemical reaction without using additional energy. Enzymes break down molecules in our body faster than they would normally break down without enzymes. On the biochemical level, enzymes work at precise temperatures and pH levels. When the temperature goes up, enzyme activity speeds up. When temperatures decrease, enzyme activity slows down. If an enzyme is at too high of a temperature, it stops functioning. Stomach enzymes function in a more acidic environment (low pH) and intestinal enzymes work in a more alkaline environment (high pH). Enzymes only react with substrates that are specific to that enzyme. When a substrate is accepted by the enzyme, the end result is a product. This product becomes the substrate for the next enzyme in the pathway.

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(Wolfe, 2000)

Importance of Aldolase B Enzyme
-Glucose and fructose are the components that make up sugar (sucrose). -In order to make ATP (energy), glucose and fructose need to go through glycolysis and enter the Krebs cycle. -Fructose needs enzymes to break it down further, before it can enter the glycolysis process. -Initially, fructose is broken down by the enzyme fructokinase into fructose-1-phosphate. -The substrate fructose-1-phosphate (F-1-P) is then further broken down by an enzyme aldose B to form two products—DHAP and glyceraldehyde. These two products are what enter glycolysis to make ATP. (Hudon-Miller, Enzymes, 2012)

In hereditary glucose intolerance (HFI), there is a mutation of the aldolase B enzyme which prevents it from functioning. If aldolase b isn’t available to breakdown F-1-P, then the by-products (DHAP and glyceraldehyde) do not enter the Krebs cycle to form ATP (energy). Fructose-1-phosphate builds up and triggers decrease in phosphate production. The phosphate production is
needed to make ATP in the electron transport chain. This leads to low energy for the liver and eventually liver failure. Build of F-1-P sends signals to glucokinase to remain in cell and reduce release of glucose. This leads to a drop in blood sugar (hypoglycemia).(High Fructose, n.d.)

Page 2 Role of Enzymes Essay

Diagram of Lock and Key Model
Cori Cycle
For needed energy, a molecule of glucose is broken down through a process called glycolysis to form 2 ATP’s. The by-product is lactic acid. During intense, anaerobic muscle activity, anaerobic hydrolysis occurs. The Cori Cycle is activated to recycle theaccumulated lactic acid back into useable energy. The lactic acid travels through the bloodstream to the oxygen-rich liver and is converted back to glucose by a process called gluconeogenesis. The glucose is then returned to the muscle to resupply it with energy. This conversion process uses up 6 ATP’s to make 2 ATP’s for the muscle to reuse. This creates a net loss of 4 ATP’s. The Cori cycle is meant to be a temporary shift of energy production from the oxygen-depleted muscles to the liver. (Hudon-Miller, Cori, 2012)

If the this conversion process continues to occur within a single cell, it would be considered futile. The single cell’s glucose would be used and then resynthesized over and over again to the point where it will eventually become depleted of all ATP and die. (The Cori Cycle, n.d.)

Dynamic Krebs (Citric Acid) Cycle
Electron Transport Chain
After the Krebs cycle, electrons from the products, FADH2 and NADH, will continue to be oxidized by the electron transport chain (E.T.C.). The protons (H+) from these products move across the mitochondrial membrane to create a differential charge which causes ADP to be phosphorylated by ATP synthase and create additional ATP (approximately 34). Ultimately, 1 glucose molecule going through glycolysis, Krebs cycle, and the electron transport chain can make about 38 ATP’s. (Energy III, 2009)

Defect Preventing ADP from Converting to ATP
Hypothetically, if the enzyme citrate synthase is defective, citrate would not be available to react to the next enzyme (aconitase) to produce isocitrate and other substrates in the citric cycle. The Krebs cycle would come to a halt and the by-products ATP, NADH and FADH2 would not be produced. Without NADH and FADH2, phosphorylation would not be triggered in the electron transport chain, and in effect, ATP proliferation would not continue. (Ophardt, 2003)

Role of Coenzyme Q10
As part of the electron transport chain, the role of Q10 is to help with the transfer of electrons from NADH and FADH2 across the mitochondrial cell membrane. When this transfer occurs, additional energy is generated by the hydrogen ions released to the intermembrane. The build-up of hydrogen ions in the intermembrane forces the hydrogen ions to move back into the matrix through ATP synthase. The re-introduction of hydrogen ion into the matrix triggers oxidative phosphorylation. This causes ADP to convert to ATP. (Sanders, 2013)

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