It is stated in this paper that most cancer cells demonstrate increased glycolysis. The use of this metabolic pathway for the generation of ATP as a source of energy is thought to be one of the most basic metabolic alterations during malignant transformations. The research has stated that this metabolic alteration may evolve during cancer development. The most obvious metabolic alterations in cancer cells are the increase in aerobic glycolysis which is dependent on a gycolytic pathway for the generation of ATP. It targets the glycolytic pathway and may kill the malignant cells. This paper considers the characteristics of the glycolytic pathway in cancer, the inhibition of glycolysis and the probable applications in cancer treatment.
The Warburg effect came was around over 80 years ago when the experiment demonstrated normal cells in comparison to malignant cells. It had shown significant increased levels ofglycolytic activity even without the presence of enough oxygen. This phenomenon was termed metabolic alteration in malignant transformation. Some of the mechanisms that have been suggested to affect the energy metabolism were mitochondrial defects, adaption to hypoxic environment in cancer tissues, oncogenic signals and abnormal expression of specific metabolic enzymes.
It was stated that the combination of glycolytic inhibitors and DNA damaging agents were also a suggested strategy to kill cancer cells. Even though several glycolitic inhibitors are promising for anticancer activity, there are potential concerns and challenges. The inhibition of glycolysis can be toxic to brain tissues, testis tissues and even retina tissues.
This paper was very in depth in content for me to understand, but after a few times of reading the paper began to interest me. I like the fact that it was a good research of glycolithic inhibitors for anti cancer activities. It even gave a step by step process of glycolysis within the paper. It was very informative.
This paper’s objective was to observe the relationship between the consumption of high fructose corn syrup in beverages and how they affect obesity. In addition to the simple sugar of fructose, it also took into consideration the effect of sucrose on the alarming increases of obesity statistics. Since it is more economically convenient to use High-fructose corn syrup or the use of fructose instead of sucrose it has become more favoured. It is used in carbonated beverages, baked goods, canned fruits, jams, jellies and dairy products. If this HFCS is used in so many products especially consumed in the United States of America; it constitutes largely to the major source of fructose in an individual’s daily dietary intake.
When large amounts of fructose are ingested; they supply an unregulated source of precursors for hepatic lipogenesis. The desire for this sweetener reduces the intake of solid food; and enhances caloric consumption. The sweet taste preference of humans by the major source of soft drink consumption is an important contributor to the epidemic of obesity. It was suggested that these HFCS should be replaced with non-caloric sweeteners. Even total Calcium intake by milk from individuals had decreased due to the increase of the usage of HFCS products mainly soft drink consumption and even juices.
So for these few months of Biochemistry; I learnt a lot from the lectures, the assignments, the blogging, the tutorials, the experimental write ups and the teaching links up on myelearning. The tutorials for me was a bit challenging because it is just brain wrecking and a lot of pressure. Other than that this course is a challenging but a good experience.
The Citric Acid Cycle is also called the Krebs Cycle or the tricarboxylic acid cycle which is a series of chemical reactions within the cell which is responsible for the breaking down of food substances into Carbon dioxide energy and water.
The enzyme triose phosphate isomerase rapidly inter-converts the molecules dihydroxyacetone phosphate and glyceraldehyde phosphate. Glyceraldehyde phosphate is removed as soon as it is formed to be used in the next step of glycolysis.
Net result for steps 4 and 5: Fructose 1, 6-bisphosphate (C6H10O6P2) ↔ 2 molecules of Glyceraldehyde phosphate (C3H5O3P1)
The enzyme triose phosphate dehydrogenase serves two functions in this step. First the enzyme transfers a hydrogen (H–) from glyceraldehyde phosphate to the oxidizing agent nicotinamide adenine dinucleotide (NAD+) to form NADH. Next triose phosphate dehydrogenase adds a phosphate (P) from the cytosol to the oxidized glyceraldehyde phosphate to form 1, 3-bisphosphoglycerate. This occurs for both molecules of glyceraldehyde phosphate produced in step 5.
B. Triose phosphate dehydrogenase + 2 P + 2 glyceraldehyde phosphate (C3H5O3P1) → 2 molecules of 1,3-bisphosphoglycerate (C3H4O4P2)
The enzyme phosphoglycerokinase transfers a P from 1,3-bisphosphoglycerate to a molecule of ADP to form ATP. This happens for each molecule of 1,3-bisphosphoglycerate. The process yields two 3-phosphoglycerate molecules and two ATP molecules.
2 molecules of 1,3-bisphoshoglycerate (C3H4O4P2) + phosphoglycerokinase + 2 ADP → 2 molecules of 3-phosphoglycerate (C3H5O4P1) + 2 ATP
The enzyme phosphoglyceromutase relocates the P from 3-phosphoglycerate from the third carbon to the second carbon to form 2-phosphoglycerate.
2 molecules of 3-Phosphoglycerate (C3H5O4P1) + phosphoglyceromutase → 2 molecules of 2-Phosphoglycerate (C3H5O4P1)
The enzyme enolase removes a molecule of water from 2-phosphoglycerate to form phosphoenolpyruvic acid (PEP). This happens for each molecule of 2-phosphoglycerate.
2 molecules of 2-Phosphoglycerate (C3H5O4P1) + enolase → 2 molecules of phosphoenolpyruvic acid (PEP) (C3H3O3P1)
The enzyme pyruvate kinase transfers a P from PEP to ADP to form pyruvic acid and ATP. This happens for each molecule of PEP. This reaction yields 2 molecules of pyruvic acid and 2 ATP molecules.
2 molecules of PEP (C3H3O3P1) + pyruvate kinase + 2 ADP → 2 molecules of pyruvic acid (C3H4O3) + 2 ATP