Cellular respiration involves a compilation of metabolic activities that occur inside the cell. Different food molecules are oxidized in the process such as glucose being turned into water and carbon dioxide. During this process, 32 molecules of a product known as adenosine triphosphate (ATP) are produced. It is this product that the body uses as energy. The body requires energy (ATP) since it is essential for all the activities of life. During this process, a lot of oxygen is needed whereby the glucose and oxygen are availed to the cells via the blood stream. The respiration process is exothermic in nature. This process occurs in two different states; the breaking down of glucose into pyruvic acid (glycolysis) and the complete oxidation of pyruvic acid into water and carbon dioxide. It occurs partially in the mitochondrion and the cytoplasm (Kent, 2000).
C 6 H 12 O 6 + 6O 2 6CO 2 + 6H 2 O+ ENERGY
Autopsy Report
Organelles Involved in Process
The primary organelle involved in respiration is the mitochondrion. It is at times referred to as the “cell’s powerhouse” for all the 32 molecules of the ATP are produced in this organelle. The respiration process occurs in multiple different steps. However, most of them occur in various parts of the mitochondrion except glycolysis (Wegrzyn et al.,2009).
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Another organelle that was also present cell’s cytoplasm. Glycolysis happens in the cell’s cytoplasm. The cytoplasm is made up of the water-based solution of salts and nutrients, cytosol and other different organelles that is found in inside the cell. It is in this organelle where glycolysis takes place, and transforms glucose into two molecules of pyruvic acid. These two molecules are later transferred to the mitochondria whereby the remaining process of energy generation occurs (Starr, 2009).
Function Interrupted
The function of the cell that was interrupted was cellular respiration, particularly the chain of electron transport. This is the process by which the cell breakdowns glucose to produce energy. Every living cell has to respire to produce energy. Two primary respiration types occur within the cell include aerobic and anaerobic respiration. With the following symptoms of hypoxia (massive cell death in tissues of the lungs, kidney, and liver), significant mitochondrial tissue damage indicates that the interrupted function was aerobic respiration (Sies and Brüne,2007). Aerobic respiration requires a lot of oxygen for it to take place. Hypoxemia means that there was a lack of oxygen. Despite the people dying of hypoxemia, their level of oxygen was still very high at 1110 mm Hg whereas the normal range is 75-100 mm Hg. Hence, this factor contradicts the cause of the death, which is believed to be hypoxia.
The Loss of Function Caused the Deaths
In the body, once cellular respiration fails, the level of oxygen decreases and this leads to cell death. Respiration is a vital process which leads to the provision of the required energy for the cellular activities of the body. Hypoxemia being the cause of death, it means that the cells were undergoing temporary anaerobic respiration. Anaerobic respiration leads to breaking down of the pyruvic acid into lactate. More accumulation of lactate in the bloodstream leads to the formation of lactic acidosis that affects the health of the organism.
A high concentration of lactic acid in the blood causes cell death. It also reduces the amount of ATP generated during the anaerobic process. Lactic acid impedes the normal functioning of glutamine synthetase reaction (a critical biochemical reaction process in the brain). Glutamine synthetase reaction is essential in facilitating metabolism and excretion of nitrogenous wastes. Excess ammonia is dumped by the body on glutamate to produce glutamine. The glutamine is transported via the bloodstream to the kidney. It is here that the free ammonia ion is excreted in the urine after the terminal amino group becomes hydrolyzed by glutaminase. With the hypoxemic conditions, it means more buildup of excess ammonium in the cells which is very toxic. Since the cells are metabolically active, more nitrogenous wastes are produced, hence disrupting their normal pH levels. Such condition is fatal for the cell and can result in the death of the person (Schiffer et al., 2003).
Explanation of Apoptosis
Two ways that can result in the death of a cell include apoptosis and necrosis. Through necrosis, the cell usually dies as a consequence of an external force, and it is usually a messy affair. It can be an infection, poisoning, body injury, etc. Apoptosis is seen as a “civil way” by which a cell dies through “committing suicide.” It is far better than necrosis and is at times referred to a programmed cell death. This process follows a controlled, anticipated routine. Caspases proteins are triggered when the cell is compelled to “commit suicide.” These proteins destroy the cells components that allow it to survive. It is through the production of DNases that destroys the cell’s DNA within its nucleus. The particular cell shrinks sending distress signals that are answered by the macrophages. These clean up all the shrunken cells within the body ensuring they do not cause damage (Potten and Wilson, 2004).
Association of Disease and Disruption to Normal Organelle Functions
An organelle can contribute to the development of a disease through its normal functioning or dysfunctional state.Once an organelle is affected by a disease, it can also affect other organelles leading to a disease development in them. Once the diseases affect the organelles, they affect their normal functioning. This can lead to the development of various diseases. For instance, in this case, the mitochondrion was affected. This organelle has the duty of generating about 90% of the entire energy needed by the body. In case they become affected by a disease, they start failing thus less energy is produced within the cell. Failure of these organelles leads to cell death and injury within the cells found in the brain, heart, lung, kidney, and liver. Different organelles in the body also are affecting by other diseases and it reduces their normal functioning.
Subcellular Metabolite Analysis
Role of Metabolite in Cellular Respiration
Glucose is the simplest form of sugar. It is thus the principal substrate needed by the body to produce energy. The cellular respiration process involves three critical processes namely; glycolysis, Krebs’s cycle and oxidative phosphorylation. Glucose provides energy in the bonds of each of the three steps. During glycolysis, the glucose molecule enters the cell and is converted to form pyruvate, water, and reduced electron carriers by the cells’ cytoplasm. Pyruvate is a product of glucose formed during the glycolysis.
The product is then converted into acetyl-coenzyme-A and CO2 which is used to kick start the Krebs cycle. NADH is the most predominant electron carrier. It can also exist in its oxidized positive ions state as NAD+, which is also a substrate. It is in its free state, and it can pick up other electrons, unlike NADH that has an additional proton and two electrons. During cellular respiration, NAD+ plays the role of an oxidizing agent. It picks up other particles that result as catabolic products of glucose. It turns into NADH that goes ahead to deposit the electrons and is regenerated back into NAD+. This makes NAD+ the energy shuttle (Chiras, 2012).
Affected Pathway
Abnormalities: presence of extremely higher levels NADH than NAD+ levels.
Hypothesis: ETC was impaired due to the extremely smaller amounts of NAD+ than NADH.
Extensive examination of the impaired cells revealed that the levels of ATP in the mitochondria were minuscule. However, the levels of acetyl coenzyme (CoA) and pyruvate were normal. However, some abnormalities were seen in two metabolites; NAD+ and NADH. Their normal levels are 75 µM and 50 µM respectively. However, from the analysis, the average patient's levels for the two were ten µM and 400 µM. NAD+ is the energy shuttle of the cell. It was an indication that the levels of NADH had increased to abnormal levels. This was an indication that the two electrons carried by the metabolite were not being passed forward to its final destination causing a "traffic jam” among the metabolite. This also resulted in the reduction in numbers of NAD+. From the analysis, it was an indication that there was a problem in the electron transport chain process.
Role of Cyanide
Electron transport chain is the final process of cellular respiration. It involves a series of molecules that are found in the mitochondrion membrane. The protons and electrons from the Krebs cycle are accepted by the first molecules of the membrane. They are passed from one molecule to another until they finally react with protons and oxygen forming water. The absence of oxygen hinders the occurrence of this process causing a “traffic jam” of electrons for they cannot be transferred. With the ETC stopping, there cannot be a generation of ATP. The victims, in this case, had high levels of oxygen in their blood. This was an indication that was something hindering the cells oxygen usage (Toole and Toole, 2004).
The victims were found to have suffered from cyanide poisoning after the toxicology analysis was carried out. Inside the mitochondrion, it has different membrane layers made up of embedded proteins and bilayer of phospholipids. These proteins within the membrane act as a passageway for the electrons allowing ATP generation. Cytochrome C is found at the end of the ETP passing the electron to be final acceptor, oxygen. The oxygen binds with the protons to form water and thus process continuous with ATP being generated. Cytochrome C, the last protein, and which was inhibited by cyanide from passing the electron to oxygen. This leads to the whole chain grinding to a stop thus no ATP was formed (Toole and Toole, 2004).
Artificial respiration or oxygenation would not have saved the victims for the toxicological reports showed they died out of cyanide poisoning. According to subcellular metabolite analysis report, at the time of their death, the patients' oxygen levels in the blood were higher than normal. The report implies that the patients did not need any more oxygen. Therefore, cyanide inhibited reparation by blocking molecules involved in passing electrons to oxygen. This means that their tissues would still be unable to use the extra oxygen added in their bodies.
References
Chiras, D. D. (2012). Human biology . Sudbury, MA: Jones & Bartlett Learning.
Kent, M. (2000). Advanced biology . Oxford: Oxford University Press.
Potten, C. S., & Wilson, J. W. (2004). Apoptosis: The life and death of cells . New York: Cambridge University Press.
Schiffer, R. B., Rao, S. M., Fogel, B. S., & Ovid Technologies, Inc. (2003). Neuropsychiatry . Philadelphia, PA: Lippincott Williams & Wilkins.
Sies, H., & Brüne, B. (2007). Oxygen biology and hypoxia . San Diego, Calif: Academic Press.
Starr, C. (2009). Biology: The unity and diversity of life . Belmont, CA: Brooks/Cole, Cengage Learning.
Toole, G., & Toole, S. (2004). Essential A2 biology for OCR . Cheltenham: Nelson Thornes.
Wegrzyn, J., Potla, R., Chwae, Y. J., Sepuri, N. B., Zhang, Q., Koeck, T. & Moh, A. (2009). Function of mitochondrial Stat3 in cellular respiration. Science , 323 (5915), 793-797.
