Cellular Metabolism Case Study Part 1: 1. Given the autopsy report the massive cell quit in the kidneys, lungs, thymus, and heart indicate that the damage occurred at the cellular level, the parts of cellular respiration that occur in the mitochondrion. more than specifically, the poison directly affected the mitochondrion and in doing so it suggests that cellular respiration was disrupted. 2. The cellular deal that would be damage by arsenate would affect the cellular move of glycolysis which occurs in the cytosol of a cell. In the information provided in the case study it states that arsenate privy replace inorganic phosphate in the timber of glycolysis that produces 1, 3-biphospholglycerate from glyceric aldehyde 3-phosphate. This yields 1-arseno-3-phosphoglycerate. Therefore, glycolysis proceeds but the ATP molecule that would be generated from 1, 3-biophosphoglycerate is lost. 3. The cellular processes that would be impaired by rotenone would affect the cellular process of the electron go chain which occurs within the mitochondrion of a cell. In information provided it states that rotenone is an agent that would inhibit the electron delight chain within the mitochondrial therefore would affect the electron ictus chain. Part 2: 1.
I think that the specific cellular process that was affected by the poison was the first footmark in the electron transport chain. The very low levels of nicotinamide amp dinucleotide+ and the high levels of NADH indicate that the initial step in the electron transport chain was disrupted. Particularly, the function of NADH dehydrogenase was inhibited by the r! otenone poison. NADH dehydrogenase is tractable for converting the electron carrier, NADH, to NAD+. 2. If NAD+ had been administered to the women, she probably could have not been saved. The low levels of NAD+ in the cells are simply a symptom of the poison. The problem is that the rotenone prevents the transfer of electrons from NADH to the electron transport...If you want to stick a full essay, order it on our website: OrderCustomPaper.com
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