Cellular Metabolism Case Study Part 1: 1. Given the autopsy report the massive cell use up 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 impaired by arsenate would affect the cellular influence of glycolysis which occurs in the cytosol of a cell. In the information provided in the case study it states that arsenate can replace inorganic phosphate in the timber of glycolysis that produces 1, 3-biphospholglycerate from glyceraldehyde 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 wou ld affect the cellular process of the negatron 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 have a go at it chain within the mitochondrial therefore would affect the electron captivate 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 group A dinucleotide+ and the high levels of NADH indicate that the initial step in the electron transport chain was disrupted. Particu larly, the function of NADH dehydrogenase wa! s inhibited by the rotenone poison. NADH dehydrogenase is gentle 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 make a full essay, order it on our website:
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