There is a proposal that pyrazole could protect against the damaging effects of alcohol on the liver that result from prolonged decrease in the ratio of [NAD+]/[NADH] caused by the oxidation of alcohol. ( NAD+ is required for several key dehydrogenation steps in the pathway of glucose synthase. NADH promotes the accumulation of fat in the liver cells) Assuming that pyrazole is not toxic and that it is transported to the liver, evaluate its potential as an antidote to liver damage in treating chronic alcoholism. Would it be a reasonable therapeutical candidate? Explain. Please explain and please don't copy bartleyby answer.

There is a proposal that pyrazole could protect against the damaging effects of alcohol on the liver that result from prolonged decrease in the ratio of [NAD+]/[NADH] caused by the oxidation of alcohol. ( NAD+ is required for several key dehydrogenation steps in the pathway of glucose synthase. NADH promotes the accumulation of fat in the liver cells) Assuming that pyrazole is not toxic and that it is transported to the liver, evaluate its potential as an antidote to liver damage in treating chronic alcoholism. Would it be a reasonable therapeutical candidate? Explain. Please explain and please don't copy bartleyby answer.

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter17: Metabolism: An Overview

Section: Chapter Questions

Problem 14P

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One of the consequences of ethanol addiction is fattyliver disease, an illness in which liver cells accumulatetriacylglycerols, the esters derived from glycerol and fattyacids. Ethanol is oxidized in the cytoplasm of liver cells byalcohol dehydrogenase and aldehyde dehydrogenase to yieldacetate and 2 NADH. Acetate is then transported into themitochondrion, where it is converted to acetyl-CoA andmetabolized by the citric acid cycle. When alcohol is consumed in excessive quantities, the resulting high levels ofNADH cause metabolic abnormalities, one of which is highlevels of fatty acid synthesis. Fatty acid synthesis, also acytoplasmic process, uses acetyl-CoA as a substrate andNADPH as a reducing agent. Determine how a high level ofcytoplasmic NADH provides a source of NADPH for fattyacid synthesis.
One consequence of ethanol addiction is fatty liver disease, an illness in which liver cells accumulate large amounts of triacylglycerols, the esters derived from glycerol and fatty acids. Ethanol is oxidized in the cytoplasm of liver cells by alcohol dehydrogenase and aldehyde dehydrogenase to yield acetate and 2 NADH. Acetate is then transported into the mitochondrion, where it is converted to acetyl-CoA and metabolized in the citric acid cycle. When alcohol is consumed in excessive quantities, the resulting high levels of NADH cause metabolic abnormalities, one of which is high levels of fatty acid synthesis. Fatty acid synthesis, also a cytoplasmic process, uses acetyl-CoA as a substrate and NADPH as a reducing agent. Speculate about how a high level of cytoplasmic NADH provides a source of NADPH for fatty acid synthesis.
The oxidation of glyceraldehyde 3-phosphate to 1,3-bisphosphoglycerate, catalyzed by glyceraldehyde 3- phosphate dehydrogenase, proceeds with an unfavorable equilibrium constant ( K'eq= 0.08; ΔG′° = 6.3 kJ/mol), yet the flow through this point in the glycolytic pathway proceeds smoothly. How does the cell overcome the unfavorable equilibrium?
Suppose a patient has correctly diagnosed GALT (galactose-1-phosphate uridylyltransferase) deficiency. Would this patient have lower steady state levels of NADPH in the presence of normal steady state glucose levels? Why is NADPH an important byproduct of the pentose phosphate pathway anyways?
What is the overall net reaction for the Pyruvate Dehydrogenase Complex? What enzyme(s) in the Citric Acid Cyclecatalyze(s) substrate-level phosphorylation? What enzyme(s) in the Citric Acid Cyclecatalyze(s) decarboxylation reactions? What enzyme(s) of the Citric Acid Cyclecatalyze(s) reactions in which NAD+or FAD is reduced to NADH or FADH2, respectively?
During Krebs cycle, the conversion of isocitrate to alpha-keto glutarate involves all of the following reactions/mechanisms except Reduction of isocitrate Reduction of NAD+ Decarboxylation of isocitrate Oxidation of isocitrate
The oxidation of glyceraldehyde 3-phosphate to 1,3-bisphosphoglycerate by glyceraldehyde 3-phosphate dehydrogenase has an unfavourable equilibrium constant (K'eq= 0.08; G′° = 6.3 kJ/mol), yet the flow at this point in the glycolytic pathway is smooth. How does the cell get out of the unfavourable equilibrium?
When the cells of our body are in dire need to synthesize Ribose 5 phosphate and it has already enough supply of NADPH, reverse non oxidative pathway of the HMP shunt pathway takes place. If the cell has 10 glucose 6 phosphate molecules, how many of these would be converted to Fructose 6 phosphate and how many to form glyceraldehyde 3 phosphate respectively to synthesize maximum number of Ribose 5 phosphate? 8:2 2:8 4:6 6:4
If α-ketoglutarate is removed from TCA cycle and used to make glutamate, how many of each of the cofactors (not intermediates) and high energy molecules in the TCA cycle are lost? How much ATP does this equate to (NADH = 2.5 ATP, FADH2 = 1.5 ATP)?
Briefly describe the biological rationale for each of the following allosteric phenomena: (a) activation of pyruvate carboxylase by acetyl-CoA; (b) activation of pyruvate dehydrogenase kinase by NADH; (c) inhibition of isocitrate dehydrogenase by NADH; (d) activation of isocitrate dehydrogenase by ADP; (e) inhibition of α-ketoglutarate dehydrogenase by succinyl-CoA; (f) activation of pyruvate dehydrogenase phosphatase by Ca2 +.
In the complete b-oxidation of stearic acid (18:0), a) how many moles of acetyl CoA are produced? b) how many times would the fatty acid pass through the fatty acid spiral for complete oxidation? c) what is the total ATP produced in the citric acid cycle? d) how many moles of NADH are produced? e) how many moles of FADH2 are produced? f) how many moles of ATP are produced after all NADH are reoxidized in the respiratory chain? g) how many moles of ATP are produced after all FADH2 are reoxidized in the respiratory chain? h) how many moles of ATP are produced from the complete oxidation of stearic acid?
In the complete b-oxidation of stearic acid (18:0), a)how many moles of acetyl CoA are produced? ________ b)how many times would the fatty acid pass through the fatty acid spiral for complete oxidation? ________ c)what is the total ATP produced in the citric acid cycle? ________ d)how many moles of NADH are produced? ________ e)how many moles of FADH2 are produced? ________ f)how many moles of ATP are produced after all NADH are reoxidized in the respiratory chain? ________ g)how many moles of ATP are produced after all FADH2 are…