Metabolism of Ethanol
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| Metabolism of alcohol inthe liver produces | Acetate
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| Ethanol + NAD --> Acetaldehyde + NADH | Alcohol dehydrogenase (ADH)
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| Acetaldehyde + NAD --> Acetate + NADH | Acetaldehyde dehydrogenase (ALDH)
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| Ethanol metabolism occurs mainly in the | Liver
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| Ethanol metabolism oxidizes ethanol to | Acetate
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| Ethanol metabolism reduces NAD+ to | NADH
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| What is the intermediate occuring in ethanol metabolism | Acetaldehyde
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| Two process for convertin gethanol to acetaldehyde exist | Alcohol dehydrogenase (ADH) or the MEOS system
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| With the MEOS system what is not produced | NADH
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| In the case of moderate ethanol consumption, what catalyzes the conversion of ethanol --> acetaldehyde | Alcohol dehydrogenase (ADH)
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| With higher/chronic levels of ethanol consumption, what catabolizes an increasing percentage of the ethanol --> acetaldehyde | Microsomal Ethanol Oxidizing System (MEOS)
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| Where does teh MEOS system occur | On the endoplasmic reticulum
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| What enyzmes is used in the MEOS system | Cytochrom P450 enzyme CYP2E1
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| What is the cytochrome P450 enzyme which oxidizes ethanol to acetaldehyed in the MEOS process | CYP2E1
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| What besides ethonal is oxidized in the MEOS system | NADPH
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| What is used as the ultimate oxidzing agent by cytochrome P450 enzymes | Molecular O2
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| Does CYP2E1 have a higher or lower Km for ethanol than does hepatic ADH | Higher
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| What does ethanol do to other P450 systems | Inibits them
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| The acetate produced from ethanol is activated to | Acetyl CoA
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| Acetyl CoA from Acetate from Ethanol can be used for | TCA cycle, Fatty acid synthesis, Cholesterol biosynthesis, Ketone body synthesis
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| The NADH from ethanol metabolism may be reoxidized via hepatic | Oxidative Phosphorylation or Dehydrogenase Reactions
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| Acetate from ethanol metabolism can be exported from teh liver to extrahepatic cells where it is | Activated to acetyl CoA and catabolized via the TCA cycle in these cells
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| What are three big users of acetate | Skeletal muscle, Heart, and Kidney
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| The ability to metabolize ethanol varies widely from person to person due to the occurrence of | Polymorphism inthe enzymes of ethanol metabolism
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| How many isoenzymes of alcohol dehydrogenase are specific for ethanol | Three of five
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| What isoenzymes of ADH are most specific for ethanol and occur in the liver | ADH 1 and ADH 2
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| Which as the higher Km ADH 1 or ADH 2 | ADH 2
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| Which ADH isoenzyme occurs in the upper GI tract | ADH 4
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| How many isoenzymes of acetaldehyde dehydtrogenas are there | Two, ALDH 1 and ALDH 22
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| Where do the isoenzymes of ALDH occur | Liver
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| Which ALDH isoenzyme is mitochondrial | ALDH 2
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| Which ALDH isoenyzme is cystosolic | ALDH 1
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| What is the major ALDH isoenzyme | ALDH 2
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| Which ALDH isoenzymes has the higher Km | ALDH 1
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| The commone genetic variant of this ALDH isoenzyme has relatively low activity that causes toxic levels of acetaldehyde to accumulate leading to nausea, vomiting, and avoidance of ethanol (homozygotes) | ALDH 2
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| Increased ethanol ingestin results in the induction of the genes for | ADH and ALDH
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| The genes for CYP2E1 are induced in response to | Increased ethanol levels
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| Degradation of CYP2E1 is inhibited by | High ethanol levels
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| NADH levels from high/chronic ethanol ingesting and catabolism may exceed the liver's ability to reoxidize NADH via | Oxidative phosphorylation
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| ADH and ALDH are not regulated b y | NADH/NAD or ATP/ADP-AMP levels
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| The amount of ethanol catabolizm occuring depends on the amount of | Ethanol present
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| Excessive high hepatic NADH levels... TCA Cycle activity | Decreases
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| Isocitrate dehydrogenase is ... by NADH | Allosterically inhibited
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| Excessive high hepatic NADH levels... Beta oxidation | Decreases
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| Excessive high hepatic NADH levels... Glycolysis | Decreases
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| Excessive high hepatic NADH levels... Glycerol-3-phosphate production | Increases
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| Excessive high hepatic NADH levels...Lactate production from pyruvate | Increses
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| Excessive high hepatic NADH levels...Malate prduction from oxaloacetate | Increases
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| A fatty liver may develop because of increased triglyceride synthesis due to | Increased glycerol-3-phosphate syntehsis and decreased beta oxidation
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| Liver damage due to excess acetaldehyde leades to decreased | Protein synthesis, Lipoprotein synthesis, Liporotein export
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| Ketoacidosis may occur with highchronic ethanol ingesting because of | Decreased TCA cycle, Excess Acetyl CoA, Increased ketone body production, Decrease ketone body utilization
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| There is decreased ketone body utilization in high/chronic ethanol ingesting because | The heart and kidney prefer to catabolize acetate over ketone bodies
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| Lactic acidosis may occur with high/chronic ethanol ingestion because | High NADH levels increase lactate prduction from pyruvate
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| At high levels of lactate the liver imports and uses ... amounts of lactate | Decreased
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| Lactate competes with uric acid for excretion by the kidney resulting in | Gout
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| Hypoglycemia in a fast may occur with high/chronic ethanol ingestion because ... hepatic lactate uptake occurs | Decreased
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| A decrease in lactate uptake by the liver cause pyruvate from transamination of alanine to be converted to ... instead of ... | Lactate, Glucose
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| Dihydroxyacetone phosphate is converted to | Glycerol=3-phosphate
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| Hyperglycemia may occur with hihg-chonric ethanol ingetion in a | Fed state
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| Acetaldehyde binds to | Amino acids
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| Acetaldehyde causes ... protein syntehsis | Decreased
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| Lipoprotien syntehsis is decreased due to lack of necessary | Apoproteins
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| Acetaldehyde binds to glutathione decreasing its | Antioxidant activity
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| Increased CYP2E1 activity in the MEOS system ... free radical formation | Increases
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| To correct for hepatic damage the liver attempts wound healing and connetive tissue syntehsis is | Increased
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| What connective tissue is especially used in hepatic repair | Collagen
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