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