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WVSOM -- Biochem
WVSOM ETOH metabolism
| Question | Answer |
|---|---|
| Carbons from EtOH catabolism are further catabolized by? | citrate synthase |
| What enzyme helps ethanol go to acetaldehyde? | Alcohol dehydrogenase or MEOS system |
| What is produced when ethanol is broken down to acetaldehyde? | NADH + H+ |
| What is the enzyme responsible for taking acetaldehyde to acetate? | acetaldehyde dehydrogenase (ALDH) |
| What is produced in the reaction from acetaldehyde to acetate? | NADH + H+ |
| Where does ethanol metabolism take place? | liver |
| What is the intermediate product in the conversion of EtOH to acetate? | acetaldehyde |
| Is acetaldehyde toxic? | yes |
| Moderate ethanol consumption uses which enzyme? | ADH |
| What is used to catabolize EtOH in higher and chronic levels of consumption? | microsomal ethanol oxidizing system (MEOS) |
| Where does MEOS take place? | endoplasmic reticulum |
| What enzyme is used to oxidize EtOH to acetaldehyde in the MEOS process? | CYP2E1 (cytochrome P450) |
| What is oxidized besides EtOH in MEOS? | NADPH |
| What is the ultimate oxidizing agent in MEOS? | molecular O2 |
| What is O2 reduced to in MEOS? | H2O |
| What has a higher Km? CYP2E1 or ADH? | CYP2E1 |
| How is NADH reoxidized in the liver? | oxidative phosphorylation and dehydrogenase reactions |
| What will abnormally high amounts of NADH due in chronic ethanol consumption? May cause hepatic dehydrogenase reactions to occur in the reverse direction and has a negative impact on hepatic metabolism | |
| Acetaldehyde in the bloodstream is a _______________. | pathological occurance |
| Where is acetate used extrahepatically? | heart, kidney and skeletal muscle |
| Why do people have different alcohol metabolism? | There are 5 different classes of isoenzymes of Alcohol Dehydrogenase so the rates vary person to person |
| Which isoenzymes are most specific for metabolism in the liver? | ADH1 and ADH2 |
| Which has the higher Km, ADH1 or ADH2? | ADH2 |
| Which isoenzyme works in the intestines? | ADH4 |
| How many isoenzymes are present for ALDH? | 2 |
| Where is ALDH2? | mitochondria |
| Where is ALDH1? | cytosol |
| Which has the higher Km? ALDH1 or ALDH2? | ALDH1 |
| What does the genetic variant of ALDH2 do? | has low activity so that toxic levels of acetaldehyde accumulate |
| What causes genes to produce more ADH and ALDH? | ethanol ingestion |
| High levels of NADH would decrease the activity of? | TCA cycle glycolysis and β oxidation |
| What is the cause of excessive EtOH consumption? | high hepatic NADH |
| What happens with too much hepatic NADH? | will exceed the liver’s ability to oxidize NADH |
| How does the body determine how much EtOH is catabalized? | amount of ethanol present |
| High NADH levels would increase the activity of an NADH/NAD+ using dehydrogenase in the direction of? | NADH oxidation/substrate reduction |
| Abnormally high NADH increases? | glycerol 3-p synthesis, pyruvate -> lactate, and oxaloacetate -> malate |
| How does increased EtOH decrease TCA? | inhibits isocitrate dehydrogenase. |
| How does increased EtOH decrease β-oxidation? | Decreased NAD+ substrate / increased NADH product slows this process. |
| How does EtOH decrease glycolysis? | glyceraldehyde 3-P is inhibited due to decreased availability of its NAD+ substrate |
| How does high hepatic NADH levels increase glycerol 3-P production? By glycerol-3P dehydrogenase from the glycolytic pathway intermediate Dihydroxyacetone phosphate | |
| What causes A fatty liver from? | TG and glycerol 3-P increases with a decrease in lipoprotein production resulting in excess fat in the liver |
| Liver damage from excess acetelaldyhyde results in? | decreaed protein synthesis, lipoprotein synthesis and lipoprotein export |
| Why does ketoacidosis occur in chronic EtOH ingestion? | abnormally high NADH decreases TCA cycle and acetyl CoA levels rise due to acetyl CoA entering the TCA cycle being decreased. This results in an increased ketone body production |
| Why is there decreased ketone body utilization occurring? | kidney and heart preferably catabolize acetate rather than ketone bodies. |
| Why does lactic acidosis occur with chronic EtOH? | high NADH levels increase lactate production and decreases its conversion to pyruvate so there is a build up |
| What disease results from lactic acidosis? | gout |
| Why does gout occur with lactate acidosis? | lactate competes with uric acids for excretion |
| Why does hypoglycemia occur with chronic ETOH consumption? | decreased hepatic lactate uptake occurs and pyruvate from tansamination of alanine is converted to lactate instead of glucose to hypoglycemia occurs. BOTTOM LINE – NOT ENOUGH GLUCONEOGENESIS |
| The presence of glutathione ___ free radical levels? | decreases |
| What happens with abnormally high acetealdehyde levels? | binds to glutathione |
| What pathological event occurs with binding of acetealdehyde to glutathione? | increase in free radicals |
| MEOS and CYP21E result in _______ levels of free radicals. | increased |
| What results from acetyladelhyde binding to amino acids? | decreased protein production |
| What happens when the liver tries to heal itself? | fibrosis and thereby cirrosis |
Created by:
tjamrose