3.6-ALCOHOL!!! Flashcards
Since the two main reactions involving alcohol use dehydrogenase’s…WHAT by product are we making a lot of?
NADH!! We are taking H’s off things, and filling up all of our taxi cabs! It explains all of the problems w/ EtOH consumption.
What is the general legal limit for DUI?
80mg/dL or .08g/dL
What two features allow EtOH to be absorbed EVERYWHERE in the body? What is its method of absorption?
Polar AND hydrophobic. Best of both worlds!…. Diffusion
Where is 80% of EtOH absorbed? What about the other 20%? Where is it mostly OXIDIZED (dehydrogenated!)
80% in s.i. and 20% in liver…Mostly oxidized in the Liver (some in stomach and si)
About how much EtOH goes unabsorbed and expelled through sweat, urine, feces, breath, saliva, and milk?
10%
What is the product of the first reaction of EtOH oxidation? REGARDLESS of route taken..(there are 4 routes)
Acetaldehyde=freaking toxic
Which EtOH oxidation pathway begins in the cytosol and is for naive drinkers?
Alcohol Dehydrogenase
Which EtOH oxidation pathway is inducible (for habitual drinkers) and occurs in the Smooth ER? What is the main enzyme in this system? (Dr.T would be upset if I get this wrong)
the Cytochrome P450 system MEOS (microsomal-EtOH-Oxidating-System)…. Main enzyme: Cytochrome-Y-2-E-1
What is the major EtOH oxidation rxn in the Brain/CNS happening in peroxisomes?
Catalase Dependent Oxidation
What is “first pass” EtOH oxidation? (its the same rxn as ADH, this is unique c/o location)
Gastric Oxidiation
What is the easiest enzyme to become saturated? Where is the enzyme housed? What is the hardest?
Alcohol Dehydrogenase in the mitochondria….vs MEOS a 1000x difference!!
What is the second reaction of EtOH oxidation? What is the enzyme?
Acetaldehyde–>Acetate using Acetaldehyde Dehydrogenase 2
What are the two ways the end product of Acetakdehyde dehydrogenase can be used?
Acetate can then be used to build stuff (acetate—>acetyl-CoA—>fat) or used for energy 30kJ/g
What are the three NEGATIVE outcomes of EtOH metabolism?
1.Acetaldehyde is an adduct (clingy and disruptive) 2. Increases ROS (reactive oxygen species) 3. Fills up all the taxi cabs (high NADH/NAD+ ratio)
What might be the leading cause for the almighty HANGOVER?
the build up of Acetaldehyde (very close to formaldehyde=toxic!!)
WHERE is the second step (acetaldehyde dehydrogenase) occurring?
In the mitochondria (weird, more breaking down in mitochondria)
What are the two main structural features of Alcohol Dehydrogenase?
Its a DIMER and it has ZINC in it!
What is the general name for the different classes of ADH? What is the main class of these?
Isozymes=iso enzymes…Class I most important
Rank the effectiveness of the ALDH2s: 1/1, 1/2, & 2/2 (converting acetaldehyde to acetate)
1/1 > 1/2 > 2/2.. I’d definitely a 2/2
What is the ONE main reason for ALL the negative effects of Alcohol in the body? Hyperlactacidemia, hyperuricemia, hypoglycemia, ketosis, hyperlipemia, fatty liver, adducts, abnormal protein trafficking….
DECREASED NAD+/NADH ratio
Why in the world would alcohol cause hypoglycemia?!
GNG gets suppressed because excess NADH goes towards making more MALATE and LACTATE instead of glucose
What does EtOH do to ADH to cause dehydration?
EtOH inhibits AntiDiureticHormone, so you pee out more becoming dehydrated!
What is the build up of lactate called coupled with dehydration?
Lactic Acidemia
What is the result of a build up of acetyl-CoA when glycogen stores are depleted and GNG is suppressed?
Ketonemia!
