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60 Cards in this Set

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pyruvate has three complexes what are its complexes?
• αKG dehydrogense
• Branched chain dehydrogense
• PDH complex
pyruvate has three complexes what are its cofactors?
TPP
lipoic acid
coenzyme A
NAD
FAD
TPP: what does it do? vitamin?
decarboxylation
vitamin B1 (thiamine)
Iipoic acid: vitamin, function
Accepts Acetyl group
lipoic acid (B4)
function of Coenzyme A? vitamin?
Final acceptor =>AcCoA
Panthenoic acid (B5)
NAD: what does it oxidize? end product? vitamin?
oxidizes FADH2 => NADH
Niacin (B3)
FAD: what does it oxidizes? what is the end product?
oxidizes Lipoic Acid => FADH2 Riboflavin(B2)
5 fates of pyruvate
1) Lactate
2) Alanine
3) Acetate
4) OAA
5) Acetyl CoA
Lactate: aerobic/anaerobic? what does it use? NADH =>?
• Anaerobic
• Uses LDH
• NADH => NAD+
Alanine: aerobic/anaerobic, when is it formed?, what transaminase does it use?, when is it increased?
• Anaerobic, formed due protection from overproduction of lactic-acid
• Uses ALT
• increases during exercise leaks"into-blood
Acetate: ethanol=>?, NAD+=>, enzyme
Ethanol => Acetaldehyde
NAD+=>NADH
Alcohol dehydrogenase
Acetaldehyde⇨Acetate: NAD+, enzyme, what drug block this enzyme and what does it lead to?
• NAD+⇨-NAD
Acetaldehyde dehydrogenase
• Disulfuam and Metronidazole inhibit this enzyme⇨ Acetaldehyde⇨N /V
Macrosteatosis: (4), how do alcoholics get heart failure?
• large fat droplets
• Atherosclerosis
• High Ketone
• Acetone smell
• Acidosis⇨GABA connection⇨heartfailure
Microsteatosis:
• Reye's syndrome
• Acetaminophen
• Pregnancy
Alcoholics pathogenesis of fatty liver
• High NADH; body thinks you're in a high energy state
• Inhibits gluconeogenesis, causing hypoglycemia
• Then use fat, leading to hyperlipidemia/fatty liver
Alcoholics: tx
• Tx: thiamine +Glucose (to prevent lactic acidosis)
• Thiamine deficient alcoholics: have even less AcCoA ⇨ more lactic acid
OAA: enzyme, cofactor, describe
• Anapleuritic
• Pyruvate Carboxylase
• Cofactor: Biotin
Acetyl CoA: when does it work, function, uses what enzyme and NAD =>
• If 02 is present
• removes CO2
• Uses Pyruvate Dehydrogenase
• NAD+ ~ NADH
Pyruvate Dehydrogenase:
structure, # of proteins,steps and cofactors
• Quaternary
• Three proteins
• Five steps
• Five cofactors
• Five vitamins
Pyruvate Dehydrogenase:
• Allosteric Activator:
• Allosteric Inhibitor:
• Rate limiting enzyme for
• rxn
• Allosteric Activator: pyruvate
• Allosteric Inhibitor: Acetyl CoA
• Rate limiting enzyme for Krebs cycle
• NAD+ ~ NADH
4 fates of acetyl CoA
FA
ketones
cholesterol
kreb cycle
Acetyl CoA ⇨ FA
acetyl CoA decarboxylate
Acetyl CoA ⇨ ketones
HMG coA synthase
Acetyl CoA ⇨ cholesterol
HMG CoA reductase
Acetyl CoA ⇨ kreb cycle
isocitrate dehydrogenase
Kreb Cycle Components:
"Cindy Is Kinky, So She Forniates More Often"
• Isocitrate
• αKG
• Succinyl CoA
• Succinate
• Fumarate
• Malonate
• OAA
Isocitrate
inhibits what enzyme
inhibits PFK-1
αKG
rxn involved in
transamination
Succinyl CoA
make what and how
-uses odd-chain FA, makes ringed structures (Ex: heme)
AcetylCoA:
what pathway it uses it?
FA synthesis; ketogenesis
Isocitrate Dehydrogenase
rate limiting enzyme
Succinate Dehydrogenase: location, another name and energy it makes
attached to mitochondria wall, ETC II (FADH2)
TCA Substrates: Pyruvate
Gly, Ala, Ser "Elastase victims"
TCA Substrates: Acetyl-CoA
Lys, Leu, "Bulkies" (Phe,Tyr, Trp)
TCA Substrates: OAA
Asp, Asn
αKG
glu and gln
fumarate
Phe and tyr
OAA + AcCoA ⇨ Citrate:
citrate synthase
Citrate ⇨ Isocitrate: enzyme, function of citrate, what is the citrate shuttle?
• Uses aconitase
• Citrate: Allosteric Inhibitor of PFK. Allosteric activator for FA synthesis
• Citrate shuttle: feeds acetyl CoA into fatty acid-synthesis
αKetoglutarate ⇨Succinyl-CoA: enzyme, what does it release? NAD+ =>
• Uses αKetoglutarate Dehydrogenase
• Releases C02
• NAD+⇨NADH
Isocitrate ⇨ α-Ketoglutarate: enzyme, what does it do? and reaction
• Uses isocitrate Dehydrogenase
• Regulatory step
• Releases CO2
• NAD+⇨NADH
αKetoglutarate
is the intermediate for all transaminase reactions
α-Ketoglutarate + Ala ⇨ glu + pyr
what builds up in concentration during periods of high transamination
glutamate, Aspartate, Alanine
what happens during amino acid breakdown?
Glutamate is still increasing, holding area for amine groups until shunted into Urea cycle.
what transaminase in the most important?
20 transaminases, one for each amino acid; AST/ALT most important
All transaminases uses what vitamin as a cofactor? presentation if there is a deficiency?
Vit B6 as a cofactor. if there is a deficiency, it causes neuropathy
Succinyl-CoA ⇨ Succinate: enzyme, function
• Uses succinyl CoA Synthetase
• Split sulphur bond to make GTP
Succinyl CoA is responsible for: (6)
1. Heme synthesis
2. Porphyrin ring substrate
3. Odd chained fatty acids feed into Succinyl-CoA.
4. Odd numbered fats break down into Propionic acid
5. Propionic CoA carboxylated becomes Methylmalonic acid CoA, which is then mutated to succinyl-CoA via Methylmanonyl mutase
(vit B12 factor) .
Succinate ⇨ Fumarate: enzyme, what does it form?
• Succinate Dehydrogenase is the only Kreb Cycle enzyme firmly anchored to the inner mitochondial membrane; attached to Complex II
• Forms FADH2
Fumarate ⇨ Malate: enzyme, what is added?
• Uses Fumarase
• Adds H20
Malate ⇨ OAA: enzyme, rxn
• Uses malate dehydrogenase
• NAD+⇨NADH
ATP count:
Glycolysis:
Kreb:
G-3P shuttle:
Malate-Asp shuttle
Glycolysis: 8 ATP "8 hrs = 1 work-day"
Kreb: 24ATP "24 hrs = 1 day"
G-3P shuttle: 4 ATP
Malate-Asp shuttle 6 ATP
Malate-Asp shuttle: where do products end up? when is it used?
Product ends up in cytosol, This shuttle is dominant since the G3P shuttle-is wastefull
G-3P shuttle: when is it used?
Used a great need of energy is needed; i.e. the need supercedes the waste
• Rapid Growth: Ages 0-2,4-7; puberty
• Rapid Division: pregnancy, cancer, burns, crush injuries
OAA => Aspartate: enzyme, what is added, how does the cycle work?
AST- aspartate Transaminase
Add NH3
Asp travels out to cytoplasm and gets converted back to OAA by AST
OAA => Malate: rxn, how does the cycle go? energy wasted?
• NADH => NAD+
• Malate travels back into mitochondria; converts to OAA; regains NADH
• No energy wasted
Viral Hepatitis:
Virus destroys cell membrane => 1 AST, 1 ALT leak out
Alcoholic Hepatitis:
Alcohol dissolves all membranes => 1 ALT, 2 AST leak out
Glycerol 3-Phosphate Shuttle:
DHAP => G-3-P:
glycerol 3 dehydrogenase
NAD=>NADH+
G-3-P => DHAP: what is formed? ATP lost? why is it 36-38 ATP made?
• FADH is formed
• 2 Atp is lost due to running the cycle twice.
• The reason for 36-38 ATPs per mole glucose in textbooks depends on which shuttle is used