Citric Acid Cycle and Oxidative Phosphorylation Flashcards
Reason why TCA won’t occur anaerobically
NADH and FADH2 will accummulate (ETC is off)
The ultimate fate of acetyl CoA in TCA
Oxidation to CO2
Hormone that controls TCA activity
None. It happens irrespective of the fed or fasting state.
Only TCA enzyme not found in the matrix of mitochondria
Succinate dehydrogenase (in the inner mitochondrial membrane)
Major control enzyme in TCA, inhibited by NADH and ATP (high energy availability states) and activated by ADP
Isocitrate dehydrogenase
TCA enzyme that requires thiamine-lipoic acid-CoA-FAD-NAD concoction like PDH
Alpha-ketoglutarate DH
Catalyzes the substrate-level phosphorylation in TCA
Succinyl CoA synthetase (“synthetase” are enzymes catalyzing reactions that involve ATPs/GTPs, vs mere “synthases”)
TCA enzyme that also functions in ETC
Succinyl DH, moonlights in ETC as “Complex II”
Exit point in the TCA cycle for Fatty Acid Synthesis
Citrate via Citrate Shuttle
Exit point in the TCA cycle for Heme Synthesis
Succinyl CoA
Exit point in the TCA cycle for Gluconeogenesis
Malate via Malate Shuttle
Entry point in the TCA cycle for Urea cycle
Fumarate
Shuttle(s) of NADH to ETC (transport from cytoplasm to mitochondria)
Malate shuttle (3 ATP) and Glycerol phosphate shuttle (2 ATP)
Shuttle(s) of FADH to ETC (transport from cytoplasm to mitochondria)
Glycerol phosphate shuttle (2 ATP)
Final electron acceptor in the ETC
Oxygen
Enzyme in Complex I of ETC
NADH Dehydrogenase
Complex II of ETC
Coenzyme Q (a lipid)
Complex III of ETC
Cytochrome b/c1 (an Fe/heme protein)
Complex IV of ETC
Cytochrome a/a3 (a Cu/heme protein); Cytochrome oxidase is the enzyme involved
Inhibitors of Complex I
Barbiturates, rotenone (Complex I has an enzyme, it is “inhibitable”)
Inhibitors of Complex III (cyt b/c1)
Antimycin
Inhibitors of Complex II (CoQ)
Doxorubicin
Inhibitors of Complex IV
Cyanide, CO (Complex IV has an enzyme, it is “inhibitable”)
Inhibitor of the F0F1 complex
Oligomycin (F1 has an enzyme, ATP synthase; it is “inhibitable”)
Myocardial-specific creatine kinase
CK-MB (other markers that can be used: Trop I, Trop T, LDH)
Headache, nausea, tachycardia, tachypnea, lips and cheeks turn a cherry-red color are caused by this ETC inhibitor
Carbon monoxide poisoning
Term used for substances that decrease the proton gradient, which causes decreased ATP synthesis, increased oxygen consumption, and increased oxidation of NADH
Uncouplers, causing increase in rate of ETC without ATP synthesis, energy is released as heat (eg. 2,4-Dinitrophenol, high-dose aspirin and salicylates, thermogenin)
Thermogenin is commonly known as _____, which protects newborns from hypothermia
“Brown fat”.
Superoxide, hydrogen peroxide, and hydroxyl radical are collectively known as
Reactive oxygen species (produced by PMNs to kill bacteria by oxidative burst; also increased in reperfusion injury)
MELAS
Mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes
Leber hereditary optic neuropathy, MELAS, Ragged red muscle fiber disease are examples of
Mitochondrial DNA diseases (mutations)
Rate of oxidative phosphorylation is dependent on
Availability of ADP (accummulation of ADP signals need for ATP synthesis; ADP also allosterically activates the rate controlling enzyme in TCA)
Location of TCA
Mitochondria
Inhibitor of the rate controlling enzyme of TCA
NADH inhibits isocitrate DH
Location of ETC and Oxidative Phosphorylation
Mitochondrial inner membrane (Cell membrane in prokaryotes)
Shuttle required for cholesterol and fatty acid synthesis in hepatocytes
Citrate shuttle
Shuttle required for the hepatic conversion of pyruvate to glucose
Malate-aspartate shuttle
High doses of nitroprusside inhibits what metabolic pathway
ETC. Cyt a/a3 (Complex IV) is inhibited by nitric oxide, plus metabolism of nitroprusside yields small quantities of cyanide
Intracellular increases in AMP would increase activation in what enzyme
PFK-1
