Flashcards in oxidative phosphorylation poisons, gluconeogenesis stuff, HMP shuttle Deck (17):
What poisons inhibit electron transport? Mechanism?
rotenone, antamycin A, cyanide, CO. decr. the proton gradient, block ATP synthesis
What poisons are ATP synthase inhibitors?
oligomycin. inhibits mitochondral ATP synthase. incr. the proton gradient, but no ATP b/c electron transport stops
What are uncoupling agents for oxidative phosphorylation?
2,4 dinitrophenol (used illicitly for weight loss; aka 2,4 DNP), aspirin (fevers often occur after aspirin overdose), thermogenin in brown fat.
increases the permeability of the membrane, causing decr. proton gradiant and incr. O2 consumption. ATP synthesis stops, but electron transport continues: produces heat
Irreversible enzymes of gluconeogenesis
pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose-1,6-bisphosphatase, glucose-6-phosphatase
What is the Cori cycle?
this is one way that skeletal muscle can get more glucose during exercise. skeletal muscle uses glycolysis to make pyruvate and is forced to anaerobic pathways to produce lactic acid. lactic acid travels through bloodstream to liver, where it is a substrate for gluconeogenesis (lactate by lactate dehydrogenase to pyruvate to glucose). glucose goes to muscle
pyruvate carboxylase: location, function, requirements, regulatory agents
in mitochondria. converts pyruvate to oxaloacetate. first step of gluconeogenesis (pypass for the irreversible pyruvate kinase rxn of glycolysis). requries biotin (B7) and ATP. activated by acetyl CoA
phosphoenolpyruvate carboxykinase. location, requirements
in cytosol (malate shuttle). oxaloacetate is converted to phosphoenolpyruvate. requries GTP
Fructose-1,6-Bisphosphatase: location, regulatory agents
in cytosol. fructose 1,6-BP to fructose-6-P. cirtate increases it (citrate buildup might suggest slowed TCA), fructose 2,6 bisphosphate decreases it.
Where does gluconeogenesis occur (organ)? Why? What happens if you are missing enzymes? What are fato sources for gluconeogenesis?
occurs primarily in liver; 10% in kidney. can't occur in skeletal muscle because skeletal muscle has no glucose-6-phosphatase. enzyme deficiencies cause hypoglycemia. sources include odd-chain fatty acids, which can enter TCA as succinyl CoA (even chain fatty acids can't be sources).
What is the HMP shunt? Purpose? Where in the cell does it occur? Phase?
provides a source of NADPH from abundantly available glucose-6-P (used for glutathione reduction inside RBCs, fatty acid and cholesterol biosynthesis). Fructose 6-P is at the end of the shunt. also yields ribose for nucleotide synthesis and glycolytic intermediates.
2 phases (oxidative and non-oxidative, both of which occur in the cytoplasm). no ATP used or produced.
(if confused, remember that I don't know the normal enzyme that brings glucose-6-P to fructose-6-P in glycolysis)
Oxidative HMP shunt: reversible? rate-limiting? enzymes? products? requirements? regulation?
irreversible. it is rate limiting. uses glucose-6-P dehydrogenase. inhibited by NADPH (makes sense- the whole point of the shuttle is to make NADPH). products: CO2, 2NADPH, ribulose-5-P1.
Nonoxidative HMO shunt: reversible? rate limiting? enzymes? products? requirements? regulation?
reversible. not rate-limiting. uses phosphopentose isomerase, transketolases. REQUIRES B1. reactants: ribulose-5-P1.
Products: ribose-5-P1, G3P, and fructose-6-phosphate.
no real regulation
How does lactoferrin function in the immune system?
found in secretory fluids and neutrophils. inhibits microbial growth via iron chelation.
Why is glucose-6-phosphate dehydrogenase deficiency a problem? Manifestations?
glucose-6-dehydrogenase is important for the oxidative, rate limiting step of the HMP shuttle. It helps produce NADPH. NADPH is needed to keep glutathione reduced. Reduced glutathione detoxifies free radicals and peroxides. Decr. NADPH in RBCs leads to hemolytic anemia from poor RBC defense against oxidizing agents. Infection also precipitates hemolysis.
Triggers for G-6-PD problems?
infections, and oxidizing agents like sulfonamides, primaquine (for malaria), anti-TB drugs, fava beans.
Findings in G6PD deficiency
Henize bodies: oxidized hemoglobin preciptiated within RBCs
Bite cells: phagocytic removal of Heinz bodies by splenic macrophages.