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25 Cards in this Set
- Front
- Back
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-why is dark meat dark?
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dark meat is rich in (slow twitch) muscle and uses (fatty acids) as fuel. breaks down FA through oxphos. has lots of mitochondria, which have lots of iron in it because of the iron sulfur centers. There is also iron present in heme
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-which proteins in the ETC contain heme?
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complex III, cyto C, complex IV
**Unlike hemoglobin where goal is to keep iron in fe2+ state, constant transition to switch from fe3+ --> fe2+ |
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T/F: uncoupling oxidative phosphorylation blocks respiration
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false: things that uncouple oxphos – does NOT block respiration (does not block flow of e-) .. Blocks PRODUCTIVE USE of PROTON GRADIENT
BUT uncoupling can have physiological purposes as well (ie. brown fat) |
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protein ionophores
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- a lot of poisons are protein ionophores -- wrap around proton, allow it to pass through membrane, gradient collapse and lose all nrg to heat
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what is brown fat good at?
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heat generation!
uncoupling protein allows proton to return to mitosol w/o creating ATP uncoupling of oxidative phosphorylation |
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[] blood glucose?
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5 mMol always, no matter well fed, fasting, starving. controlled by liver
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NAD+ is derived from
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Niacin
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FMN is derived from
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Riboflavin
FMN: triple ring structure that accepts e- Covalently attached to amino acid of a particular protein Different version of FMN = flavin adenine dinucleotide just as we saw w/ NAD, have adenine nucloetide covalently attached FMN covalently attached to protein. FAD is nucleotide cofactor, not covalently bound, but usually tightly bound and has same function. FMN present in COMPLEX I !!! |
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FAD is derived from
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Riboflavin
FMN: triple ring structure that accepts e- Covalently attached to amino acid of a particular protein Different version of FMN = flavin adenine dinucleotide just as we saw w/ NAD, have adenine nucloetide covalently attached FMN covalently attached to protein. FAD is nucleotide cofactor, not covalently bound, but usually tightly bound and has same function. FMN present in COMPLEX I !!! |
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Two ways that e- can flow through the ETC?
What delivers the electrons to each? Protons pumped out from each? ATP yield from each? |
1.
I --> Q --> III --> Cyto C --> IV --> O2 Electrons via NADH 10 protons pumped out (4 from 1, 4 from 3, 2 from 4) 2.5 ATP/NADH *complete oxidation of glucose yields 30 or 32 molecules of ATP (4 protons required to make 1 atp) 2. II --> Q --> III --> Cyto C --> IV --> O2 Electrons via Succinate 6 protons pumped out (4 from 3, 2 from 4) 1.5 ATP/Succcinate *complete oxidation of glucose yields 30 or 32 molecules of ATP (4 protons required to make 1 atp) |
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Flow of e- through complex I?
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2e- --> FMN --> Fe-S --> Q
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Q
-Structure -Aka? |
Q aka ubiquinone --> structure: benzoquinone with isopreniod side chain. side chain is very hydrophobic and allows it to be soluble in intermembrane of mitochondria
mechanism of e- carrying not important, just note that ring structure is important in acceptance of e- and transfer to next species in complex |
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Iron-Sulfur Centers
oxidation state of iron? |
-Present in complex I
-E- transferred from NADH --> FMN --> iron sulfur centers --> Q - irons are chelated from sulfurs from cysteine or elemental sulfur -iron can be in fe3+ state (acceptor for e-) or fe2+ state fe3+ --reduced--> fe2+ -Iron responsible for making dark meat dark |
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F0F1 ATPase
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F0f1 atpase (F0 in the membrane, F1 outside)
not only atpase, atp synthase identical to similar kinds of structures you can find in other tissues and other organelles in other locations, uses nrg of hydrolysis of atp to derive nrg that does work that helps to pump protons from inside to outside (or one side of membrane to other) to generate proton gradient atp synthase in mitochondrial membrane is identical but works in reverse. In intermembrane side proton gradient is present, that is dispersed as proton reenters the mitosol. if you collapse proton gradient (eg. asphyxiation) get atp synthase working WRONG WAY in mito matrix.. Can start hydrolzying atp WE DONT DO THIS because of the IF1 inhibitor If you have ischemia (no O2), proton gradient collapses s low atp demand of atp by other sources glycolysis working anerobically --> that produces pyruvate as end product (- charge) .. Can also make lactic acid (also -) create – charged molecules and LOWER pH in cytosol (bc glycolysis occurs in cytosol) what does that mean for the mito matrix? Have high H+ concentration, H+ goes back into matrix in exchange for stuff like POTASSIUM which provides a + charge to NEUTRALIZE – CHARGE ON PYRUVATE. ACID pH IN CYTOSOL GET LOW pH IN MITOSOL AS WELL. pH low on cytosol eventually communicated in mitosol as well bc you have eflux of metal ions from mitosol to cytosol to make adjustment in pH reduction in pH an inhibitor of F1 called IF1 gets activated – ACTIVATED AT LOW pH, binds to f1, shuts down ATPase!!!! This is why even though thermodynamically H+ should be pumped back into intermembrane space in ischemic conditions, this will NOT OCCUR. |
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What provides most of the ATP produced in aerobic cells?
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Ox Phos provides most of the ATP produced in aerobic cells.
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Hydrolysis of ATP by ATP synthase during ischemia is prevented by ?
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the IF1 inhibitor
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The rate of respiration and oxidative phosphorylation are generally limited by ?
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the level of ADP
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Complete oxidation of glucose to carbon dioxide and water yields ?
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30 or 32 molecules of ATP.
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Transport of ATP, ADP, and Pi?
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Making atp inside mito matrix, must be mechanism to transport it out to the cytosol. Really concerned with getting it across inner membrane – have transporter can easily cross outer membrane
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Heat generation in brown fat is an example of?
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UNCOUPLING OF OXIDATIVE PHOSPHORYLATION
Type of adipose tissue – brown fat especially rich in MITOCHONDIRA, this is what makes them brown (the iron in the mito) brown fat is good at HEAT GENERATION because it has protein – the UNCOUPLING PROTEIN – it’s a PROTON CHANNEL so you create proton gradient, have high gradient on intermembrane side, as proton returns into mitosol, energy is released in form of heat RATHER than used to do work to generate ATP when we do that, call this UNCOUPLING OF OXIDATIVE PHOSPHORYLATION because production of proton gradient through respiration is UNCOUBLED from the process of ATP production also a lot of poisons that are PROTON IONOPHORES – wrap around proton, allow to pass through membrane, proton gradient collapses and lose all their energy to HEAT, prevents ATP production |
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How does cyanide poisoning work?
How can you treat it? Why does that treatment work? |
-Cyanide inhbits the cytochrome oxidase step (cyto c --> iv)
-it binds Fe3+ in the heme of the cytochrome a,a3 component (tissue asphyxia) CYANIDE POISONING -inhibits cytochrome oxidase step - receives e- from cyto c and transfers them to oxygen to produce water. -Complex 4 has heme in its structure as well as a,a3 -cyanide binds to Fe3+ in heme, keeps it from accepting more e- thus flow of e- blocked how would you treat cyanide poisoning? -Inhalation of amyl nitrite or intravenous infusion of NaNO2 - this converts oxyhemoglobin to methemoglobin – reservoir of heme in blood so large doesn’t matter if you convert some portion of that to Fe3+ (usually don’t want this to happen). How is treatment beneficial? -cyanide instead of binding to vital tissues binds to Fe3+ in methemoglobin to allow patients own enzymes to act on cyanide to convert to harmless thyocyanite --> gives patient time to detoxify cyanide! |
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What is the role of glycolysis in muscle?
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Production of lactic acid under anaerobic conditions, which regenerates NAD+ needed to drive glycolysis in the forward direction.
Lactate is released into the bloodstream and delivered to the liver where it is converted back to glucose. It is able to store glucose in a polymeric form called glycogen so that abundant glucose is available on demand. Recall that fast twitch and slow twitch muscles use different energy sources/metabolic pathways: FAST TWITCH: glucose --> pyruvate --> lactic acid --> blood --> liver --> glucose SLOW TWITCH: glucose --> pyruvate --> acetyl-coA --> ATP *predominately fatty acids metabolized |
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What is the role of glycolysis in the liver?
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-Its major function is maintaining blood levels of glucose, and it plays a general function of processing metabolic fuel.
-It is the major site where excess glucose from the diet is converted to fatty acids, which will be transported to the adipose tissue for storage. -It can also store glucose in the form of glycogen -It can also convert fatty acids to ketone bodies, a form of metabolic fuel that acts as a soluble version of fatty acids -The liver is the major source of gluconeogenesis, the synthesis of glucose from carbon sources such as lactic acid and the carbon skeletons of glucogenic amino acids -Recall that glycolysis is not only used to metabolize glucose and derive energy but also to make intermediates (like citrate for FA synthesis) which are important starting points for anabolic reactions like fatty acid synthesis and gluconeogenesis |
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What is the role of glycolysis in the brain?
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Glucose is aerobically catabolized to CO2 and H2O. Reducing equivalents in NADH must be delivered to the mitochondria
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What is the role of glycolysis in red blood cells?
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Since RBCs lack mitochondira, glycolysis is essential for energy production, and lactate is the end product.
*Recall that RBC has no mitochondria, no nucleus |
