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56 Cards in this Set

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What cofactor does riboflavin (Vitamin B2) form?
FAD (flavin adenine dinucleotide)

Flavin proteins accept electrons from NADH and donate it to cytochromes
What cofactor does niacin (vitamin B3) form?
NAD+/NADP+ (nicotinamide adenine dinucleotide)

NAD --> Catabolic
NADP --> Anabolic
Is the catalytic role of niacin and riboflavin in bound or soluable form?
They are both catalytic in their oxidized, tightly bound form and accept electrons in this form.
What are Iron-Sulfur proteins?
Integral membrane proteins also called non-heme iron.

Iron coordination bonding with sulfur in the cystine and elemental forms.

It acts as a redox electron carrier.

The iron alternates between Fe2+ and Fe3+
What is the role of sulfur in electron transport?
Found in iron-sulfur proteins.

It binds non-heme iron. Typically, the exterior sulfur is in cysteine form and the interior is in elemental, inorganic sulfide form.
What's the difference between ubiquinone and ubiquinol?
Ubiquinone (Coenzyme Q) is a mobile hydrogen carrier that is not not permanently associated with a protein. It can generate free radicals.

Ubiquinol (Coenzyme QH2) is the reduced (has 2 extra electrons) form of ubiquinone.
What makes ubiquinone (CoQ10) membrane compatible?
10 isoprene units make it fat soluble.
Ubiquinone transfers electrons from ___ to ___.
Complex I (NADH Q Reductase) to Complex III (Cytochrome Reductase)
What are Cytochromes?
Integral membrane proteins (except cytochrome c) that contain iron in the form of an iron-porphyrin, usually a heme group.

Similar to iron sulfur proteins, the iron alternates between Fe+2 and Fe+3.

In most cytochromes (except cytochrome a/a3) heme iron bound to 2 amino acid side chains rather than one (prevents binding of molecular oxygen, CO, etc.)
What metal does cytochrome oxidase use?
Cu2+
Which cytochrome is soluable and not bound in the mitochondrial membrane?
Where is it located?
Cytochrome C, inner mitochondrial space.
What do cytochromes have in common with myoglobin?
Heme group
Composition of: Complex I (NADH-Q reductase)
FMN and several iron-sulfur centers
No cytochromes
Composition of: Complex III (QH2, Cytochrome C reductase)
Cytochrome b (iron-sulfur protein)
Cytochrome C1
Composition of: Complex IV (Cytochrome oxidase)
Contains 2 heme a groups (cytochromes a and a3 each near a copper ion)
Composition of: Complex II (Succinate Q reductase)
Electrons transferred directly to ubiquinone, no cytochromes
What three enzymes can transfer electrons from FADH2 to CoQ?
Succinate Dehydrogenase
Glycerol phosphate dehydrogenase
Fatty acyl-CoA dehydrogenase.
What transfers electrons to CoQ?
Complex I (NADH Q Reductase) and Complex II (Succinate Q Reductase)
What transfers electrons to Cytochrome C?
Complex III (Cytochrome C Reductase)
What transfers electrons to Oxygen? What metal ion actually reduces the oxygen to water?
Complex IV (Cytochrome oxidase), Copper.
What is the energy of electron flow used for?
Pumping protons out of the matrix into the IM space, harvesting the concentration gradient for ATP synthesis
What is the chemiosmotic hypothesis?
Energy drop at each complex is coupled to a proton pump. The proton gradient created by these pumps is coupled to ATP synthesis. 10 times higher concentration outside, and negative charge on the inside.
What is oxidative phosphorylation?
Where does it take place?
Oxygen consumption coupled to ATP synthesis. Pressure from the proton gradient drives ATP synthase in a forward direction. Oxygen pulls electrons through the ETC, the pumps push the protons out, and the built up gradient pushes protons back into the matrix. Inner mitochondrial membrane.
What is the system of electron carriers that are coupled to ATP synthesis called? Where are they located?
Respiratory chain, inner mitochondrial membrane.
Where is ATP synthase located?
Inner mitochondrial membrane
What is ATP synthase composed of?
Proton channel (Fo) + ATP synthase (F1). O= oligomycin-sensitive factor.
Why is part of ATP synthase called an ATPase?
In the absence of a sufficient proton gradient, ATP synthase DOES NOT synthesize but rather hydrolyzes ATP.
What is ATP translocase?
Integral inner mitochondrial protein that carries ADP into the matrix and ATP out of the matrix.
Follow the path of electrons for the Glycerol phosphate shuttle.
NAD + e- = NADH (via glycolysis) then it gives it to...
DHAP + e- = Glycerol Phosphate then it gives it to...
FAD +e- = FADH2 which finally gives it to...
Q + e- = QH2 (which is not reversible.)

This all happens from the cytosol to the inner membrane. Does not go into the matrix.
Follow the path of electrons for the Malate-Aspartate shuttle.
NAD + e- = NADH
OAA + e- = Malate (cytoplasm)
Malate then goes through two membranes into the mitochondrial matrix in exchange for a aketoglutarate coming out.

Malate --> OAA donates e- back to an NADH which then goes to the ETC.

Reversible. OAA gets turned into aspartate, which can then leave to the cytoplasm as a glutamate comes in. The glutamate is converted to aketoglutarate, which goes out when the malate comes in.
Where is glycerol dehydrogenase located?
Both in the mitochondria (inner space) and cytoplasm. DHAP <--> Glycerol phosphate.
Why can't OAA get across the inner mitochondrial membrane?
There's no transporter for it. (Or for acetyl-CoA and NADH) See malate shuttle. OAA needs to be turned into malate, which goes into the matrix, then comes back out... and is converted back into OAA in cytosol. NADH is used when OAA is turned into Malate, then is reformed the other way.

OR- OAA --> Malate --> Pyruvate --> shuttled... Pyruvate converted back to malate in matrix.

To get back out, OAA+ AcetylCoA = Citrate. Citrate can be transported out.
What is respiratory control?
Tight coupling between ETC and ADP concentrations. If ADP is absent, ETC stops. It prevents unnecessary consumption of O2 when ATP is adequate.
IF uncoupled, (protons flow around ATP synthase), then ETC rate is as fast as the O2 supply. ***** important.
What is the rate limiting step for ETC?
Rate depends on substrate availability: NADH, O2, ADP, PO4
What is the rate limiting factor in respiratory control?
ADP
What happens to pyruvate dehydrogenase when energy charge drops and NAD+/NADH increases?
More NAD+ than NADH. Less NADH = less inhibition of PDH. More PDH activity turns more pyruvate into Acetyl-CoA, which makes NADH from NAD+. Increases TCA cycle.
What does antimycin A do?
Poison inhibits cytochrome reductase (complex III).
What does rotenone and amytal do?
Barbituates: Inhibits NADH Q Reductase (Complex I), does not affect FADH2
What does Cyanide do?
Inhibits electron flow, works on cytochrome oxidase (Complex IV). CO and Azide work in the same manner. Shuts down the ETC b/c no reaction with O2
What does Oligomycin do?
Inhibition of Fo of ATP synthesis. Uncouples oxidative phosphorylation. Reduces ATP/ADP ratio.
What does Dinitrophenol (DNP) do?
Carries protons across the mitochondrial membrane. Reduces the proton to oxygen ratio.
What does atractyloside do?
Inhibits translocation. Less ATP in cytoplasm, more ATP in matrix.
What does Valinomycin do?
Makes inner mitochondrial membrane permeable to potassium, interrupting membrane potential.
What does arsenate do?
Competes with phosphate for ATP synthesis.
When rototone or amytal are inhibiting electron flow, how many ATP's are made from NADH? FADH2?
Blocks NADH-Q reductase (Complex I). NADH: 0; FADH2: 2 ATP.
When azide is inhibiting electron flow, how many ATP's are made from NADH and FADH2?
Blocks Complex IV, so none
Name a poison that can block proton flow back into the matrix
Oligomycin- blocks at Fo. Also blocks flow of e- through ETC (b/c tight coupling)
Name poison that facilitates the flow of protons across inner membrane from inner membrane space into the matrix.
DNP and pentachlorophenol.
With DNP, if ATP can't be made from shunted protons, what happens to the energy?
Released as heat, causing hyperthermia. Brown fat- we have a natural uncoupler protein. Electric blankset in thoracic area in infantss.
How does pentachlorophenol lead to acidosis? and hyperthermia? ** Think, boy eats paint on fence.
Free flow of protons into matrix. ETC slows down, NADH is not used, which increases NADH concentration. ADP is not made into ATP. The Malate-Aspartate shuttle reverses. ATP translocase reverses. PFK is then stimulated by AMP and ADP. NADH and lactic acid increases.

BUT- ETC is still okay, NAD+/NADH is still okay, but protons diffuse, released as heat.
What's the P/O ratio?
The number of high energy phosphate bonds formed for each oxygen atom consumed
How many ATP from NADH?
3
How many ATP from FADH2?
2
How many ATP per glucose?
36-38
Which poison can keep ADP from exchanging with ATP? What happens to energy change in cell? Does electron flow speed up or slow down?
Atractyloside. Stops ATP synthesis. Halts electron flow.
Compare mechanism of arsenate action in mitochondrion with action in glycolysis?
Glycolysis: Arsenate binds with G3P, so substrate level phosphorylation with phosphoglycerate kinase is hindered. Instead of making ATP, Arsenate is removed.

In mitochondria, arsenate competes with PO4, binds to ADP during ATP synthesis. Arsenate gets into the mitochondrion through the phosphate transporter.