Mkgrady8 Electron Transport And Oxidative Phosphorylation

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composition of the electron transport chain

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flavoproteins, iron-sulfur proteins (non-heme iron), cytochromes (contain heme), ubiquinone (isoprene tail that is fat soluble), copper (part of cytochrome oxidase), most components are obtained from the diet

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flavoproteins

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comes from riboflavin in the diet; accept electron from NADH and donate to cytochromes

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iron-sulfur proteins

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also called non-heme iron, iron coordination bonding with sulfur, acts as redox electron carrier (acceptor/donor)

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ubiquinone

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aka coenzyme Q10; contains isoprene tail (10 isoprene units); can generate free radicals; fat soluble and compatible with membranes

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cytochromes

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integral membrane proteins; contain heme; iron alternates between Fe+2 and Fe+3 (same as iron-sulfur proteins); bound to 2 aa (prevents oxygen binding); cytochrome oxidase also uses CU++); end step of electron transport chain

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ETC multi-proteins complexes

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NADH-Q reductase (complex I); succinate-Q reductase (complex II); cytochrome reductase (complex III); cytochrome oxidase (complex IV)

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chemiosmotic hypothesis

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each complex coupled to proton pump; proton gradient contains the energy for ATP synthesis (10x higher concentration outside, greater than 10x will change energetics (blocks pumps and electron flow))

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oxidative phosphorylation

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oxygen consumption coupled to ATP synthesis; pressure from the proton gradient drives ATP synthase in forward direction (1. oxygen pulls electrons through the ETC 2. pumps push protons out 3. gradient pushes protons back in); ATP synthase can run backwards so it is also called mito ATPase

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respiratory control

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if ADP is absent ETC stops; very tight coupling between the ETC and ADP concentrations but if oxidative phosphorylation is uncoupled (protons flow around ATP synthase) then ETC rate is as fast at the O2 supply; VERY IMPORTANT COMCEPT

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oxidative phosphorylation poisons

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oligomycin- inhibition of ATP synthase (reduced ATP/ADP); dinitrophenol (DNP)- uncouplers (reduced P/O ratio)= high energy bonds/oxygen atom, P/O ratio: NADH=3 and FADH2=2; atracytoside- inhibition of translocation (reduced ATP/ADP ratio in cytoplasm, increased ATP/ADP ratio in matrix so won't transport the ATP across the membrane); cyanide- inhibition of electron flow (like hypoxia/anoxia)

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glycerol phosphate shuttle

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NADH donates electrons to DHAP (dihydroxyacetone phosphate) with the help of glycerol phosphate dehydrogenase and in the process the DHAP becomes glycerol phosphate; glycerol phosphate donates to FAD (in complex II) with the help of mitochondrial dehydrogenase phosphate; FADH2 donates to coenzyme Q (not reversible) this shuttle enters at coenzyme Q

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malate-aspartate shuttle

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NADH donates electrons to OAA with the help of malate dehydrogenase and making malate from OAA in the process; malate transported and donates e back to NAD+ so malate then becomes OAA again; aspartate is transported out of the mito when malate is transported in; NADH donates e to electron transport chain (reversible); this shuttle enters at NADH-Q reductase (just like any other NADH found inside the matrix); if you are hypoxic then this NADH can go back out the shuttle (because it bounds up) and will combine with pyruvate to form lactate= lactic acidosis; THIS SHUTTLE IS REVERSIBLE WHERE THE GLYCEROL PHOSPHATE SHUTTLE IS NOT

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creatine

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derived from arginine, glycine, SAM; creatine (phospho)kinase (APK)- reversible phosphorylation by ATP so energy storage; popular athletic supplement

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creatinine

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nonenzymatic degradation of creatine phosphate; utilized in urinalysis as test of glomerular filtration rate (GFR); so you use creatine kinase in the muscle to get ATP and in the process creatine becomes creatine phosphate which breaks down into creatinine which is excreted in the urine

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steps in ischemic injury

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1. ET slows down 2. NADH increases and ADP increases 3. MA shuttle reverses and ATP translocate reverses 4. PFK stimulated AMP/ADP 5. NADH and lactic acid increases 6. lysosomes go boom

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lactic acidosis from poisons

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cyanide poisoning- blocks ETC (stimulates anoxia) produces lactic acidosis; pentachlorophenol- ETC is OK and NAD+/NADH is OK but 1. ATP/ADP drops 2. PFK activity increased 3. pyruvate increased 4. lactate increased

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1 NADH = how many ATP at the end of the electron transport chain

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3

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what if you start at the Q

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that means that you entered as FADH2 and you make 2 ATP because you only go through 2 complexes

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prefrontal pause: how does proton flow through the proton channel affect the flow of electrons through the ETC?

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permissive allowing proton flow would reduce buildup of protons which are coupled to proton pumps which in turn would allow electron flow; this is the basis for respiratory control blocking proton channel eventually blocks electron flow; so these actions are coupled= to have outflow of electrons you need inflow of electrons

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the only thing that can slow down or stop electron flow

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if you have too HIGH of a buildup of electrons and it can no longer push any more over

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rhotinone and amytal

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poisons; prevents NADH Q reductatase from working so they stop the electron transport chain form working; so will also prevent use of O and will prevent production of H2O FROM NADH but you also have entry of G from FADH (from succinate) so you sill still have production of 2 ATP+use of O2+production of H2O form this

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anamycin A

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a poison; prevents the working of cytochrome reductase so there is no entry into the electron transport chain so there is no production of anything from THIS pathway

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cyanide, azide, and CO

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poisons; prevents cytocrome reductase from working so it also prevents any entry into the electron transport chain

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when you use one of these poisons then upstream

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the complexes fill up upstream

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flavin is found where

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in the reductases as FMN; this is where electrons can come into the electron transport chain (the other entry point is coQ (complex II))

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atractyloside

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inhibits ATP/ADP translocase which is a transporter across the inner mito membrane that delivers ATP to the IM space and ADP to the matrix; so this causes a buildup of things on the wrong sides

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oligomycin

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inhibition of ATP synthesis by inhibiting ATP synthase so you will again get reduced ATP/ADP

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thermogenin

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allows movement of H+ back into the cell; it isn't coupled to anything; this powers the brown fat in infants

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dinitrophenol (DNP)

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can easily transport across the mito membrane if you attached a proton to it; it will then drop the proton, leave, grab a proton, go back in, etc and this will relieve the proton gradient and release heat; is an uncoupled molecule because electron flow is not coupled to ATP synthesis; reduced P/O ratio- ATP produced per O2 consumed so basically lots of protons crossing and combining with oxygen but not a lot of ATP produced

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if ADP is low

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protons can't flow back in

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prefrontal pause: will pentachlorophenol cause a pt's body temp to increase or decrease and why? hint: consider what has been uncoupled

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increased due to release of energy that would have been captured in ATP (this compound is equivalent to DNP)

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prefrontal pause: a 65 yr old male is admitted to the ER and he is having shortness of breath and fatigue. imaging studies show that he has about 90% blockage in his coronary circulation. what pump is most directly affected by his ischemia?

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proton pumps; lowered oxygen so mito don't have it so nothing to receive electrons and no generation of ATP