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19 Cards in this Set
- Front
- Back
Ox phos (overview)
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-2 stages are neede to male ATP:
REDOX- coupled e- xport uses reduced cofactors NADH & FADH2 to make a proton gradient PHOSPHORYLATION- ADP is phosphorylated by ATP synthetase using the proton gradient |
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NADH oxidation
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-IMPORTANT SUBSTRATE
-done by catelytic redox carriers tht are integral membrane proteins in inner memb of mit0 -inc E change -protons of mito matrix are translocated to cytosol & creates the proton gradient -this inc H+ outside of cell |
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e- transport assembly
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2 e- from NADH & succinate are xported to O2 via e- xfering cofactors
-all are integral memb proteins except succ & Coq -their cofactors undergo redox rxns -CoQ is mobile & hydrophobic -NADH & succ are soluble |
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Complex 1
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-is a multiprotein enzyme that shuttles e- through the memb
-NADH is oxidized & sends e- to complex 1 -complex 1 sends e-s to coQ -which sends 2-4 H+ across memb. |
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CoQ (umbiquinone)
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-coenzyme
-only accepts e- from complex 1 -donates only to complex 3 |
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Complex 2
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-is a multiprotein complex
-is succinate dehydrogenase -memb bound |
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Complex 3
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-is multiprotein complex
-is QH cytochrome reductase -sends e- to cytochrome C |
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Cytochrome C
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-coenzyme
-accepts e- from comp 3 -donates them to complex 4 |
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Complex 4
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-is multiprotein complex
-cytochrome oxidase -has heme proteins -accepts e- from cytochrome C -donates them to O2(IMPORTANT SUBSTRATE) -O2 is then converted to H2O -2 H+ are pumped across membrane |
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Complex 5 (ATP synthase/ATPase)
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-is multiprotein
-has 2 parts: F1=lumen,F0=membrane(roter) -H+ go through the complex -this charges the complex & phosphorylates ADP->ATP |
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Coenzymes
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-flavoproteins: H+ carriers,integral memb proteins,
-iron/sulfur proteins:e- carriers,integral proteins -cytochrome: e- carriers, all int memb protein expt cyto C -ubiquinone: mobile,H+ carrier,hydrophobic |
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Regulation of Ox phos
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-ATP synthesis is by ADP(rt limiting)availability & proton gradient
-availability of O2 is the RATE LIMITING STEP in ischemic conditions & pulmonary impairment -Pi is RATE LIMITING STEP when Pi is depleted (fructose overload b/c it takes up Pi)comp 5 can't phosphorylate ADP->ATP -if not enough O2 complex 4 is charged but no )2 to be the e- carrier so NADH backs up & H+ gradient is too high |
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What happens during vigorous musc activity
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cytosolic ADP inc
-ADP/ATP translocase exchanges ADP w/ ATP & protons flow back into ATP sythase -results in inc rates of e- xport |
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Ox phos inhibitors
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Rotenone:
inhibits e- flow through comp 1,e-s can't get to umbiquinone Antimycin A: e-s can't flow through comp 3,e-s can't get to cyto C Cyanide & Azide: binds to comp 3 Oligomycin: block proton flow through complex 5,ATP can't be made which leads to buildup of steep proton gradient which inhibits e- flow 2,4DNP,pentachlorophenol & uncouplers: dissipate proton gradient by xporting H+ on inner mito memb, ATP can't be made Valinomycin: makes inner mito memb permeable to K+ , dissipates memb pot Arsenate: competes for Pi for ATP synth. & results in an ATP analog that switches back to Pi & ADP Atractyloside: blocks ATP/ADP antiporter in inner mito memb, no ADP=no ATP=no e- flow |
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Experiment
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-adding mito will dec O2 levels
-adding ADP will dec the rate of O2 consumption -adding oligomycin will dec rt. of consumtion & inc proton gradient -add DNP will inc rt. of consumption b/c the uncoupling will alleviate the proton gradient & give the 1st part of the chain the chance to pump protons |
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Complex 4 deficiency:Cytochrome C oxidase
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-affects heart & neurons
-28% of chain defects -heterogenous -hypotonia,growth retardation, cardiomyopathy -encephalopathy,liver failure,lactic acidosis |
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Complex 1 deficiency
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-has 37 nuclear encoded subunits
-7 mito encoded subunits -locus heterogeneity,mitochondrial inheritence -exercise intolerance,lactic acidemia,weakness, norm resp. rt w/ succinate |
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Reactive oxygen species ennzymes (ROS)
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Superoxide dismutase:
-in cytosol & mito dangerous superoxide to H2O2 mutation of SOD1 gene is the cause of familial ALS -Catalase: (peroxisomes) H2O2=>H2O & O2 -Peroxidases: react H2O2 w/ organic substrates i.e. glutathione peroxidase |
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Cellular O2 control
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*1 e- to O2 forms O2-
*superoxide dismutase forms H2O2 & w/ catalase=>H2O *this rxn forms harmless O2 byproducts *deficiency leads to disease state -H2O2 & hydroxyl radical react w/ Fe2+ & enter the radical chain rxns -this leads to lipid peroxidation memb damage,genotoxic damage,aging,CA,damage to oxidative tissues |