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19 Cards in this Set

  • Front
  • Back
Ox phos (overview)
-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
NADH oxidation
-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
e- transport assembly
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
Complex 1
-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.
CoQ (umbiquinone)
-only accepts e- from complex 1
-donates only to complex 3
Complex 2
-is a multiprotein complex
-is succinate dehydrogenase
-memb bound
Complex 3
-is multiprotein complex
-is QH cytochrome reductase
-sends e- to cytochrome C
Cytochrome C
-accepts e- from comp 3
-donates them to complex 4
Complex 4
-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
Complex 5 (ATP synthase/ATPase)
-is multiprotein
-has 2 parts:
-H+ go through the complex
-this charges the complex & phosphorylates ADP->ATP
-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
Regulation of Ox phos
-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
What happens during vigorous musc activity
cytosolic ADP inc
-ADP/ATP translocase exchanges ADP w/ ATP & protons flow back into ATP sythase
-results in inc rates of e- xport
Ox phos inhibitors
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
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
makes inner mito memb permeable to K+ , dissipates memb pot
competes for Pi for ATP synth. & results in an ATP analog that switches back to Pi & ADP
blocks ATP/ADP antiporter in inner mito memb, no ADP=no ATP=no e- flow
-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
Complex 4 deficiency:Cytochrome C oxidase
-affects heart & neurons
-28% of chain defects
-hypotonia,growth retardation, cardiomyopathy
-encephalopathy,liver failure,lactic acidosis
Complex 1 deficiency
-has 37 nuclear encoded subunits
-7 mito encoded subunits
-locus heterogeneity,mitochondrial inheritence
-exercise intolerance,lactic acidemia,weakness, norm resp. rt w/ succinate
Reactive oxygen species ennzymes (ROS)
Superoxide dismutase:
-in cytosol & mito
dangerous superoxide to H2O2
mutation of SOD1 gene is the cause of familial ALS
(peroxisomes) H2O2=>H2O & O2
react H2O2 w/ organic substrates i.e. glutathione peroxidase
Cellular O2 control
*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