Biochem: Oxidative Phosphorylation
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| How are electrons transported to NAD, FAD, FMN, Q, cytochrome? | hydride ions to NAD and hydrogen atoms to FAD, FMN, Q, transported as electrons to cytochromes
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| What is the standard reduction potential? | tendency to gain electrons for a given redox pair
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| Negative reduction potential? | tendency of the reduced partner to lose electrons increases
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| Positive reduction potential? | tendency of the oxidized partner to lose electrons increases
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| With respect to reduction potential, electrons will move? | from the partner with a negative reduction potential to the partner with a positive reduction potential
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| What is the P/O ratio? | ATP formed:Oxygen atom reduced
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| P/O ratio for NADH? | 3 ATP:1 NADH
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| P/O ratio for FADH2? | 2 ATP:1 FADH2
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| Why are 2.5 ATP synthesized for each NADH instead of three? | because it takes 4 protons to make an ATP and NADH oxidation only transports 10 protons
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| What is Mitchell's hypothesis/chemiosmotic theory? | proton pumps establish a chemiosmotic gradient in which complex 1, 3 and 4 pump protons into the intermembrane space giving it a high pH and positive charge as compared to matrix. Energy generated by proton gradient drives ATP synthesis
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| What couples oxidation to phosphorylation? | the proton gradient
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| The electron transport chain is stopped if | the energy to move protons out of the matrix is smaller than the energy lost to heat, if energy of gradient is not dissipated
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| What is the Fo domain of the F1/F0 ATPase? | spans the inner membrane, the proton channel
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| What is the F1 domain of the F1/F0 ATPase? | extended out into the matrix, the catalytic subunit
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| How is F1 held into place? | S and b2 subunits
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| Describe rotational catalysis | when a proton is transferred the rotator stalk (gamma-epselon subunit) has a conformational change and rotates on the immobile F1 subunit, catalyzing ATP
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| What is the function of oligomycin? | inhibits ATP synthase by binding to the F0 domain thus closing the proton channel, electron transport is halted
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| What is a symptom of oligomycin? | lactic acidosis in the blood
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| What molecules uncouple electron transport from phosphorylation? | uncoupling proteins:cause proton's to leak across inner mito membrane: UPC1, ionophores, 2,4-Dinitrophenol, CCCP, FCCP
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| What happens to energy released from electron transport that is not coupled to phosphorylation? | Released as heat called nonshivering thermogenesis
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| Where does nonshivering thermogenesis occur and how? | UCP1/thermogenin causes heat production in brown fat by making a pore in the inner mito membrane and dissipating the proton gradient
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| What is irreversible uncoupling or ETC block? | ETC block
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| What is the effect of 2,4-Dinitrophenol (DNP)? | used as dyes, preservatives, pesticides, dangerous diet agent, binds protons on one side and moves in to the other because it is fat soluble
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| Effects of CCCP and FCCP? | lipid soluble weak acids which are powerful uncouplers
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| What uncouplers are found naturally in the body? | UPC1 in brown fat, UPC2 & UPC3 found in other cells.
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| What is UPC2 & UPC3 used for clinically? | target for weight loss but can increase risk of diabetes in pancreas beta cells
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| Examples of ionophores | gramicidin, valinomycin, nigericin
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| Function of gramicidin | channel forming by dimerization to form beta-helix
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| Function of valinomycin | associtaed with carying K across bilayers, keeps ion distribution in accordance with the Nernst equation when at equilibrium
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| Function of Nigericin | mobile carrier, H+/K+ antiporter, can move across lipid membranes b/c it's carboxyl group and a K+ makes the charged ion neutral
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| Function of Adenine nucleotide translocase? | antitransporter of ATP and ADP, symport of Pi and H+
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| What is the function of Atractyloside? | glycoside that binds outward faceing intermembrane space portion o fthe adenine nucleotide transporter, inhibits transporter
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| Function of Bongkrekic acid? | binds the inward facing matrix portion of the adenine nucleotide transporter, inhibits transporter
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| What is the effect of inhibition of ADP/ATP transport? | inhibit ATP production/stall ETC
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| What is the function of NSAIDS on oxidative phophorylation? | can uncouple ox phos, decrease ATP synthesis, inhibit adnenine nucleotide translocase
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| How is cytochrome C is released from the mito during apoptosis? | pore formation in the outer mito membrane
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| What genes are encoded by the mito genome? | complex 1, 3, 4, 5
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| What is a major signal/symptom of ETC and ox phos disorders? | lactic acidosis
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| What kind of inheritance is seen in ETC and oxidative phosphorylation disorders? | maternal inheritance, autosomal dominant, recessive or sex-linked, mutations in one or more of the 13 proteins coded on the mito genome
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| What diseases are caused by mutation in mito DNA of complex 1? | Leber's hereditary optic neuropathy (LHON), LHON Dystonia, mito encephalomyopathy-lactic acidosis-stroke like episodes (MELAS)
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| Diseases caused by mutation of mito DNA of complex 5? | Leigh's Disease, myoclonic epilepsy with ragged-red fibers (MERFF), neuropathy-ataxia-and retinitis pigmentosa (NARP)
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| How many of the genes for oxidative phosphorylation are coded by mito DNA? | 13 of 120
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| What affects mutation rate of mito DNA? | more ATP atissue needs, the more it is affected by mito defects because mutation rate is 10x greater than nuclear DNA
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| What is the usual inheritance of mtDNA diseases? | maternal
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| What is mitochondrial myopathy? | abnormal proliferation of mito
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| What is Leber hereditary optic neuropathy? | bilateral loss of central vision occurs due to neuroretinal degen
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| What is Leigh syndrome? | Affects the brainstem and basal ganglia and is charcterised by defects in mito oxidative phosphorylation
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| What is rhabdomyolysis? | breakdown of muscle due to injury, toxins or metabolic disease which leads to high [] of myoglobin in both plasma and urine
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| What is ragged red fibers? | pathological hallmark of mtDNA disease characterized by subsarcolemmal accumulation of abnormal mito in the muscle fiber, which stain red with a Gomori trichrome stain
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