Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
SGU: Oxidative Phosp
Biochem: Oxidative Phosphorylation
| Question | Answer |
|---|---|
| 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 |
| What is the standard reduction potential? | tendency to gain electrons for a given redox pair |
| Negative reduction potential? | tendency of the reduced partner to lose electrons increases |
| Positive reduction potential? | tendency of the oxidized partner to lose electrons increases |
| With respect to reduction potential, electrons will move? | from the partner with a negative reduction potential to the partner with a positive reduction potential |
| What is the P/O ratio? | ATP formed:Oxygen atom reduced |
| P/O ratio for NADH? | 3 ATP:1 NADH |
| P/O ratio for FADH2? | 2 ATP:1 FADH2 |
| 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 |
| 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 |
| What couples oxidation to phosphorylation? | the proton gradient |
| 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 |
| What is the Fo domain of the F1/F0 ATPase? | spans the inner membrane, the proton channel |
| What is the F1 domain of the F1/F0 ATPase? | extended out into the matrix, the catalytic subunit |
| How is F1 held into place? | S and b2 subunits |
| 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 |
| What is the function of oligomycin? | inhibits ATP synthase by binding to the F0 domain thus closing the proton channel, electron transport is halted |
| What is a symptom of oligomycin? | lactic acidosis in the blood |
| 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 |
| What happens to energy released from electron transport that is not coupled to phosphorylation? | Released as heat called nonshivering thermogenesis |
| 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 |
| What is irreversible uncoupling or ETC block? | ETC block |
| 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 |
| Effects of CCCP and FCCP? | lipid soluble weak acids which are powerful uncouplers |
| What uncouplers are found naturally in the body? | UPC1 in brown fat, UPC2 & UPC3 found in other cells. |
| What is UPC2 & UPC3 used for clinically? | target for weight loss but can increase risk of diabetes in pancreas beta cells |
| Examples of ionophores | gramicidin, valinomycin, nigericin |
| Function of gramicidin | channel forming by dimerization to form beta-helix |
| Function of valinomycin | associtaed with carying K across bilayers, keeps ion distribution in accordance with the Nernst equation when at equilibrium |
| 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 |
| Function of Adenine nucleotide translocase? | antitransporter of ATP and ADP, symport of Pi and H+ |
| What is the function of Atractyloside? | glycoside that binds outward faceing intermembrane space portion o fthe adenine nucleotide transporter, inhibits transporter |
| Function of Bongkrekic acid? | binds the inward facing matrix portion of the adenine nucleotide transporter, inhibits transporter |
| What is the effect of inhibition of ADP/ATP transport? | inhibit ATP production/stall ETC |
| What is the function of NSAIDS on oxidative phophorylation? | can uncouple ox phos, decrease ATP synthesis, inhibit adnenine nucleotide translocase |
| How is cytochrome C is released from the mito during apoptosis? | pore formation in the outer mito membrane |
| What genes are encoded by the mito genome? | complex 1, 3, 4, 5 |
| What is a major signal/symptom of ETC and ox phos disorders? | lactic acidosis |
| 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 |
| 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) |
| 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) |
| How many of the genes for oxidative phosphorylation are coded by mito DNA? | 13 of 120 |
| 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 |
| What is the usual inheritance of mtDNA diseases? | maternal |
| What is mitochondrial myopathy? | abnormal proliferation of mito |
| What is Leber hereditary optic neuropathy? | bilateral loss of central vision occurs due to neuroretinal degen |
| What is Leigh syndrome? | Affects the brainstem and basal ganglia and is charcterised by defects in mito oxidative phosphorylation |
| What is rhabdomyolysis? | breakdown of muscle due to injury, toxins or metabolic disease which leads to high [] of myoglobin in both plasma and urine |
| 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 |
Created by:
mnoronha
Popular Biochemistry sets