Oxidative phosphorylation pdf answer key

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Oxidative phosphorylation pdf answer key

Pierre Cardol, ... Diego Gonzalez-Halpen, in chlamydomonas' original book, 2009 OxPHOS, is defined as an oxidation-driven electron transfer chain of the toy, poured into atp synthesis through an electrochemical transmembrane gradual transition (Fig. 13.1). Historically, bovine heart mitochondria have been the system of choice for the structural characterization of oxphos aocritic complexes (Saraste, 1999), because they can be purified in relatively large quantities. The yeast Saccharomyces cerevisiae, which is convenient for a large variety of molecular genetic tools (Bonnefoy and Fox, 2002), has become a model organism to study the biogenesis of mitochondrial compounds (Barrientos et al., 2002; Herman And Neofert, 2003) and the effect of mutations on OXPHOS components (Fisher et al., 2002). In contrast, the mitochondria of photosynthetic organisms were poorly characterized by a biochemical perspective, mainly because of the difficulties in achieving preparations without loroplast contaids. Neverthon though, the characterization of mitochondrial components in Arabidopsis through proteumic approaches progressed significantly (Millar et al., 2005). Figure 13-1. Oxy phosphor system (OXPHOS) in the inner membrane of the plant mitochondria. Electrons are transmitted from NADH and NAD(P)H to coenzyme Q (Q) using type I NADH:ubiquinone oxidoreductase or composite I (I) and type II alternative NADH dehydrogenases (NDA; located on the inner face (int) or external (ext) of the inner membrane. Some electrons from organic acid oxidation are also transmitted to Q using succinate dehyroganase or composite II (II). Electrons are then transmitted from cosidodocate c reduced (QH2) to cytochrome c (cyt c) through ubiquinol:cytochrome c oxydordoctase or composite III (III) and then oxygen via cytochrome c oxydaz or IV complex (IV). A replacement oxide azid (AOX) can then bypass complex III and IV by transferring electrons directly from QH2 to oxygen. The outer reactions brokered by complexes I, III, and IV are combined with protons (H1) to transfer from the matrix into intermembrane space. The energy associated with proton gradient is used to produce ATP by complex V (ATP synthase) or dissipated by crippling proteins (UCP). Chlamydomons is an attractive model for the study of mitochondria in single-celled photosynthetic organisms because it allows for a combination of classic biochemical approaches with genetics, and because photosynthesis-impaired mutations can increase heterotropics, and breath-impaired mutants as binding phototrops. Early work with chlamydomons mitochondria included a linear genomic sequence of 15.8 kb (gray and pit, 1988; Michaelis et al., 1990; see chapter 12), the biochemical characterization of enriched fragments of several OXPHOS complexes (Thea, 1994), and a sequence of several nuclear genes encoding polypeptides participating in OXPHOS In 1988, 1988, 1988, 1988, 198 Franz and Falk, 1992; Attia and Fransen, 1996; Nourani and Fransen, 1996; Perez-Martinez et al., 2000, 2001; Dinant et al., 2001; Funes et al., 2002a; Atia et al., 2003). At the same time, it characterized a number of chlamydomons mutations influenced by mitochondrial components (Matagne et al., 1989; Dorotho et al., 1992; Colin et al., 1995; Duvi and Mattan, 1999; Ramtkel et al., 2001, 2004; Cardol et al., 2002, 2006, 2008; Ramkel et al., 2004; see Chapter 12), and Procedures for Obtaining the Purified Mitochondria Were Developed (Ericsson et al., 1995; Nourni and Fransen, 1995). In particular, wall-impaired mutants have allowed isolation of mitochondrial preparations without thylakoid components. Then, the main mitochondrial complexes of chlamydomons were solved with blue polyacrylamide (BN-PAGE) electrophoresis (Van Lees et al. 2003; Cardol et al., 2004), which enables N-terminal sequencing or bi-blood mass spectrometry analysis of individual sub-units. The genome sequence enabled the prediction of chlamydomonas OXPHOS (Cardol et al., 2005), whose main components are schematically displayed in the form of 13.1. This chapter summarizes the knowledge of oxphos components of chlamydomons and the components involved in their biogenesis. We also treat alternative dehydrogenases and oxidases which specifically are photosynthetic organisms, and some other mitochondrial components associated with OXPHOS. If necessary, we refer to components of polytumala sp., a colorless algae closely related to chlamydomons (Pr?schold et al., 2001; See also Volume 1, Chapter 1).D.A. Bender, in the Encyclopedia of Food Science and Nutrition (2nd edition), 2003This knowledge of the processes involved in electron transport and oxidative phosphoration came from studies using inhibitors.1.Rotenone, the active ingredient of insecticide derris powder prepared from the roots of the nico lonchocarpus catany plant. The same effect is seen in the presence of amital (amobarbital), a sedative in the barbiturate, which again inhibits I complex. These two compounds inhibit malat oxidation, which requires complex I, but not succinate, which reduces ubiquinone directly. The addition of uncoupler has no effect on malate oxidation in the presence of these two inhibitors of electron transport, but results in uncontrolled oxidation of succinate.2.Antimycin A, an antibiotic produced by spp strep. used in antif mushroom slayer that are parasitic on rice. It inhibits complex III, thus inhibiting the oxidation of both malate and succinate, since both require complex III, and the addition of uncoupler has no effect.3.Cyanide, azid, carbon monoxide and irreversibly bind to the iron of cytochrome a3, thus inhibiting complex IV. Again, these compounds inhibit oxidation of both malate and succinate, since both rely on cytocratic oxydage and, again, the addition of No effect.4.Oligomycin, a therapeutic useless antibiotic produced by spp strep. oligomycin inhibits the transport of protons across the stem of the primary particle. The result is a delay of oxidation of both malate and concise, since, if the protons cannot be transferred back into the matrix, they will accumulate and delay further electron transport. In this case, the addition of uncoupler permits the re-entry of protons across the crista membrane, Hence the uncontrolled oxidation of bedding.5.Atractyloside (Glaxside plant) and bongkrekic acid (a toxic antibiotic created by Pseudomona cocovenans grown on coconut ? it is named after bongkrek, a fermented coconut mold product in Indonesia, that becomes highly toxic when Ps. cocovenans grows on the mold). Both compounds inhibit the transport of ADP and ATP over the mitochondrial membrane. Bongkrekic acid repairs nucleotides for protein transport on the matrix side of the membrane so that they cannot be released, while atractyloside has a higher affinity for transport protein than ADP, and therefore competes with it for transport into the matrix. Larry R. Engelking, in the textbook of Veterinary Physiological Chemistry (3rd edition), 2015?Explain how Malata Ferry operates in transferring the equivalents from the cytoplasm to mitochondria, why it matters, and how Glo, Asp, -KG = and Mel are transported across internal mitochondrial membranes.?Explain why the Malat ferry is of a more universal vessel than simply Glycerol 3-P Shuttle. ? Describe the cells and membranes of mitochondria, and locate the respiratory compositions they contain.?Define oxidative phosphorilation and cellular respiration.?Detect the final recipient of electrons at ETC.?Detect how the four protein compounds and two PORTABLE ETC electron explorers work.?Compare the processing of reducing reduction The equivalents from FADH2 to those of NADH in ETC.?Explain how ATP is produced during oxidative phosphoral and how it passes into cytoplasm.?Show how the effects of inhibitors differ from those of the uncoupler of oxidative phosphorilation.?Noted how thermogene , fatty acids, norepinphrine and thyroxine can contribute to an endogenous mitochondrial heat generation.?Discuss how peroxisomal oxidation can contribute to endogenous heat generation (see Chapter 55).?Identify known inhibitors to stop cellular respiration, and identify the site where each inhbitor operates. Generuso G. Gascon, Genneroso Gascon, Genneroso Gasco and Bruce Cohen, in the textbook of Clinical Neurology (third edition), 2007 Various oxidation defects occur in the brain, although how they relate to migraine production is speculative. Migraine affects as much as 25% of the population and is often seen as maternal relatives of patients with diseases of oxidative phosphorilation. Malignant migraine refers to three conditions: migraine patients who turn out to have MELAS; Migraine patients who are relatives of patients with oxidative phosphorilation diseases, who do not respond to the usual contraceptive drugs; And migraines developing strokes. Blood should be tested for biochemical defects and mtDNA of oxidative phosphorylation. If blood tests are negative, muscle biopsy should be done for routine pathology, histochemistry and microscopelectrons, oxidative phosphorylation biochemistry, and mtDNA analysis to include southern blob analysis for redesigned mtDNA. Management is not specific. The prognosis is unknown and depends on whether more specific mutations are found to be related. James C. Blackstock, in the Biochemistry Manual, 1989Oxididative phosphorylation may be delayed at various stages by a variety of agents (table 13.3) who have proved invaluable in its experimental investigation. Electron transport may be delayed in several locations. Rutnon and Ideal Evergate ATP Synthesis is driven by electrons derived from NADH but this FADH2 initiative continues. The action sites of electron transport inhibitors have been corrodating by the 'croissant technique' in which carriers before blockage are reduced more and those beyond the more oxidative. Table 13.3. Some inhibitors of oxidative phosphorilationThe script of inhibitionAgentComment Electronrotenone traffic Reduces ubiquinone and oxidation simultaneously of complex centers I FeSAmytalAntimycin AInhibits electron transfer from cytocochrome b562 to ubiquinoneidron cyanidogen sol esul Fidvines to Fe3+ of cytochrome a and a3Azide carbon monoxideBinds to Fe2+ of cytochrome a and a3Inner membrane2,4-DinitrophenolAre anionic in pH 7.0, may incentivize to be lipophilic and soluble in the membrane. Protons are transmitted via membrane and transport H4 from canceled cyanide-p-trifluoromethoxyphenylhydrazonevalinomycinrenders pervading membranes to K+ which may disable EmNigericinAbol Hishes H4 Gradient by K+H+ exchange SynthesaoligomicinBinds to OSCP Stalk and Blocker H+poreDCCDReacts with Proteolipid Binding DCCD of F0 Component and Blocker H+ PoresAdenine Subject KnockoutideAtractylosideBinds to External Conformation to Prevent Interaction ADPBongkrekic Bindings to Internal Conformation to Prevent INTERACTION ATP Foss Supply Mercerial hypnotisminda for lawidative sulphydryl phosphorylation groups may be delayed by agents who do not impair electron traffic but prevent phosphorillation by assimilation of transit Color transmembrane proton. Such agents, e.g. 2,4-dinitrophenol and carbonyl cyanide-p-trifluoromethoxyphenylhydrazone, are called uncouplers because they separate the two functional aspects of oxidative phosphorilation. Ionophores, e.g. valinomicin and nigericin, are also fat-soluble substances that promote the transfer of cations across the membrane. They may function by inserting into the membrane to form a pore or as mobile suppliers which disperse through the membrane. Oligumicin B and DCCD inhibit oxidation By blocking the proton pore of ATP synthesis. Michio Hirano M.D., in the current treatment of neurological diseases (7th edition), 2006OXPHOS requires coordinated transfer of electrons using four multiunit enzymes (complex I through IV) that produce proton color transition across the inner mitochondrial membrane. The electrochemical color transition is used by the Complex V for the production of adenosine triposphate (ATP). Four OXPHOS enzymes (complex I, III through V) contain sub-units

encoded in both mitochondrial DNA (mtDNA) and nuclear DNA (nDNA), while sub-units of II consist of encoded in nDNA only. The dual genetic sources of OXPHOS enzymes account for a number of unusual characteristics of mitochondrial encephalomyopathy.mtDNA is a small (16.6 kilobase [kb]) bicircular molecule The strand encoded only 37 genes: 22 transfer RNAs (tRNAs), 2 ribosumal RNAs (rRNAs) and 13 polypeptides which are sub-units of OXPHOS enzymes. Unlike nDNA, which features autosomal chromosomes and sex paired in each cell, mtDNA exists in hundreds to thousands of copies per cell. Changes of mtDNA may be present in some molecules (heteroplasmia) or overall (homoplasmia). Most mutations of MTDNA are heteroplasmic. When the share of mtDNA mutation exceeds a critical level, OXPHOS is compromised (threshold effect). The share of mtDNA mutation can vary from organ to organ (tissue division). Because the brain muscle and skeleton have high energy requirements, mitochondrial disorders usually manifest as encephalomiopathy. The tissue distribution of mtDNA mutations is determined by the dispersion of genoms during mitosis (mitotonic separation). The mitochondrial genomic is inherited through motherhood (maternal inheritance). Therefore, mtDNA mutations are passed from mothers to all their children, but only girls and not boys are able to pass the mutations on to their children. Intriguingly, single deletions of mtDNA occur randomly and are rarely transmitted to maternally.S. Rubinstein-Litwak, in the Encyclopedia of Food Science and Nutrition (second edition), 2003 Oxidative phosphorilation also known as the electron transport chain. It includes the resulting reactions to the synthesis of ATP from ADP+Pi. Heat can also be generated when ATP production is not a babe from the respiratory chain. Oxidative phosphoration is the main source of ATP in aerobic organisms. During the sourness of fuel molecules, FADH2 and NADH play a major role as the main electron carriers taking the electrons to the ultimate receiver, oxygen (O2). The transfer of electrons from NADH and FADH2 to O2 occurs in the inner membrane of the mitochondria. During this transfer, several protons are sucked out of the mitochondrial matrix, creating a proton gradient. Finally, with the help of ATPase, an ATP synthesis complex, the protons flow back into the energygenerating matrix needed to generate ATP. Electrons are transferred from NADH to O2 A chain of three large protein compounds. Each complex is an electron-guided proton pump that contains several oxidation reduction centers. The electron carrier groups that take the electrons from NADH and FADH2 to O2 are flavin, iron-sulfur clusters, macaques and copper ions (Fig. 5). Figure 5. Oxidative plex I, also known as NADH-Q reductase, involves the first process that through the electrons from the NADH are transmitted. NADH binds to flavoprotin, plebin mononucleotide (FMN), transferring its two high potential electrons and losing its hydrogen molecules. The result is FMNH2 and NAD+. From there, the electrons are transferred to Coenzyme Q, also known as ubiquinone Q, on their way to Compound III. Coenzyme Q is also the entry point for FADH2 electrons to the grid. While some energy is lost as heat, ATP is also generated in the same response by bonding ADP+Pi. Complex III is the second proton pump in the electronic transport chain. At this point, the electrons from coenzyme Q are transferred to cytochrome b and then cytochrome c, a water-soluble protein, on their way to complex IV. During the transfer, some protons are pumped again out of the mitochondrial membrane. A second integrated response causes atp formation. Complex IV, also known as cytochrome oxide azid then or cytochrome a, plays a role in transferring the electrons from cytochrome c to O2. In the latter stage, the electrons bind to O2 to form H2O. The net response from any glucose molecule that enters glycolysis and continues through the TCA cycle and oxidative phosphoration is: glucose + 6O2 +36ADP + 36Pi6CO2 +36ATP +6H2O.. When there is not enough energy to turn ADP into ATP, mitochondrial electron transport is uncoupled from ATP synthesize by proton leakage. The result is the release of energy as heat. Reflected proteins (UCP) are known to be responsible for leaks that sometimes occur during oxidative phosphorilation. Three un paralyzed proteins have been found. Thermogenic or UCP1 is present in brown fat tissue, UCP2 is present in several tissues, and UCP3 is primarily present in the skeletal muscle. UCP play a role in energy metabolism by limiting the synthesis of ATP and energy bloating as heat, thus reducing the efficiency of energy production. Yunjoon Jung, Andrew S. Burke, current topics in developmental biology, 2014 Hasty phosphorilation in the mitochondrial electron transport chain produces ROS, which is highly reactive and toxic mitochondrial (Mt) DNA, leading to a reduction in mitochondrial functions (Kujoth et al., 2005; Trifunovich et al., 2004). With age, increased levels of ROS were observed along with functioning mitochondria and considered to be the cause of aging (Berthit & Larson, 2013; Tryponovich et al., 2004). Can mtDNA mutations affect life expectancy and aging? Homozyg nook-in mice engineered to pronounce mtDNA polymerase that have flawed reading proof, show growing Mutant and mutant points, related to reduced life intransification and phenotypes for premature aging (Kujoth et al., 2005; Trifunovich et al., 2004). In addition, mice lacking exonuclease polymerase mtDNA to display neural function and hematopoietic fathers and progeria phenotype (Ahlqvist et al., 2012). Conversely, the introduction of random point mutations mtDNA to the mouse model was not enough to reduce life expectancy (Edgar et al., 2009). Therefore, the extent of mtDNA damage or a specific mutation in the mitochondrial genum will affect the effect on the stem cell. Eleonora Grandi, Donald M. Bers, Cardiac Electrophysiology: From Bedside Cell (6th Edition), 2014 Oxidative Phosphorilation is the primary source of energy for metabolic/contraction working from cardiac myocytes. Mitochondria provide the ATP needed for shrinking function and transporting sarculami and sarcoplasmic ion, which is responsible for electrical activity from Yozeit. Energy drives ion transport processes through their dependence on proton driven force and potential phosphorylation, as well as by direct transport across mitochondrial internal membranes (it has been shown that mitochondrial Ca2 + transport can affect Ca2 + cytoplasm65 signals). On the other hand, energy requires a change in response to the activation of myofilaments and, to a lesser extent, NKA, SERCA, and PMCA.31 pairing of mitochondrial energy to ECC models and therefore it is necessary to investigate the central role of energy in regulating myocyte mechanical activity and ion concentration paths, especially in impaired metabolic situations under pathological conditions, such as ischemia and heart failure (HF). To link the metabolism and treatment to Ca2+ (shape) thro cells, Michailova et al66,67 expanded the Winslow et al23 model by combining descriptions of Ca2+ and Mg2+ hoarding and transportation by atp and ADP, and regulating mgATP of ion transporters (NKA, SERCA, and PMCA). Matsuoka et al68 together modeled mitochondrial metabolism69 for their electrophysiological model56 and simulated nicotinamide adenine dinucleotide (NADH) and mitokondrial caTs following an increase in workload. The Aururek Group has extensively studied heart energies both experimentally and theoretically. Cortassa et al70 has developed the first integrated metamaterial model of heart energy metabolism that takes into account mitochondrial matrix-based processes such as tricarboxylic acid cycle, oxidative phosphoration, and Ca2+ dynamics. This model was then combined with models of electrophysiological, Ca2+-treatment,43 and force-generation61 subsyst sets of myocyte of the heart to study the complex dynamics of the response of the bio-energy mitochondria to changes in myocyte contraction and electrical activity.71 The formulation explicitly incorporates the cytoplasmic processes that consume ATP related to the transport of power and ion, As well as the cross processes in the ATP related to the transport of ion power as well as The Kinase Creatine response. Changes in electrical activity and contraction of myocyte identify with mitochondrial energy through ATP, Ca2+, and Na+ concentrations in mitochondrial matrix cells. Extensions of this model have been used to study the mechanisms of oxidative stress.72,73C.F. Currie, on the horizons of bioenergistics, the 1972 law-phosphorilation first described more than 30 years ago, has been the subject of a biochemistry historian. Our interest in the subject was stimulated by 3 papers by Herman Kalckar that appeared between 1937 - 1939, because then I learned another reaction which causes the absorption of phosphate into the amorgeny - the phosphor reaction. We confirmed Kalkar's findings that kidney extract without oxidative cells required the absorption of disorganized phosphate and we did a component analysis of the phosphor system. Later Colwick, Kalker and I joined forces and did more detailed research on cell-free preparations of heart, brain and liver. Meanwhile Ochoa, who has previously shown that oxidation of pyruvate in brain extracts gave P:O Ratio of 2, arrived at the lab in St. Louis. I mention these facts because the question arises as to why, having identified the importance of the problem, none of us have continued for a very long time to work on this issue. On my own behalf, I felt that solving the problem was far away and also that with limited resources available we needed to put our primary effort into the study of phosphorus. Phosphorus.

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