Electron transport pathway

FIGURE 21.6 Proposed structure and electron transport pathway for Complex I. 

FIGURE 21.21 A model for the electron transport pathway in the mitochondrial inner membrane. UQ/UQH9 and cytochrome e are mobile electron carriers and function by transferring electrons between the complexes. The proton transport driven by Complexes I, III, and IV is indicated. 

Mitchell s chemiosmotic hypothesis. The ratio of protons transported per pair of electrons passed through the chain—the so-called HV2 e ratio—has been an object of great interest for many years. Nevertheless, the ratio has remained extremely difficult to determine. The consensus estimate for the electron transport pathway from succinate to Og is 6 H /2 e. The ratio for Complex I by itself remains uncertain, but recent best estimates place it as high as 4 H /2 e. On the basis of this value, the stoichiometry of transport for the pathway from NADH to O2 is 10 H /2 e. Although this is the value assumed in Figure 21.21, it is important to realize that this represents a consensus drawn from many experiments. 

Consider the oxidation of succinate by molecular oxygen as carried out via the electron transport pathway... 

Write a balanced equation for the reduction of molecular oxygen by reduced cytochrome e as carried out by complex IV (cytochrome oxidase) of the electron transport pathway. 

The third reaction of this cycle is the oxidation of the hydroxyl group at the /3-position to produce a /3-ketoacyl-CoA derivative. This second oxidation reaction is catalyzed by L-hydroxyacyl-CoA dehydrogenase, an enzyme that requires NAD as a coenzyme. NADH produced in this reaction represents metabolic energy. Each NADH produced in mitochondria by this reaction drives the synthesis of 2.5 molecules of ATP in the electron transport pathway. L-Hydroxyacyl-... 

A hypothesis for the oxidation of purines in the presence of this enzyme has been elaborated by Bergmann and his colleagues. It postulates that the purine, often in one of its less prevalent tautomeric forms, is adsorbed on the protein, or the riboflavin coenzyme, of the enzyme then hydration occurs under the influence of the electronic field of the enz5rme, and this must involve a group that is not sterically blocked by the enzyme but which is accessible to the electron-transport pathway of the riboflavin moiety. Finally, the secondary alcohol is assumed to be dehydrogenated in this pathway to give a doubly... 

Fig. 1. Proposed electron transport pathway in D. gigas NiFe-hydrogenase. Selected distances are given in angstroms. Modified with permission from Ref. (157).

Electron-Transport Pathway Linked to the Use of CO2 as a Terminal Electron Acceptor in Acetogens... 

Figure 14.1. Proposed electron-transport pathway in the acetogenic bacteria M. thermoacetica and M. thermoautotrophica. Cyt., cytochrome MTi/FD//, methylene tetrahydrofolate dehydrogenase Fd, ferredoxin Fp, flavoprotein H2ase, hydrogenase.

Electron-Transport Pathway Linked to Use of Nitrate, DMSO, and Thiosulfate as Terminal Acceptors... 

III (column 3 versus column 5), inhibition of the uncoupled electron transport rate was only partially relieved. Thus, the compounds appear to have two effects (a) the more sensitive is an effect on the ATP-generatlng pathway and (b) a second, but weaker, effect involved the electron-transport pathway. 

Comparative responses obtained with quercetin and narlngenin are shown in Traces D and E, respectively. Quercetin and narlngenin, at concentrations that completely inhibited photophosphorylation, inhibited the ADP-stimulated rate of 0 utilization 70 and 82%, respectively. FCCP restored the rate to 12 and 42% of the original rate for quercetin and narlngenin, respectively. The failure to obtain complete recovery can be attributed to interference with a component of the electron-transport pathway, at these same concentrations, as evidenced by data presented in Table II. Similar results were obtained with the remainder of the representative compounds. The results reinforce the postulate that the primary effect Imposed by the allelochemlcals on thylakolds is energy transfer inhibition with a secondary effect imposed on the electron-transport pathway. 

Partial reactions. Through the use of various electron donors and acceptors, it is possible to bracket specific sites on the electron-transport pathway associated with the action of inhibitors (23-25). Attempts to identify the slte(s) of interaction of the allelochemlcals on the electron-transport pathway were generally... 

Results obtained from the partial reactions, chlorophyll fluorescence, and binding studies did not provide any clues relative to interactive sites on the electron-transport pathway for the allelochemicals. No evidence was obtained to specifically implicate Interference with the protein of PS II. Additionally, insofar as they could be analyzed, none of the allelochemicals affected PS I-associated electron transport between the site of donation by DPIPH and acceptance by methyl vlologen. 

In the studies with Isolated chloroplasts and thylakolds, the primary effect of the phenolic allelochemlcals was on the ATP-generating pathway, i.e., energy transfer inhibition. The compounds acted on the electron-transport pathway at higher concentrations, but the exact slte(s) remain to be identified. These may be located on the oxidizing side of PS II or around the PQ pool. The sites are not associated with PS I. The compounds did not act as uncouplers. 

When little NADP+ is available to accept electrons, an alternative electron transport pathway is used. The high-energy electron donated by photosystem I passes to ferredoxin, then the cytochrome bf complex, then plastocyanin and back to the P700 of photosystem I. The resulting proton gradient generated by the cytochrome bf complex drives ATP synthesis (cyclic photophosphorylation) but no NADPH is made and no 02 is produced. 

A full comprehension of the specific sites involved in the inhibitory action of herbicides and the mechanisms through which inhibition is produced will be achieved only when the uncertainties associated with the sequence and interrelation of components in the electron transport pathway, the numbers and locations of phosphorylation sites, and the mechanism of phosphorylation have been resolved. 

Electron Acceptors. Compounds classified as electron acceptors can compete with some component of the electron transport pathway and subsequently be reduced. Ferricyanide, PMS, and FMN, which are used to study partial reactions of the photochemical pathway, operate in this manner. However, they are not phy-totoxic. 

The thermogenic mechanism best understood in plants is a cyanide-insensitive nonpho-sphorylating electron transport pathway that is found only in plant mitochondria (Raskin et al., 1987). This pathway is distinct from the electron transport pathway involved in mitochondrial ATP production, and is under the control of calorigens, molecules that can lead to a... 

Thermogenic systems based on uncoupling proteins or on the alternative electron transport pathways found in mitochondria of certain plants represent what in many ways is the sim-... 

Several types of effects are ascribed to thyroid hormones. T3 and T4 control heat production in the organism by affecting the electron transport pathway (see Chapter 17). Apparently these hormones stimulate electron transport, thereby producing more ATP. The latter is used to increase the activity of Na+/K+ pumps throughout the organism, in the process of which ATP is hydrolyzed and heat... 

Several inherited disorders are associated with faulty operation of the electron transport pathway. ATP production is diminished in such cases. These disorders are known as mitochondrial myopathies, and they are associated with the absence of specific polypeptide chains found in complexes I, III, or IV. In many cases, the problem may be traced to specific lesions in mitochondrial DNA, which codes for at least 13 polypeptide chains found in these complexes. Myopathies are tissue specific some affect the heart, others the skeletal muscle. Many are accompanied by lactic acidosis, because the inability to reduce NADH normally results in its accumulation and the channeling of pyruvate toward lactic acid production. In complex I disorders, the oxidation of FADH2 is not impeded. In complex III lesions, neither NADH nor FADH2 can be oxidized. However, use has been made by B. Chance and colleagues of menadione (Chapter 6) and ascorbic acid in such cases. The former can oxidize UQH2, whereas ascorbate can oxidize menadione and reduce cytochrome c. Marked clinical improvement in affected patients follows such treatment. 

Fig. 1. Abbreviated Z-scheme for the light reactions of oxygenic photosynthesis showing electron transport pathways to carbon fixation and hydrogen production.

The system depends on an electron transport pathway that transfers electrons from NADPH through a flavoprotein (NADPH cytochrome P-450 reductase) to cytochrome P-450 that is the terminal oxidase of the chain (10). The xenobiotic first forms a complex with the oxidized form o cytochrome P-450 which is reduced by an electron passing down the chain from NADPH. The reduced cytochrome P-450/substrate complex then reacts with and activates molecular oxygen to an electrophilic oxene species (an electron deficient species similar to singlet oxygen) that is transferred to the substrate with the concommitant formation of water. Cytochrome P-450 thus acts primarily as an oxene transferase (2). Substrate binding is a relatively nonspecific, passive process that serves to bring the xenobiotic into close association with the active center and provide the opportunity for the oxene transfer to occur. 

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