Oxidative phosphorylation cellular respiration

Mitochondria, which are cytoplasmic organelles involved in cellular respiration, have their own chromosome, which contains 16,569 DNA base pairs (bp) arranged in a drcalar molecule. This DNA encodes 13 proteins that are subunits of complexes in the electron transport and oxidative phosphorylation processes (see Section 1, Chapter 13). In addition, mitochondrial DNA encodes 22 transfer RNAs and two ribosomal RNAs. 

Kalckar, who showed that aerobic cells make ATP from ADP and Pj by a process that depends on respiration. At that time it was unclear that this oxidative phosphorylation occurred in mitochondria or that it involved NADH. Resolution of these questions had to await development of methods for preparing mitochondria free of other cellular constituents, and for presenting NADH on the matrix side of the inner membrane. When these methods were devised in... 

Figure 17.3. Cellular Respiration. The citric acid cycle constitutes the first stage in cellular respiration, the removal of high-energy electrons from carbon fuels (left). These electrons reduce O2 to generate a proton gradient (middle), which is used to synthesize ATP (right). The reduction of O2 and the synthesis of ATP constitute oxidative phosphorylation.

Oxidative phosphorylation is the culmination of a series of energy transformations that are called cellular respiration or simply respiration in their entirety. First, carbon fuels are oxidized in the citric acid cycle to yield electrons with high transfer potential. Then, this electron-motive force is converted into a proton-motive force and, finally, the proton-motive force is converted into phosphoryl transfer potential. The conversion of electron-motive force into proton-motive force is carried out by three electron-driven proton pumps—NADH-Q oxidoreductase, Q-cytochrome c oxidoreductase, and... 

Observable phytotoxic actions of propham and chlorpropham on the intact plant are the inhibition of root and epicotyl growth and reduction of transpiration and respiration. Symptoms found at the cellular level are absence of spindle development abnormal root cell growth inhibition of messenger RNA, protein and amylase synthesis and inhibition of photosynthesis and oxidative phosphorylation (Ennis, 1948 Moreland and Hill, 1959). 

It is well established that Q is a component of the respiratory chain and plays a critical role in respiration and oxidative phosphorylation. It was thought that the presence of (X was confined exclusively to the inner mitochondrial membrane and its sole function was to serve as the redox component of the respiratory chain. However, this belief has been modified as it has been shown that Q is present in all cellular membranes examined. The major part of Q is present in the reduced form in human and animal tissues, and serves as an important antioxidant. In fact, it has been shown that QH2-IO, the reduced form of Q IO, efficiently scavenges free radicals and it is as effective as ct-tocopherol in preventing peroxidative damage to lipids, considered the best lipid-soluble antioxidant in humans. The antioxidant and prooxidant properties of mitochondrial ubiquinone have recently been reviewed. ... 

In phase 2 of cellular respiration, the energy derived from fuel oxidation is converted to the high-energy phosphate bonds of ATP by the process of oxidative phosphorylation (see Fig. 2). Electrons are transferred from NADH and FAD(2H) to O2 by the electron transport chain, a series of electron transfer proteins that are located in the inner mitochondrial membrane. Oxidation of NADH and FAD(2H) by O2 generates an electrochemical potential across the inner mitochondrial membrane in the form of a transmembrane proton gradient (Ap). This electrochemical potential drives the synthesis of ATP form ADP and Pi by a transmembrane enzyme called ATP synthase (or FoFjATPase). 

Because of the role of mitochondria in cellular respiration and energy production, efforts to elucidate the mechanism of thyroid hormone action in metabolism and calorigenesis have focused on mitochondrial studies. Thyroid hormones in vitro are known to uncouple oxidative phosphorylation in isolated mitochondria, but these effects occur at unphysiological doses of T4. In physiological concentrations, T4 increases adenosine triphosphate (ATP) formation and the number and inner membrane surface area of mitochondria (21), but T4 does not reduce the efficiency of oxidative phosphorylation. Furthermore, 2,4-dinitrophenol, a classic uncoupler of oxidative phosphorylation, can neither relieve hypothyroidism nor duplicate other physiological effects of thyroid hormones. 

Van der Meer et al. [59] have described the regulation of mitochondrial respiration on the basis of the principles of irreversible thermodynamics. According to these authors, and thus in contrast to the view of Holian et al. [53], the entire system of oxidative phosphorylation in the hepatocyte is displaced from equilibrium. They observed a linear relationship between the rate of oxygen consumption and the affinity of the entire oxidative pho.sphorylation system, a term which includes the cytosolic phosphate potential, the mitochondrial NADH/NAD ratio and the partial pressure of oxygen. They concluded that the adenine nucleotide translocator may be a rate-limiting step in cellular oxidative phosphorylation. 

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