Mitochondrial oxidation of

Insects poisoned with rotenone exhibit a steady decline ia oxygen consumption and the iasecticide has been shown to have a specific action ia interfering with the electron transport iavolved ia the oxidation of reduced nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD) by cytochrome b. Poisoning, therefore, inhibits the mitochondrial oxidation of Krebs-cycle iatermediates which is catalysed by NAD. 

Note The.se P/O ratios of 2.5 and 1.5 for mitochondrial oxidation of NADH and [FADHg] are consen.sns values. Because diey may not reflect actual values and because these ratios may change depending on metabolic conditions, the.se estimates of ATP yield from glucose oxidation are approximate. 

Senior, A.E. Shenatt, H.S.A. (1968). Biochemical effects of the hypoglycaemic compound pent-4-enoic acid and related non-hypoglycemic fatty acids. Oxidative phosphorylation and mitochondrial oxidation of pyruvate, 3-hydroxybutyrate and tricarboxylic acid-cycle intermediates. Biochem. J. 110,499-509. 

Biguanides such as metformin are thought to inhibit mitochondrial oxidation of lactic acid, thereby increasing the chance of lactic acidosis occurring. Fortunately, the incidence of lactic acidosis in clinical practice is rare. Patients at greatest risk for developing lactic acidosis include those with liver disease or heavy alcohol use, severe infection, heart failure, and shock. Thus, it is common practice to evaluate liver function prior to initiation of metformin. 

Xanthothricin 308 stimulated oxidation of NADH and NAD-linked substrates by rat liver mitochondria, yeast mitochondria, and Ehrlich ascites tumor cells (74MI1, 74MI3). It also stimulated mitochondrial oxidation of succinate, pyruvate, or malate. The antibiotic xanthothricin was obtained... 

Tsai, Su-Chen, Steinberg, D., Avigan, J., Fales, H. M. Studies on the stereospecificity of mitochondrial oxidation of phytanic acid and of a-hydroxyphytanic acid. J. Biol. Chem. 248, 1091-1097 (1973). 

Amino-4-cyclopropylidenebutanoic acid (2S)-56, is a methylenecyclopro-pane substituted alanine which can be considered as a non-natural isomer of hypoglycine A 51. It has recently been synthesized racemic [61] and enantiome-rically pure [62]. Biological assays have shown that at relatively high concentration the 5,6-methanoamino acid 56 inhibits the metabolism of pyruvate into glucose, but 56 is not active in inducing the mitochondrial oxidation of fatty acids,Eq. (21) [63]. 

Decreased metabolism of lipids. Decreased mitochondrial oxidation of fatty acids is another possible cause of ethanol-induced steatosis. Other possible causes are vitamin deficiencies and the inhibition of the mitochondrial electron transport chain. 

Antiretroviral nucleoside analogues have been associated with hepatic steatosis and lactic acidosis. These compounds require phosphorylation to active triphosphate derivatives by cellular phosphokinases. The triphosphate nucleotide inhibits the growing proviral DNA chain, but it also inhibits host DNA polymerases, and this can result in compensatory glycolysis and lactic acidosis. Abnormal mitochondrial oxidation of free fatty acids causes the accumulation of neutral fat in liver cells, and this manifests as hepatomegaly with macrovesicular steatosis. Hepatic steatosis and lactic acidosis have been reported previously with zidovudine, didanosine, zalcita-bine, Combivir (zidovudine plus lamivudine), and lamivudine. Of 349 Australian patients studied for 18 months (516 patient-years) taking NRTIs only two had severe lactic acidosis (847). 

Ramsay RR, Salach JI, Singer TP (1986) Uptake of the neurotoxin l-methyl-4-phenylpyridine (MPP+) by mitochondria and its relation to the inhibition of the mitochondrial oxidation of NAD+-linked substrates by MPP+. Biochem Biophys Res Commun 134 743-748. 

The GTP formed as described above yields ATP [via nucleoside diphosphokinase]. The reduced coenzymes (4 NADH and FADH2) feed electrons into the mitochondrial electron transport chain (ETC) to yield 14 ATP per pyruvate oxidized (12 ATP/4 NADH and 2 ATP/FADH2) through the process of oxidative phosphorylation as described in Section 13.5. This total yield of ATP corresponds to a total of 32 ATP per glucose oxidized plus a further 6 ATP from mitochondrial oxidation of NADH generated in glycolysis, that is, 38 ATP per glucose oxidized. 

P-Oxidation mitochondrial oxidation of fatty acids--> Energy ... 

The biosynthetic reactions involve a series of condensation processes and are distributed between cytosol and microsomes. All of the carbons of cholesterol are derived from acetyl-CoA, 15 from the methyl and 12 from the carboxyl carbon atoms. Acetyl-CoA is derived from mitochondrial oxidation of metabolic fuels (e.g., fatty acids) and transported to cytosol as citrate (Chapter 18) or by activation of acetate (e.g., derived from ethanol oxidation) by cytosolic acetyl-CoA synthase (Chapter 18). All of the reducing equivalents are provided by NADPH. 

Urea formation is energetically expensive, requiring the expenditure of 4 mol of ATP per mole of urea formed. However, NADH is produced when fumarate is reconverted to aspartate. How many ATP molecules are produced by the mitochondrial oxidation of the NADH What is the net ATP requirement for urea synthesis ... 

In plants, stored carbohydrates, mostly in the form of starch, are hydrolyzed to glucose. Glycolysis then produces pyruvate, which is transported into mitochondria, as in animal cells. Mitochondrial oxidation of pyruvate and concomitant formation of ATP occur in photosynthetic cells during dark periods when photosynthesis is not possible, and in roots and other nonphotosynthetlc tissues all the time. I... 

Mitochondrial Oxidation of Fatty Acids Is Coupled to ATP Formation... 

Mitochondrial oxidation of fatty acids is the major source of ATP in mammalian liver cells, and biochemists at one time believed this was true in all cell types. However, rats treated with doflbrate, a drug used to reduce the level of blood lipoproteins, were found to exhibit an increased rate of fatty acid oxidation and a large Increase in the number of peroxisomes in their liver cells. This finding suggested that peroxisomes, as well as mitochondria, can oxidize fatty acids. These small organelles, =0.2-1 pm in diameter, are lined by a single membrane (see Figure 5-21). They are present in all... 

In this section we first discuss the magnitude of the proton-motive force, then the components of the respiratory chain and the pumping of protons across the inner membrane. In the following section we describe the structure of the ATP synthase and how It uses the proton-motive force to synthesize ATP. We also consider how mitochondrial oxidation of NADH and FADH2 Is controlled to meet the cell s need for ATP. 

Continued mitochondrial oxidation of NADH and the reduction of O2 are dependent on sufficient ADP being present. This phenomenon, termed respiratory control, is an Important mechanism for coordinating oxidation and ATP synthesis in mitochondria. 

Fenaminosulf reduces respiration in sensitive fungi. Thus, it inhibits the mitochondrial oxidation of nicotinamide adenine dinucleotide (NADH) in Pythium (Tolmsoff, 1962). On the other hand, in nonsensitive fungi (Rhizoctonia solani) a reductase has been identified which decomposes the active substance. But... 

With this in mind, the balanced equation for the mitochondrial oxidation of NADH is as follows ... 

Problem 22.69. True or false In the mitochondrial oxidation of fatty acids, the hydration of the enoyl-CoA derivative results in the chiral o-hydroxy derivative. 

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