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Oxidation metabolic

Physiological Role of Citric Acid. Citric acid occurs ia the terminal oxidative metabolic system of virtually all organisms. This oxidative metabohc system (Fig. 2), variously called the Krebs cycle (for its discoverer, H. A. Krebs), the tricarboxyUc acid cycle, or the citric acid cycle, is a metaboHc cycle involving the conversion of carbohydrates, fats, or proteins to carbon dioxide and water. This cycle releases energy necessary for an organism s growth, movement, luminescence, chemosynthesis, and reproduction. The cycle also provides the carbon-containing materials from which cells synthesize amino acids and fats. Many yeasts, molds, and bacteria conduct the citric acid cycle, and can be selected for thek abiUty to maximize citric acid production in the process. This is the basis for the efficient commercial fermentation processes used today to produce citric acid. [Pg.182]

Hurst (19) discusses the similarity in action of the pyrethrins and of DDT as indicated by a dispersant action on the lipids of insect cuticle and internal tissue. He has developed an elaborate theory of contact insecticidal action but provides no experimental data. Hurst believes that the susceptibility to insecticides depends partially on the cuticular permeability, but more fundamentally on the effects on internal tissue receptors which control oxidative metabolism or oxidative enzyme systems. The access of pyrethrins to insects, for example, is facilitated by adsorption and storage in the lipophilic layers of the epicuticle. The epicuticle is to be regarded as a lipoprotein mosaic consisting of alternating patches of lipid and protein receptors which are sites of oxidase activity. Such a condition exists in both the hydrophilic type of cuticle found in larvae of Calliphora and Phormia and in the waxy cuticle of Tenebrio larvae. Hurst explains pyrethrinization as a preliminary narcosis or knockdown phase in which oxidase action is blocked by adsorption of the insecticide on the lipoprotein tissue components, followed by death when further dispersant action of the insecticide results in an irreversible increase in the phenoloxidase activity as a result of the displacement of protective lipids. This increase in phenoloxidase activity is accompanied by the accumulation of toxic quinoid metabolites in the blood and tissues—for example, O-quinones which would block substrate access to normal enzyme systems. The varying degrees of susceptibility shown by different insect species to an insecticide may be explainable not only in terms of differences in cuticle make-up but also as internal factors associated with the stability of oxidase systems. [Pg.49]

Neuromelanin, a dark colored pigment and product of the oxidative metabolism of dopamine, is found in the cytoplasm of dopaminergic neurons of the human substantia nigra pars compacta. Neuromelanin deposits increase with age, matching the age distribution of Parkinson s disease. In the absence of significant quantities of iron, neuromelanin can act as an antioxidant in... [Pg.164]

Chance, B., Leigh, J.S., Kent, J., McCully, K., Nioka, S., Clark, B.J., Marris, J.M., Graham, T. (1986). Multiple controls of oxidative metabolism in living tissues as studied by phosphorous magnetic resonance. Proc. Natl. Acad. Sci. USA 83,9458-9462. [Pg.151]

Histopathological examination shows the typical corelike lesions in a high proportion of muscle fibers in older patients this may amount to 100%. Most typically the cores are large and centrally-placed, but multiple cores may occur in the same fiber cross section. Most older patients show a striking predominance of type 1 (slow twitch oxidative) fibers and virtually all fibers with cores are type 1. Sometimes younger family members have more normal proportions of type 1 and type 2 fibers but, again, the cores are confined to the type 1 fibers. It is well established that muscle fiber types can interconvert due to altered physiological demands, and it is likely that fibers with cores convert to a basically slow twitch-oxidative metabolism to compensate for the fact that up to 50% of their cross sectional area may be devoid of mitochondria. [Pg.292]

Petursson H, Lader MH Benzodiazepine dependence. BrJ Addict 76 133—143,1981a Petursson H, Lader MH Withdrawal from long-term benzodiazepine treatment. Br Med J (Clin Res Ed) 283 643—643, 1981b Pichard L, Gillet G, Bonfils C, et al Oxidative metabolism of zolpidem by human liver... [Pg.158]

Certain anaerobic bacteria can reductively dechlorinate PCBs in sediments (EHC 140). Higher chlorinated PCBs are degraded more rapidly than lower chlorinated ones, which is in contrast to the trend for oxidative metabolism described earlier. Genetically engineered strains of bacteria have been developed to degrade PCBs in bioremediation programs. [Pg.140]

It appears that organisms at the top of aquatic food chains are not exposed to substantial levels of PAH in food because of the detoxifying capacity of organisms beneath them in the food chain. On the other hand, fish, birds, and aquatic mammals feeding on mollusks and other invertebrates are in a different position. Their food may contain substantial levels of PAH. Although they can achieve rapid metabolism of dietary PAH, it should be remembered that oxidative metabolism causes... [Pg.186]

The major biochemical features of neutrophils are summarized in Table 52-8. Prominent feamres are active aerobic glycolysis, active pentose phosphate pathway, moderately active oxidative phosphorylation (because mitochondria are relatively sparse), and a high content of lysosomal enzymes. Many of the enzymes listed in Table 52-4 are also of importance in the oxidative metabolism of neutrophils (see below). Table 52-9 summarizes the functions of some proteins that are relatively unique to neutrophils. [Pg.620]

With modest impairment of blood flow, this mechanism allows for preservation of oxidative metabolism without alteration in electrical function. However, when CPP and therefore CBF are sufficiently low, OEF reaches a maximum and cannot increase further. Brain tissue ceases to function electrically, resulting in a neurologic deficit. Microvascular collapse occurs, and CBV falls. If the oxygen supply falls low enough, the tissue dies. Of critical clinical importance is the observation that the amount of time it takes for tissue to suffer irreversible damage is inversely related to the severity of the ischemic insult. Tissue that is completely deprived of blood will die within a few minutes, but less severely hypoperfused tissue may survive for many hours, and may be saved by timely thrombolysis that restores perfusion, or perhaps by another therapeutic intervention. [Pg.17]

Keizer J, G d Agostino, R Nagel, F Gramenzi, L Vittozzi (1993) Comparative diazinon toxicity in guppy and zebra fish different role of oxidative metabolism. Environ Toxicol Chem 12 1243-1250. [Pg.101]

Shang TQ, SL Doty, AM Wilson, WN Howald, MP Goprdon (2001) Trichloroethylene oxidative metabolism in plants the trichloroethanol pathway. Phytochemistry 58 1055-1065. [Pg.102]

Nagata K, H Yu, M Nishikawa, M Kashiba, A Nakamura, EE Sato, T Tamura, M Inoue (1998) Helicobacter pylori generates superoxide radicals and modulates nitric oxide metabolism. J Biol Chem 273 14071-14073. [Pg.160]

Bartnicki EW, CE Castro (1994) Biodehalogenation rapid oxidative metabolism of mono- and polyhalometh-anes by Methylosinus trichosporium OB-3b. Environ Toxicol Chem 13 241-245. [Pg.370]

FIGU RE 8.1 Alternative pathways for the oxidative metabolism of naphthalene by (a) bacteria and (b) fungi. [Pg.386]

Evans WC, HN Fernley, E Griffiths (1965) Oxidative metabolism of phenanthrene and anthracene by soil pseudomonads. The ring-fission mechanism. Biochem J 95 819-831. [Pg.419]

Phenols also constitute a major source of xenobiotic exposure to the body in the form of drugs and environmental pollutants. Oxidative metabolism of these compounds can lead to physiological damage, therefore the metabolism of these compounds is of great interest. LCEC has been a powerful tool for investigating the metabolism of aromatic compounds by the cytochrome P-450 system LCEC... [Pg.25]


See other pages where Oxidation metabolic is mentioned: [Pg.139]    [Pg.547]    [Pg.408]    [Pg.409]    [Pg.283]    [Pg.287]    [Pg.292]    [Pg.272]    [Pg.330]    [Pg.428]    [Pg.163]    [Pg.409]    [Pg.889]    [Pg.921]    [Pg.944]    [Pg.944]    [Pg.243]    [Pg.259]    [Pg.270]    [Pg.126]    [Pg.143]    [Pg.165]    [Pg.231]    [Pg.263]    [Pg.40]    [Pg.133]    [Pg.41]    [Pg.310]    [Pg.321]    [Pg.75]    [Pg.118]    [Pg.124]   
See also in sourсe #XX -- [ Pg.111 , Pg.263 ]

See also in sourсe #XX -- [ Pg.464 ]

See also in sourсe #XX -- [ Pg.282 ]




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1-Nitropyrene oxidative metabolism

ALCOHOL METABOLISM Utilized-Oxidized-Reduced

ALDEHYDE METABOLISM Utilized-Oxidized-Reduced

Acetylenes, oxidation metabolism

Aerobic oxidative metabolism

Allylic Oxidation and the Metabolism of Marijuana

Anandamide oxidative metabolism

Animal metabolism oxidative processes

Benzene, biological oxidation metabolism

Biosynthesis and Metabolism of Endothelium-Derived Nitric Oxide

CARBOHYDRATE METABOLISM Utilized-Oxidized-Reduced-Acid

Carcinogenicity, oxidative metabolism

Codeine oxidative metabolism

Drug disposition oxidative metabolism

Drug oxidation metabolic enzymes involved

Energetics oxidative metabolism

Energy metabolism oxidative phosphorylation

Fatty acid metabolism beta-oxidation

Fatty acids, metabolism oxidation

Galloyl esters, oxidative metabolism

Glycogen breakdown oxidative metabolism

Hypoxia oxidative metabolism

Lipid metabolism fatty acid oxidation

Lipid metabolism, oxidative transformations

Metabolic Syndrome oxidative stress

Metabolic capability, oxidative

Metabolic oxidation products

Metabolic oxidation reactions

Metabolism beta oxidation

Metabolism nitric oxide and

Metabolism oxidation-reduction reactions

Metabolism oxidative phosphorylation

Metabolism) mitochondrial oxidation disorder

Metabolism, principles oxidation

Metoprolol oxidative metabolism

Modulation of nitric oxide metabolism

NADPH-dependent oxidative metabolism

Nitric oxide metabolism

Nitroglycerine, nitric oxide metabolism

Oxidation as a metabolic energy source

Oxidation chlorinated hydrocarbon metabolism

Oxidation diazinon metabolism

Oxidation in metabolism

Oxidation intermediary metabolism

Oxidation metabolism

Oxidation metabolism

Oxidation organophosphates metabolism

Oxidation, drug metabolism

Oxidation-reduction reactions metabolic

Oxidative Metabolism (Catabolism)

Oxidative Metabolism of Purines

Oxidative and Glycolytic Metabolism

Oxidative drug metabolism

Oxidative metabolic detoxification

Oxidative metabolic oxidation

Oxidative metabolism

Oxidative metabolism

Oxidative metabolism of xenobiotic

Oxidative metabolism pyrethroid insecticides

Oxidative metabolism pyrethroids

Oxidative metabolism reactive species formation

Oxidative metabolism slowing down

Oxidative metabolism, mitochondrial disorder

Oxidative metabolites cyclooxygenase, metabolism

Oxidative polymorphism, poor extensive metabolizers

Oxidative reactions metabolic identification

Oxidative stress and metabolism

Oxidative, Reductive, and Hydrolytic Metabolism of Drugs

Purine oxidative metabolism

Retinol metabolism, oxidative

Tamoxifen oxidative metabolism

Teratogenicity, oxidative metabolism

Xenobiotic metabolism oxidation

Xenobiotic oxidative metabolism

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