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Mitochondrial electron transporter

Hydramethylnon [67485-29-4] is tetrabydro-5,5-dimetbyl-2-(1 H)-pyrimidinone [bis-l,5-(4-trifluoromethylphenyl)-3-penta-l,4-dienylidene] hydrazone (152) (mp 189°C). It is a slow-acting stomach poison used in baits and traps to control ants and cockroaches. Its mode of action is inhibition of mitochondrial electron transport. [Pg.297]

The decline in immune function may pardy depend on a deficiency of coenzyme Q, a group of closely related quinone compounds (ubiquinones) that participate in the mitochondrial electron transport chain (49). Concentrations of coenzyme Q (specifically coenzyme Q q) appear to decline with age in several organs, most notably the thymus. [Pg.431]

FIGURE 21.3 % J and % values for the components of the mitochondrial electron transport chain. Values indicated are consensus values for animal mitochondria. Black bars represent %r red bars,. ... [Pg.679]

Protein Complexes of the Mitochondrial Electron-Transport Cham ... [Pg.681]

What Is the P/O Ratio for Mitochondrial Electron Transport and Oxidative Phosphorylation ... [Pg.702]

When induced in macrophages, iNOS produces large amounts of NO which represents a major cytotoxic principle of those cells. Due to its affinity to protein-bound iron, NO can inhibit a number of key enzymes that contain iron in their catalytic centers. These include ribonucleotide reductase (rate-limiting in DNA replication), iron-sulfur cluster-dependent enzymes (complex I and II) involved in mitochondrial electron transport and cis-aconitase in the citric acid cycle. In addition, higher concentrations of NO,... [Pg.863]

The Stoichiometry of Proton Pumping by the Mitochondrial Electron-Transport Chain 129... [Pg.107]

Polymorphonuclear leucocytes (PMNs) employ a system comprising myeloperoxidase, hydrogen peroxide, and a halide factor to kill microorganisms and tumour cells. This process is sometimes loosely called the respiratory burst , which refers to the sudden rise in oxygen consumption by the phagocytosing neutrophils that is independent of the mitochondrial electron transport chain. [Pg.193]

Other enzyme systems may also be directly or indirectly involved in the generation of ROS in the lung, including those of the eicosanoid pathway, the mitochondrial electron transport system, and aldehyde, glucose and xanthine oxidases (Parks and Granger, 1986). These systems may also be relevant to lung damage. For example, the oedematous pulmonary injury that results from cessation of blood flow for a period followed by reinstatement of... [Pg.216]

Ubiquinones (coenzymes Q) Q9 and Qi0 are essential cofactors (electron carriers) in the mitochondrial electron transport chain. They play a key role shuttling electrons from NADH and succinate dehydrogenases to the cytochrome b-c1 complex in the inner mitochondrial membrane. Ubiquinones are lipid-soluble compounds containing a redox active quinoid ring and a tail of 50 (Qio) or 45 (Q9) carbon atoms (Figure 29.10). The predominant ubiquinone in humans is Qio while in rodents it is Q9. Ubiquinones are especially abundant in the mitochondrial respiratory chain where their concentration is about 100 times higher than that of other electron carriers. Ubihydroquinone Q10 is also found in LDL where it supposedly exhibits the antioxidant activity (see Chapter 23). [Pg.877]

Mitochondria, nitric oxide synthase and arachidonic acid metabolism are sources of reactive oxygen species during ischemia-reperfusion injury. ROS generation during ischemia-reperfusion may come from several sources, including NOS activity, mitochondrial electron transport, multiple steps in the metabolism of arachidonic... [Pg.568]

FIGURE 32-7 Sources of free radical formation which may contribute to injury during ischemia-reperfusion. Nitric oxide synthase, the mitochondrial electron-transport chain and metabolism of arachidonic acid are among the likely contributors. CaM, calcium/calmodulin FAD, flavin adenine dinucleotide FMN, flavin mononucleotide HtT, tetrahydrobiopterin HETES, hydroxyeicosatetraenoic acids L, lipid alkoxyl radical LOO, lipid peroxyl radical NO, nitric oxide 0 "2, superoxide radical. [Pg.569]

Figure 5.17 The mitochondrial electron-transport chain. (From Voet and Voet, 2004. Reproduced with permission from John Wiley Sons., Inc.)... Figure 5.17 The mitochondrial electron-transport chain. (From Voet and Voet, 2004. Reproduced with permission from John Wiley Sons., Inc.)...
The desaturation process is particularly interesting as it provides an example of a microsomal (as opposed to mitochondrial) electron transport system. The enzymes responsible, fatty acyl-CoA desaturases, are examples of mixed function oxidases... [Pg.184]

Schulze-Osthoff, K., Beyaer, R., Vandevoorde, V., Haegeman, G.,and Fiers, W., 1993, Depletion of the mitochondrial electron transport abrogates the cytotoxic and gene inductive effects of TNF, MBO/. 12 3095-... [Pg.16]

NADH reoxidized by mitochondrial electron transport chain... [Pg.175]


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