ATPase mitochondrial

Although iron-sulfur proteins are found in various cellular localizations in eukaryotic cells, mitochondria are the major site of Fe-S cluster biosynthesis (Lill et ah, 1999). Deletions in nuclear genes involved in mitochondrial iron-sulfur cluster formation lead to massive accumulation of iron in mitochondria (Chapter 7). For example, deletion of ATM1, a mitochondrial ATPase, which seems to be responsible for the export of Fe-S clusters, leads to respiratory incompetence, excessive iron accumulation and leucine auxotrophy (Kispal et ah, 1999). In Ayfhl cells there is only partial loss of mitochondrial Fe-S enzymes and the cells are not leucine auxotrophs. 

Mitochondrial ATPase inhibition. Smoke extract, in the mouse brain mitochondria culture in the presence or absence of vitamin C for 60 minutes, inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner. The effect of extract on mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. The extract treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane was preserved. Nicotine produced no significant damage . Mitogenic activity. Water extract of the dried leaf, administered to mice at a concentration of 0.05%, was active on lymphocytes from mesenteric lymph node and lymphocytes B and T. Intracellular Ca level was unchanged. The extract was active on... 

Flavonoids are known to inhibit the function of many ATP-binding proteins, such as mitochondrial ATPase, myosin, Na/K and Ca plasma membrane ATPases, protein kinases, topoisomerase II, and multidrug resistance (MDR) proteins. In general, inhibition takes place through binding of the flavonoids to the ATP-binding site. Only two cases relevant to the inhibition of carcinogenesis by flavonoids" " will be discussed in detail. 

Peripheral Mitochondrial ATPase, alkaline phosphatase Readily solubilized by detergents... 

Flavonoids can affect the function of plasma membrane transport Na+- and K+-ATPase, mitochondrial ATPase, and Ca2+-ATPase. The Mg2+-ectoATPase of human leukocytes is inhibited by quercetin, which acts as a competitor of ATP binding to the enzyme. The sarcoplasmic reticulum Ca2+-ATPase of muscle is effectively inhibited by several flavonoids that were also active inhibitors of antigen-induced mast cell histamine release. 

M4. Manfredi, G., Gupta, N., Vazquez-Memije, M. E., Sadlock, J. E., Spinazzola, A., De Vivo, D. C., and Schon, E. A., Oligomycin induces a decrease in the cellular content of a pathogenic mutation in the human mitochondrial ATPase 6 gene. J. Biol. Chem. 274, 9386-9391 (1999). 

M21. Miiller-Hocker, J., Stiinkel, S., Pongratz, D., and Hiibner, G., Focal deficiency of cytochrome-c-oxidase and of mitochondrial ATPase combined with loosely coupled oxidative phosphorylation in the skeletal muscle of a patient with progressive external ophthalmoplegia An enzyme histochemical, immunocytochemical and fine structure study. J. Neurol. Sci. 69, 27-36 (1985). 

Rouslin, W. (1991). Regulation of the mitochondrial ATPase in situ in cardiac muscle role of the inhibitor subunit. J. Bioenerg. Biomembr. 23 873-888. 

Efrapeptins such as efrapeptin D (24 in Figure 5) were isolated from the entomopathogenic fungus Tolypocladium niveum. They have a unique linear peptide structure with a bicyclic amine moiety at their C-terminus and show insect toxicity by inhibiting mitochondrial ATPase.7... 

Many metabolic processes such as glycolysis, Krebs cycle reactions, photosynthesis, protein synthesis, and lipid metabolism are affected by exposure to F. Much of the action of F on these processes can be attributed to F-dependent inhibition of enzymes. Examples of enzymes shown to be inhibited by F include enolase, phosphoglucomutase, phosphatase, hexokinase, PEP carboxylase, pyruvate kinase, succinic dehydrogenase, malic dehydrogenase, pyrophosphatase, phytase, nitrate reductase, mitochondrial ATPase, urease (Miller et al. 1983), lipase (Yu et al. 1987), amylase (Yu et al. 1988), invertase (Yu 1996 Ouchi et al. 1999), and superoxide dismutase (SOD) (Wilde and Yu 1998). 

Akagi M, Inui K, Tsukamoto H, Sakai N, Muramatsu T, Yamaha M, et al. A point mutation of mitochondrial ATPase 6 gene in Leigh syndrome. Neuromus Dis 2002 12 53-5. 

Zhang, X. and Moye-Rowley, W.S. (2001) Saccharomyces cerevisiae multidrug resistance gene expression inversely correlates with the status of the F(0) component of the mitochondrial ATPase. The Journal of Biological Chemistry, 276, 47844—47852. 

Blocking of the proton gradient between NADH-Q reductase and QH2 Blocking of the proton gradient between cytochrome Cj and cytochrome c Dissociating of cytochrome c from mitochondrial membranes Inhibiting of mitochondrial ATPase (ATP synthase)... 

The answer is d. (Murray, pp 123-148. Scriver, pp 2367-2424. Sack, pp 159-175. Wilson, pp 287-317.) Oligomycin inhibits mitochondrial ATPase and thus prevents phosphorylation of ADP to ATP It prevents utilization of energy derived from electron transport for the synthesis of ATP Oligomycin has no effect on coupling but blocks mitochondrial phosphorylation so that both oxidation and phosphorylation cease in its presence. 

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