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Cell respiration, inhibition

Inhibition of cytochromes of electron transport system can be caused by cyanogenic glycosides, such as amygdalin (Fig. 11.14) in bitter almonds, Prunus amygdalus, linamarin and lotaustralin in clover and birdsfoot trefoil, or dhurrin (Fig. 11.14) in Sorghum vulgare. The potent effect of cyanide on cell respiration has given rise to a recent serious conservation problem. In Southeast Asia, divers stun fish on coral reefs with a blast of cyanide to collect them for the aquarium trade. In the process, many fish are killed and the corals bleached, because their symbionts die (e.g. Payne, 2001). [Pg.291]

Rubbo, H., Denacola, A., and Radi, R. (1994). Peroxynitrite inactivates thiol-containing enzymes of Trypanosoma cruzi energetic metabolism and inhibits cell respiration. Arch. Biochem. Biophys. 308, 96-102. [Pg.80]

Over 200 organic insecticides, designed to kill insects without excessive danger to humans and animals, are presently in use/ Many of these compounds act by inhibiting cell respiration others uncouple ATP synthesis from electron transport. [Pg.636]

Standiford, T.J., Kunkel, S.L., Liebler, J.M., Burdick, M.D., Gilbert, A.R, and Stricter, R.M. (1993). Gene expression of macrophage inflammatory protein-la fiom human blood monocytes and alveolar macroph es is inhibited by interleukin-4. Am. J. Cell. Respir. Biol. 9, 192-198. [Pg.120]

For this reason, cyanide action has been described as internal asphyxia . Although some cyanide combines with hemoglobin to form a stable nonoxygenbearing compound, cyanhemoglobin, this substance is formed only slowly and in a small amount. Therefore, death is not due to cyanhemoglobin but to inhibition of tissue cell respiration. [Pg.699]

Pyriminil toxicity occurs primarily because it inhibits NADH ubiquinone oxidoreductase activity of complex I in mammalian mitochondria resulting in preferential toxicity to high-energy-demanding cells such as nerves and pancreatic jS-cells. However, pyriminil may also act as a nicotinamide antagonist and interfere with the synthesis of NADH/NADPH, furthering neural and jS-cell toxicity. Inhibition of mitochondrial respiration in nerves causes somatic, autonomic, and central nervous system neuropathies while inhibition in jS-cell causes an immediate, irreversible insulin-dependent diabetes mellitus condition. Pyriminil also acts as a noncompetitive inhibitor of rat acetylcholinesterase. [Pg.2168]

Pavani M, Fones E, Oksenberg D, Garcia M, Hernandez C, Cordano G, et al. Inhibition of tumoral cell respiration and growth by nordihydroguaiaretic acid. Biochem Pharmacol 1994 48 1935 12. [Pg.250]

The biological action of azides is caused by HN, formed by hydrolysis (Bradbury et al.. 1957 Parochetti and Warren, 1970). The biochemical mode of action is based, according to Keilin (1936), on the paralysis of cell respiration and on the inhibition of the oxidative enzyme system of the cell. [Pg.493]

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). [Pg.621]

Warburg,11 who suggested that cell respiration is catalyzed by heavy metals contained in living cells, observed that chemicals that poison such action also inhibit similar catalytic properties in charcoal. Thus, hydrocyanic acid poisons living cells and also the catalytic properties of carbon. Both effects are ascribed to adsorption on active centers that contain iron. [Pg.279]

Lowered oxygen tension (Pq) or inhibition of cell respiration has been found to decrease contractile force in a variety of smooth muscles during spontaneous myogenic activity, or stimulation by neuroeffectors or high-K+ solution (Hellstrand et al., 1977 Ishida and Paul, 1990 Coburn et al., 1992). The sensitivity of... [Pg.381]

The toxicity of cyanide is attributed to its ability to inhibit enzyme reactions. The action of one such enzyme, cytochrome oxidase, essential for the respiration of cells is inhibited by cyanide ions. Cytochrome oxidase is a component of the mitochondrial electron transport system. It transfers electrons from cytochrome c to oxygen, forming water, while releasing sufficient free energy to permit the formation of adenosine 5 -triphosphate (ATP). The latter is essential for normal metabolic processes. Cyanide ion forms complexes with heavy metal ions such as iron and copper to stop electron transport and thus prevent ATP formation. Several enzyme reactions have been listed that cyanide can inhibit several enzyme reactions by forming complexes. [Pg.318]

The different nature of MR, as compared to hydrophobic and steric properties, can only be detected in cases where a proper selection of substituents allows this. One sueh example is the inhibition of malate dehydrogenase by 4-hydroxyquinoline-3-carboxylic acids (5), where the interaction of the ligands with the enzyme is described better by MR (eq. 36) than by Jt (pljo vs. Ji n = 13 r = 0.604 s = 0.716), and the respiration inhibition of ascites tumor cells, where the transport into or the accumulation in the cells is more appropriately described by Jt (eq. 37 same set of compounds) than by MR (piso vs. MR n = 14 r = 0.699 s = 0.554) (Table 9) [293]. [Pg.41]


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See also in sourсe #XX -- [ Pg.636 ]

See also in sourсe #XX -- [ Pg.636 ]

See also in sourсe #XX -- [ Pg.636 ]

See also in sourсe #XX -- [ Pg.636 ]




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