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Oxidative phosphorylation poisons affecting

A number of substances inhibit oxidative phosphorylation at specific locations. These may be divided into agents that affect electron transport, those that affect complex V, and those that collapse proton gradients (proton ionophores). Such substances have been used as research tools to unravel the complexities of these pathways, as poisons, and as antibiotics. Inhibition of electron transport inhibits phosphorylation, the extent of which depends on the location of the inhibition site. Thus, if complex I is inactivated, electron transport can still take place using FADH2 as an electron donor. The donor P/O ratio is then 2. [Pg.454]

Cyanide poisoning is marked by metabolic acidosis and a large anion gap. The latter is a consequence of the blocked oxidative phosphorylation and the increased rate of glycolysis. Maduh et al (1990) showed that cyanide also affects and thus the pH of the tissues. In turn, the Ca transport process is disrupted, leading to a rise in cystolic [Ca ]. Acidification depolarizes the cell membrane and changes the potassium conductance. [Pg.502]

The answer is d. (Murray, pp 123-148. Scriver, pp 2367-2424. Sack, pp 159-175. Wiison, pp 287-317.) All of the poisons shown affect either electron transport or oxidative phosphorylation. Dinitrophenol is unique in that it disconnects the ordinarily tight coupling of electron transport and... [Pg.184]


See other pages where Oxidative phosphorylation poisons affecting is mentioned: [Pg.568]    [Pg.103]    [Pg.496]    [Pg.44]    [Pg.627]    [Pg.819]    [Pg.564]    [Pg.112]    [Pg.388]   
See also in sourсe #XX -- [ Pg.92 , Pg.95 , Pg.96 ]




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