Electron transport chain azide

This type of effect can occur in all tissues and is caused by a metabolic inhibitor such as azide or cyanide, which inhibits the electron transport chain. Inhibition of one or more of the enzymes of the tricarboxylic acid cycle such as that caused by fluoroacetate (Fig. 6.7) also results in inhibition of cellular respiration (for more details of cyanide and fluoroacetate see chap. 7). 

The answer is c. (Murray, pp 123-148. Scriver, pp 2367-2424. Sack, pp 159-175. Wilson, pp 287-317.) The electron transport chain shown contains three proton pumps linked by two mobile electron carriers. At each of these three sites (NADH-Q reductase, cytochrome reductase, and cytochrome oxidase) the transfer of electrons down the chain powers the pumping of protons across the inner mitochondrial membrane. The blockage of electron transfers by specific point inhibitors leads to a buildup of highly reduced carriers behind the block because of the inability to transfer electrons across the block. In the scheme shown, rotenone blocks step A, antimycin A blocks step B, and carbon monoxide (as well as cyanide and azide) blocks step E. Therefore a carbon monoxide inhibition leads to a highly reduced state of all of the carriers of the chain. Puromycin and chloramphenicol are inhibitors of protein synthesis and have no direct effect upon the electron transport chain. 

The second type of asphyxiants is that which works at the cellular level. Here, they interfere with the mitochondrial cytochrome oxidase s function in the electron transport chain. Because this is the fuel cell for the body, energy production ceases within the cell, with cell death following close behind. The key substance implicated here is cyanide, which is usually found only in a chemical laboratory setting, but can also be a side effect of smoke inhalation. As previously mentioned, hydrogen sulfide and carbon monoxide also have some effect at this site. In addition, azides are cellular asphyxiants. The azides, along with the nitro-ate-ites, are also vasodilators and can cause headaches and hypotension. 

When they further observed that the normal nucleus contains a high proportion of mono-, di-, and trinucleotides of adenine, they claimed to have provided direct proof of their theory by demonstrating that the mono-or dinucleotides in the nucleus may be converted to ATP when oxygen is present. (The nucleotides can be extracted from the nucleus with acetate buffer at pH 5.1.) This conversion certainly suggested the existence of an intranuclear process of oxidative phosphorylation. As in mitochondria, oxidative phosphorylation in the nucleus is inhibited by uncouplers or agents blocking the electron transport chain. Nuclear oxidative phosphorylation is blocked by cyanide, azide, and antimycin A, or by dinitrophenol but, in contrast to mitochondria, it is resistant to Janus green, methylene blue, carbon monoxide, Dicumarol, and calcium. 

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