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Toxicity of cyanide: cell death or suffocation?


Function

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Hi everyone

 

An aspect of my course of energy and metabolism is the influence of cyanides in our body.

 

This is what I've written down during the course, which is confirmed by Wikipedia:

 

Cyanide ion binds with the iron-cation in cytochrome oxidase complex (cytochrome a-a3), inhibiting its possibility to continue the electron transport (the reaction 2 cyt a3-Fe2+ + 1/2 O2 + 2H+ <--> 2 cyt a2-Fe3+ + H2O is inhibited), leading to suffocation.

 

I understand that the blockage of this electron transport inhibits a normal ATP-production, leading e.g. to a reduced or completely inhibited function of the Na-K-ATPase, eventually leading to depolarization, eventually leading to brain damage and heart failure and... general death.

I don't see, however, how this cyanidic inhibition leads to suffocation because 'tissues can't use oxygen anymore'.

 

Can someone help me?

 

Thanks.

 

F.

 

EDIT: hmm... starting to figure it out: the cells use the O2 electron transfer to produce ATP (or, better, use the energy of ...). Since the O2 cannot be utilized, there'll be no ATP (or only 2 from the glycolysis) and so on.

Is this actually what's meant by "suffocation"? The disability to use O2 in the ATP production? Which means as much as "normal conditions" minus O2? So that this problem would be the same with cyanide and oxygen, as well as without both cyanide and oxygen (which is the case in 'normal', stereotypical suffocation)?

Edited by Function
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Suffocation is probably not the best way to describe cellular processes (though it is not completely wrong). The mechanisms are correct. cell death occurs due to inability to create ATP. Proximately this is caused by blocking the cytochrome c oxidase, the terminal step in the electron transfer chain to oxygen.

As the effect is similar to present tissues to hypoxic or anoxic environments it could be termed suffocation in a casual way.

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Suffocation is probably not the best way to describe cellular processes (though it is not completely wrong). The mechanisms are correct. cell death occurs due to inability to create ATP. Proximately this is caused by blocking the cytochrome c oxidase, the terminal step in the electron transfer chain to oxygen.

As the effect is similar to present tissues to hypoxic or anoxic environments it could be termed suffocation in a casual way.

 

Thanks for confirming this for me :)

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  • 4 weeks later...

The liver can metabolise cyanide. It converts it to thiocyanate.

Unfortunately, that's still toxic (though much less so)

is this toxic by the same pathway as cyanide? what i mean is it capable of inhibiting cytochrome c oxidase?

 

in relation to chronic cyanide poisoning, is there a low end dose where one could repetitively consume it without ill effects (perhaps in occasional cigarette/cigar smokers)? the konzo case seems to be on the other extreme end. the cassava plants that they are consuming can have upwards of 1 g/kg or cyanide, especially when the plant is grown in drought conditions.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC35028/

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  • 1 year later...

Suffocation is not strictly speaking inaccurate, the pathophysiological term being histotoxic hypoxia or histotoxic shock. Cyanide shuts down cytochrome c oxidase. "Tissue cannot use oxygen anymore" because the functioning of the mitochondrial electron transport chain is dependent on cytochrome c oxidase (or complex 4) passing the electrons to molecular oxygen. Inhibiting complex 4 will stop the ETC "Using" oxygen to produce the proton gradient required for ATP synthase to generate ATP, and without ATP the cell will go into histotoxic shock.

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