toxicology of CN-

Eli Lilly and Company rosshaynes at hotmail.com
Tue Jul 13 09:34:11 EST 1999

Your second assertion I believe was the correct one.  OP inhibitors such as
CN- prevent the reduction of O2 to H2O traditionally viewed as the "last
step" in the ETC.  This backlog in e-'s effectively shuts down the entire
ETC b/c if the redox potential of the last cyt/prot transfer is messed up,
the rest of the ETC will not be able to shuttle electrons or pump H+'s
accross the inner mito. mb.
Hope that helps,
Brent Gilbert <strider at udel.edu> wrote in article
<37866E1E.9009F17D at udel.edu>...
> I should be able to figure this out, but I'm still not quite sure why
> CN- is soooo toxic. I understand it inhibits the ECT by interfering with
> the reduction of O2 to water, but if the rest of ECT is unaffected, and
> protons are still being pumped out of the mitochondria, most of the ATP
> should still be formed from ADP. I can only think that either the
> bioavailability of CN- is so much greater than other inhibitors of
> oxidative phosphorylation, and that is the cause of the extreme
> toxicity, or that the prevention of reducing O2 to water "backs up" the
> rest of the electron acceptors in the chain in their reduced forms, such
> that they cannot accept any more electrons, and the proton pump stop
> working. Am I at least close?? Thanks!
> Brent Gilbert

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