toxicology of CN-

Brent Gilbert strider at udel.edu
Fri Jul 9 16:48:14 EST 1999

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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