this post was submitted on 02 Nov 2024
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[โ€“] notabot@lemm.ee 8 points 1 week ago (1 children)

Isn't one of the main issues with carbon-monoxide that hemoglobin preferentially binds with it over oxygen, and so it doesn't get expelled from your bloodstream via your lungs? You can tolerate quite large doses with little more than a headache, so I doubt you could overdose from internally generated amounts, but a large enough dose dangerously reduces your blood's oxygen carrying capacity.

[โ€“] IrritableOcelot@beehaw.org 6 points 1 week ago* (last edited 1 week ago)

Yep! The LD50 is 12.5% in air (higher than I thought, honestly) and yes the issue is that it binds preferentially to hemoglobin.

The main treatment for sub-lethal exposure is just supplying pure oxygen to kick the equilibrium the other way and slowly remove the CO from your system. It won't all come off, but your body recycles red blood cells pretty quickly, so you're back on your feet within a few hours and back to normal within a few days. However, there's no treatment for lethal doses, people have proposed using things like cobalt porphyrins (which bind CO even better than iron hemes) to more quickly sequester the CO from your hemoglobin, but that's not been trialled yet in humans.

I wasnt aware of its use as a neurotransmitter (but I'm absolutely going to look into it now), but its barely soluble in water so there must be more going on there. just like urea, it's a natural waste product, and typically one your body wants to get rid of reasonably quickly.

Edit: from a chemical perspective, NO and CO "look" electronically similar to a NO-binding protein, so I expect most of these effects of CO are actually just it activating pathways natively activated by NO.