Pharmacology
Ethanol binds to α7-nAChRs as an agonist, GABA (especially the δ subunit) as a positive allosteric modulator, 5-HT3 receptor agonist, NMDA receptor antagonist, AMPA receptor antagonist, Kainate receptor antagonist, glycine receptor agonist and an inhibitor of potassium, sodium and calcium ion channels. It also appears to cause an increase in dopamine through a poorly understood process that may involve inhibiting the enzyme that breaks dopamine down. Ethanol also appears to block the reuptake of adenosine, additionally.
The removal of ethanol through oxidation by alcohol dehydrogenase in the liver from the human body is limited. Hence, the removal of a large concentration of alcohol from blood may follow zero-order kinetics. This means that alcohol leaves the body at a constant rate, rather than having an elimination half-life.
Also, the rate-limiting steps for one substance may be in common with other substances. For instance, the blood alcohol concentration can be used to modify the biochemistry of methanol and ethylene glycol. Methanol itself is not highly toxic, but its metabolites formaldehyde and formic acid are; therefore, to reduce the concentration of these harmful metabolites, ethanol can be ingested to reduce the rate of methanol metabolism due to shared rate-limiting steps. Ethylene glycol poisoning can be treated in the same way.
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