## Ethanol as Antidote in Methanol Poisoning ### Mechanism of Action **Key Point:** Ethanol acts as a competitive substrate inhibitor of alcohol dehydrogenase (ADH), the enzyme responsible for converting methanol to its toxic metabolites. ### Stepwise Explanation 1. **Normal methanol metabolism:** - Methanol → Formaldehyde (via ADH) - Formaldehyde → Formic acid (via aldehyde dehydrogenase) - Formic acid accumulates → toxicity 2. **With ethanol present:** - Ethanol has higher affinity for ADH than methanol - ADH preferentially oxidizes ethanol to acetaldehyde - Methanol metabolism is blocked/slowed - Methanol is excreted unchanged in urine and breath - Formic acid production is prevented ### Clinical Pearl **High-Yield:** Ethanol must be given early and maintained at a serum level of **100–150 mg/dL** to be effective. Once formic acid is already formed, ethanol cannot reverse the damage. **Mnemonic: "ADH Affinity" — Ethanol > Methanol** (ethanol wins the competition for the enzyme) ### Modern Alternative Fomepizole (4-methylpyrazole) is now preferred over ethanol because: - Higher selectivity for ADH - No CNS depression - No hypoglycemia risk - Easier dosing Both work on the same principle: **competitive inhibition of ADH**. [cite:Parikh Forensic Medicine & Toxicology Ch 19]
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