Question:medium
Which of the following statements is CORRECT regarding the pharmacology of N-acetylcysteine (NAC)?
Which of the following statements is CORRECT regarding the pharmacology of N-acetylcysteine (NAC)?
Show Hint
NAC is the antidote for paracetamol toxicity and works by replenishing an important intracellular antioxidant.
Updated On: Jun 23, 2026
- It acts as a precursor for glutathione synthesis
- It is used as antidote for organophosphate poisoning
- It inhibits cyclooxygenase enzyme
- It is a specific antidote for benzodiazepine overdose
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The Correct Option is A
Solution and Explanation
N-acetylcysteine (NAC) is a key pharmacology drug with multiple mechanisms and uses.
Mechanism of action:
NAC provides $\text{L-cysteine}$, the rate-limiting substrate for glutathione (GSH) synthesis. Glutathione is the primary intracellular antioxidant that neutralizes reactive oxygen species (ROS) and toxic electrophilic metabolites. NAC also directly acts as an antioxidant via its free thiol (-SH) group.
Paracetamol toxicity -- Classic use:
Paracetamol is converted to the toxic metabolite $\text{NAPQI}$ (N-acetyl-p-benzoquinone imine) by CYP2E1 and CYP3A4. In overdose, GSH is depleted and NAPQI binds covalently to hepatic proteins, causing centrilobular necrosis.
NAC replenishes GSH, conjugates NAPQI directly (via thiol groups), and provides cysteine for further GSH synthesis.
Route of administration:
IV (Prescott protocol: 150 mg/kg over 15 min, then 50 mg/kg over 4h, then 100 mg/kg over 16h) or oral (140 mg/kg loading, then 70 mg/kg q4h x 17 doses).
Other uses: Mucolytic (breaks disulfide bonds in mucus glycoproteins), contrast-induced nephropathy prophylaxis, ARDS adjunct.
\[\boxed{\text{Precursor for glutathione synthesis}}\]
Mechanism of action:
NAC provides $\text{L-cysteine}$, the rate-limiting substrate for glutathione (GSH) synthesis. Glutathione is the primary intracellular antioxidant that neutralizes reactive oxygen species (ROS) and toxic electrophilic metabolites. NAC also directly acts as an antioxidant via its free thiol (-SH) group.
Paracetamol toxicity -- Classic use:
Paracetamol is converted to the toxic metabolite $\text{NAPQI}$ (N-acetyl-p-benzoquinone imine) by CYP2E1 and CYP3A4. In overdose, GSH is depleted and NAPQI binds covalently to hepatic proteins, causing centrilobular necrosis.
NAC replenishes GSH, conjugates NAPQI directly (via thiol groups), and provides cysteine for further GSH synthesis.
Route of administration:
IV (Prescott protocol: 150 mg/kg over 15 min, then 50 mg/kg over 4h, then 100 mg/kg over 16h) or oral (140 mg/kg loading, then 70 mg/kg q4h x 17 doses).
Other uses: Mucolytic (breaks disulfide bonds in mucus glycoproteins), contrast-induced nephropathy prophylaxis, ARDS adjunct.
\[\boxed{\text{Precursor for glutathione synthesis}}\]
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