Electrochemical evaluation of plant extracts as potential antidotes for acetaminophen poisoning

Acetaminophen, a widely used analgesic, causes severe liver damage in overdose situations due to N-acetyl-p-benzoquinoneimine (NAPQI), a toxic metabolic intermediate. Current antidotes, like N-acetylcysteine (NAC), are effective but costly and not universally accessible. There is a critical need for novel, cost-effective antidotes to mitigate acetaminophen-induced hepatotoxicity. This study investigates the electrochemical oxidation of acetaminophen in the presence of plant extracts, including pomegranate peel, pomegranate, bell pepper, black radish, and turnip, to evaluate their potential as alternative antidotes. Cyclic voltammetry (CV) and controlled-potential coulometry were employed to study acetaminophen oxidation, confirming NAPQI formation. CV analysis revealed that pomegranate peel extract exhibited superior reactivity with NAPQI, with an anodic-to-cathodic peak current ratio (I_pA/I_pC) exceeding that of N-acetylcysteine (NAC), the standard antidote for acetaminophen poisoning, by 40-45%. Coulometric experiments corroborated this high reactivity, suggesting an EC' mechanism for pomegranate peel extract and an EC mechanism for other extracts. Other plant extracts showed moderate reactivity, with bell pepper and turnip achieving 30-50% of pomegranate peel's I_pA/I_pC, indicating their potential as NAPQI scavengers. These findings highlight the varying scavenging capacities of plant extracts. The high reactivity of pomegranate peel extract with NAPQI, driven by an EC' mechanism, suggests its potential as a cost-effective, natural antidote for acetaminophen poisoning. This study introduces a novel electroanalytical approach for antidote development, elucidating interaction mechanisms between plant extracts and NAPQI. Unlike traditional methods, this electrochemical strategy offers precise, rapid assessment of antidote efficacy, providing a scalable framework for evaluating natural compounds to mitigate acetaminophen-induced liver damage.