Abstract
Objective: To describe the molecular aspects related to paracetamol and the hepatotoxic mechanism triggered by higher doses. Bibliographic review: The research performed included the absorption and phase I of biotransformation of paracetamol, which results in the formation of the toxic metabolite N-acetyl-p-benzoquinoneimine (NAPQI). Acetaminophen overdose exposes the user to acute intoxication. In these cases of intoxication, glutathione is depleted, a substance that participates in the metabolism of paracetamol converting NAPQI into mercapturic acid for subsequent renal elimination. Consequently, the toxic metabolite accumulates in the body, causing damage to the mitochondrias, deterioration of structural proteins, which can result in hepatotoxicity. In situations of intoxication, the substance N-acetylcysteine has great clinical relevance as it contributes to an increase in the concentration of glutathione and a reduction in the concentration of accumulated NAPQI. Final considerations: It is understood that the indiscriminate use of paracetamol leads to considerable health risks, including fatal outcomes due to its hepatotoxic mechanism, and it is important to educate the population by health professionals about this problem. Furthermore, it is essential to recognize the importance of using N-acetylcysteine as an antidote in cases of intoxication.