Resfar Mechanism of Action

Pharmacology: After oral administration of 100 mg/kg, N-Acetylcysteine (NAC) is completely absorbed and undergoes rapid and extensive metabolism in the intestinal wall and liver. The elimination half-life was 5-6 hours after intravenous administration. NAC is mainly excreted in the urine. The main urinary metabolite of NAC is the inorganic sulphate. However, during the acute paracetamol intoxication, the urinary metabolite of NAC may differ, being at least partially represented by complexation products of NAC or its derivatives with the toxic. In toxic pathology, NAC exerts its effects on multiple mechanisms. The best known effect regards its action as precursor of glutathione. NAC acts as precursor of cysteine needed for GSH synthesis (by deacetylation with formulation of free cysteine and by reduction of plasma cystine to cysteine with formation of oxidized NAC); increase the total amount of glutathione (GSH+GSSG), if depleted; and facilitates conversion of glutathione from the oxidized form (GSSG) to the biologically active, reduced form (GSH).
Furthermore, in paracetamol poisoning, NAC acts by reducing the reactive metabolites (e.g. NAPQI) to atoxic compounds; conjugating itself directly with said metabolites; in a specific manner as antioxidant agent; and as precursor of sulfates necessary for the metabolization of paracetamol by sulfation.
These mechanisms justify the need of early treatment (within 10 hours) in paracetamol poisoning, to prevent or minimize with maximum efficacy the occurrence of hepatic damage. Likewise important is the capacity of NAC to improve peripheral utilization of O₂, increasing delivery and peripheral extraction. In intoxications with severe hepatic insufficiency this makes its possible to prevent or correct tissutal hypoxia which represents one of the main factors responsible for the genesis of multiple organ insufficiency: this effect is evident even in the event of delayed treatment.