Mercury is a chemical element that has been known since prehistoric times and has been used over time as a component of paints, in the treatment of various diseases, and later in various industrial compounds. Mercury enters the body transcutaneously, by inhaling or by ingesting food contaminated with mercury. The most common cause of mercury poisoning is eating seafood, but people can get mercury poisoning from industrial processing, thermometers, dental work, and old paints. The most vulnerable are people at occupational risk due to chronic exposure, as well as fetuses in the intrauterine period. Mercury poisoning produces extremely serious effects on the nervous, renal, and gastrointestinal systems. The nature and extent of mercury poisoning depend on factors such as the route of exposure, the rate of exposure, the distribution and biotransformation of mercury in the body, the chemical form of mercury or the mercury compound. Both mercury in the blood and the urine should not exceed 10 μg/L. The critical values of mercury in the blood are >150 μg/L and the lethal ones exceed 800 μg/L. New diagnostic methods allow the rapid and accurate identification of the concentration of mercury in biological products. Treatment is based on the use of chelating agents. However, the prognosis of mercury poisoning is extremely variable, due to the potentially irreversible nature of the lesions.

When a new coronavirus appeared in the late 2019, identified as the cause of several cases of pneumonia in Wuhan, Paracetamol was initially reported to be the preferable antipyretic medication, choice which was detrimental to the use of other drugs. People have resorted to buying large stocks of Paracetamol and some have used it in large doses, regardless of the consequences. However, the Paracetamol (Acetaminophen) overdose remains the leading cause of death or transplantation due to acute liver failure in many parts of the world. This review aims at presenting the pharmacokinetics, the clinical signs, and the risk factors for systemic toxicity associated with Paracetamol overdose, as well as the current therapeutic approach. Paracetamol is primarily metabolized in the liver, by glucuronidation and sulfation. In case of a Paracetamol overdose, a large amount of NAPQI is conjugated with glutathione, and this process is due to a major depletion of glutathione, thus leading to hepatic necrosis, renal failure, and encephalopathy. The evaluation of serum acetaminophen levels by analytical methods is extremely useful both for the diagnosis and the therapy monitoring.