LAST FIVE YEARS’ LABORATORY BASED STUDIES TO ADDRESS ACETAMINOPHEN INDUCED HEPATOTOXICITY
Abdullah Al Mahmud Ashik and Mohammad Borhan Uddin*
ABSTRACT
Acetaminophen is a commonly used analgesic drug that is considered an over-the-counter drug. Chronic use of this analgesic drug, as well as overdose, can cause hepatotoxicity. Acetaminophen metabolism takes place within liver. Hepatotoxicity from this drug is caused by the development of the poisonous NAPQI metabolite, as well as glutathione (GSH) depletion, oxidative stress, and mitochondrial dysfunction, all of which lead to a decrease in adenosine triphosphate (ATP) storage. There are so many other factors that are responsible for acetaminophen-induced hepatotoxicity. Many studies have recently been conducted in order to establish therapeutic options by designing a new medicine to improve acetaminophen toxicity. Many investigations have been conducted in the laboratory to determine the hemodynamic effects and in several studies drugs were given intraperitoneal. The herbal medicine was also used by the researchers to significantly reduce acetaminophen toxicity. They derived a variety of natural compounds from various plants and used these items in their research. There have been numerous studies conducted in order to discover a better alternative antidote. These experiments focused on a variety of molecules, including Nrf2, c-Met, thrombospondin-1, CYP2E1, and others. These were proved only in the lab-based animal trial. In future, preclinical trials are required to better determine the safety and efficacy of these compounds.
Keywords: Hepatotoxicity, Acetaminophen, Intraperitoneal, herbal compound, antidote, NAPQI, Glutathione hormone.
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