Acetaminophen,also known as paracetamol, is widely used as analgesic and antipyretic
medication in the world and is considered to be safe at therapeutic dosages. It
is widely accepted that an overdose of acetaminophen can induce severe liver
damage in humans and in experimental animals; it is important to note that
hepatic injury induced by therapeutic dose has been reported however there are
few studies in order to identify potential triggers for this condition. There
are several evidences suggesting that hepatotoxicity of compounds might be
related to protein malnutrition condition, for example, Kwashiorkor seems to be
associated with exposure to aflatoxins.
Proteinmalnutrition can affect the pathways of acetaminophen metabolism. Acetaminophen
is metabolized by different pathways such as sulfation, glucuronidation, and
some isoforms of hepatic microsomal cytochrome P450s, such as CYP1A2 and CYP3A.
The P450 system can generate the reactive metabolite, N-Acetyl-P-Benzoquinone
Imine (NAPQI), which is subsequently detoxified through conjugation with
Glutathione (GSH) by Glutathione S-Transferase (GST). However, at higher doses,
saturation of conjugation pathways and the consequent depletion of GSH can increase
NAPQI levels NAPQI is able to bind to several hepatic proteins, and this
binding is associated with development of centrilobular necrosis. Moreover,
administration of hepatotoxic doses of acetaminophen can reduce GSH levels in
liver and kidney. It is important to note that malnutrition per se induced a
reduction in the GSH content.
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