Controversial role of intracellular iron in the mechanisms of chemically-induced hepatotoxicity.
Hepatotoxicity induced by various therapeutic agents, industrial chemicals and environmental pollutants is a well-recognized phenomenon. These chemicals are known to cause liver damage that is localized to either periportal or centrilobular regions of the liver lobule (1-3). Depending on dose, duration, and route of exposure, the resultant liver injury may regress or progress and becomes irreversible (1). Mechanisms involved in this selective, localized toxicity have been the target of extensive research efforts, and many studies produced conflicting results. As depicted in Figure 1, although many investigators implicate iron and lipid peroxidation in this process (4-9), others dispute such assertions (10-12).
Badr
M Z
MZ
Division of Pharmacology, University of Missouri-Kansas City 64108-2792.
D000433:1-Propanol / Q000633:toxicity; D000082:Acetaminophen / Q000633:toxicity*; D000818:Animals; D004317:Doxorubicin / Q000633:toxicity; D006801:Humans; D007501:Iron / Q000378:metabolism*; D015227:Lipid Peroxidation; D008099:Liver / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010084:Oxidation-Reduction; D020005:Propanols; D011809:Quinones / Q000633:toxicity*; D014812:Vitamin K / Q000633:toxicity
D020005:Propanols; D011809:Quinones; D014812:Vitamin K; D000082:Acetaminophen; C006463:allyl alcohol; D004317:Doxorubicin; D000433:1-Propanol; D007501:Iron