The involvement of free radical reactions in the pathogenesis of liver injury has been investigated for many years in a few defined experimental systems using carbon tetrachloride, excess iron or ethanol as prooxidant agents. More recently, the hepatotoxicity of several other free radical-generating compounds has been characterised mainly in the rat hepatocyte model. In particular, the mechanisms by which drugs like paracetamol, halothane, paraquat or conditions such as ischemia-reperfusion exert their damaging activity to the liver have mostly been clarified. Since we are not trying to cure diseases occurring only in rats, the likely relevance of free radical reactions also in the genesis and progression of human liver injury has been carefully considered. Increasing evidence of free radical involvement is reported for chronic ethanol intoxication and iron overload, but the most striking proof of a causative role of ree radical chain reactions, namely lipid peroxidation, in the acute lethal damage of the hepatocyte has been obtained so far in ischemic hepatitis.
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