Aromatic Anticonvulsants and their effects on mitochondrial function

This book sets out some relevant concepts and information on the role that the liver plays in the metabolic disposition of various endogenous and exogenous chemical agents including almost all drugs. During the biotransformation process highly reactive intermediate metabolites can be formed which if not properly eliminated can interact with cellular macromolecules damaging the organ. The idiosyncratic hepatotoxicity associated with the use of aromatic antiepileptics is well known and has been attributed to the accumulation of toxic intermediates formed during hepatic bioactivation. In this study we evaluated in vitro the effect of carbamazepine phenytoin and phenobarbital as well as their respective metabolites on mitochondrial function and the induction of oxidative stress in rat liver mitochondria as a possible mechanism of hepatotoxic action of these drugs. After all the studies carried out we can say that the results suggest the involvement of mitochondrial damage mediated by oxidative stress caused by the metabolites of aromatic anticonvulsants in the development of idiosyncratic hepatotoxicity induced by these drugs.