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Drug-Induced Mitochondria Toxicity
Chimaobi J. Ononamadu* (2009)
Dept of Applied biochemistry, Nnamdi Azikiwe University. Awka. Nigeria. ( Review Article)
Correspondence to: Ononamadu Chimaobi. chymaonos@yahoo.com, +2348037202476
Abstract
Mitochondria play a critical role in generating most of cell’s energy as ATP. They are also involved in other metabolic processes such as haem synthesis etc Over the years, drugs such as certain antiviral agents, lipid lowering drugs, cholesterol lowering drugs, antibiotics, analgesics and cancer therapeutics have been implicated in inducing-mitochondria dysfunction and thus drug-induced-mitochondrial toxicity. Recent advances suggest that mitochondria DNA, mitochondrial respiratory chain, oxidative phosphorylation, mitochondrial channels and mitochondrial permeability form the bulk of the target of drug-induce toxicity. In the case of Acetaminophen (Analgesic), reaction metabolite formation including ROS, glutathione depletion, alkylation of mitochondrial proteins, membrane permeability transition (MPS)/Pore formation in the inner mitochondrial membrane and release of inter membrane proteins lead to toxicity after an over dose. For antiretroviral drugs like NRTIs, termination of mitochondrial DNA-Synthesis terminates organelle replication and some other mitochondrial processes leading to toxicity. Based on the recognition of the different interplaying mechanism, it appears most promising therapeutically to target either the initiating event or central propagating mechanism to prevent toxicity
Keywords:Drug toxicity, Mitochondria, damage, hepatotoxicity, Oxidative stress, Glutathione, DNA, Cell, Metabolism
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