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These molecular alterations trigger a number of interrelated pathomechanisms, namely: i) free-thiol oxidation of proteins;6,7ii) disassembly of cytoskeleton,8,9 with plasma membrane blebbing as a major emergent;10iii) formation of mitochondrial permeability transition pores, leading to the release of mitocondrial promoters of apoptosis (cytochrome c, Smac/DIABLO) and uncoupling of the electron transport chain from ATP production, with eventual necrosis associated with ATP depletion;11iv) increased plasma-membrane peroxidation, leading to membrane permeabilization and leakage of cytosolic components;12v) oxidative breaking of DNA strands, leading to genotoxicity and carcinogenesis;13,14vi) elevation of intracellular Ca2+ levels, which facilitates mitochondrial permeability transition and activation of Ca2+-dependent proteases, endonucleases, and lipases.11,15 Due to its multiple energy-dependent functions, liver has a high mitochondrial metabolic rate, and is heavily engaged in detoxification mechanisms that involve redox-enzyme systems