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Recently, we have demonstrated that dose- and time-dependent ASA treatment of HepG2 cells caused cell cycle arrest, increase in ROS production, reduction in mitochondrial potential, and alterations in mitochondrial redox and respiratory functions [23]

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This has triggered the evolution of resistance mechanisms whereby the water-soluble toxic form of mercury, the Hg 2+ cation (either aquated or coordinated to ligands such as chloride), is reduced back to the mono-atomic elemental form, the atoms of which are volatile and can be eliminated from the organism back into the environment [87]