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Continuous liver damage due to the overproduction of ROS and inflammation by diverse endogenous and exogenous injuries, failure at the respiratory chain in mitochondria [10,11], drop-in antioxidant elements such as superoxide dismutase [12], catalase activity [13], or the elevation of lipid peroxidation [14], among other described mechanisms, working together, are involved in injuries, apoptosis, inflammation, and fibrosis [10]

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