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In the persistent presence of hepatic steatosis, there may be triggering of the oxidative stress process that is characterized in NAFLD by mitochondrial dysfunction, increased release of inflammatory mediators, increased production of oxidative stress byproducts, such as the MDA marker, or impaired redox balance, as well demonstrated by a decrease in GPx levels, or even by impaired inactivation of ROS by deficient reserves of antioxidant nutrients ( 4 , 22 )

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It tends to lower blood pressure as a secondary benefit