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Targeting this system, either by hepatocyte-specific knockout of peroxisomes or by deficiency in ACOX (which catalyzes the initial step in peroxisomal FAO), results in hepatic lipid accumulation and fibrosis, oxidative stress, and inflammation, emphasizing the role of peroximal FAO in NAFLD and NASH [108]

Studies with GPx1 knockout mice revealed an important role of this enzyme in cardiac dysfunction (Lubos et al

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Artificial overexpression of GPx1 showed an increased capacity to rescue breast cancer cells from the cell cycle arrest caused by hyperoxic stress, indicating the involvement of both peroxide-derived free radicals and nonperoxide-derived species during the deleterious process [84]