https://www.selleckchem.com/products/rin1.html
Although PCBP1-deleted livers were iron-deficient, dietary iron supplementation did not prevent steatosis; instead, dietary iron restriction and antioxidant therapy with vitamin E prevented liver disease. PCBP1-deleted hepatocytes exhibited increased labile iron and production of reactive oxygen species, were hypersensitive to iron and prooxidants, and accumulated oxidatively-damaged lipids due to the reactivity of unchaperoned iron. CONCLUSIONS Unchaperoned iron in PCBP1-deleted mouse hepatocytes leads to production of reactive oxygen spe
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