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Lycopene is generally consumed and known for its antioxidant activities.In this study,we hypothesized that lycopene can prevent iron-mediated oxidative stress,proliferation and autophagy and used a rat model of nutritional iron supplementation to confirm its intervention in these defence mechanisms.Rats received a basal diet supplemented with or without ferrous sulfate (1000 mg/kg diet) and were fed 0.9％ saline solution or lycopene solution (10,15 or 20 mg/kg body weight) by gavage for 6 weeks.We found that iron supplementation induced cell proliferation predominantly in non parenchymal cells comparing to hepatocytes,but not apoptosis.In addition,iron was accumulated within the hepatic lysosomes where it triggers autophagy as evidenced by the formation of autophagic vesicles detected by LC3-B staining.It also induced morphologic alterations of the mitochondrial membranes due to increased lipid peroxidation as shown by elevated iron and malondialdehyde concentrations in serum and tissues.Lycopene reduced iron-catalyzed lipid peroxidation by decreasing the malondialdehyde level in the liver and colon and enhancing the total superoxide dismutase activities in serum and tissues.Take together,our data suggest that lycopene prevented iron-induced oxidative stress,proliferation and autophagy at both biochemical and histological levels due to its potent free radical scavenging and antioxidant properties.