The impact of garlic, known for its
antioxidant activities, on
iron metabolism has been poorly investigated. The aim of this work was to study the effect of crude garlic pre-treatment on
iron-mediated lipid peroxidation, proliferation and autophagy for 5 weeks. Rats were fed distilled water or garlic
solution (1 g/kg
body weight) by gavage for the first 3 weeks as pre-treatment and received a basal diet supplemented or not with
ferrous sulfate (650 mg Fe/kg diet) for the last 2 weeks of treatment. Immunohistochemistry labeling and ultrastuctural observations were used to evaluate the
iron deleterious effects in the liver.
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-II 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. Garlic pre-treatment reduced
iron-catalyzed lipid peroxidation by decreasing the
malondialdehyde level in the liver and colon and by enhancing the status of
antioxidants. In addition, garlic reduced the
iron-mediated cell proliferation and autophagy by lowering
iron storage in the liver and protected mitochondrial membrane. Based on these results, garlic treatment significantly prevented
iron-induced oxidative stress, proliferation and autophagy at both biochemical and histological levels due to its potent
free radical scavenging and
antioxidant properties.