Attenuation of acute and chronic liver injury in rats by iron-deficient diet

294: R311–R320, 2008. First published November 21, 2007; doi:10.1152/ajpregu.00735.2007.—Oxidative stress due to iron dep-osition in hepatocytes or Kupffer cells contributes to the initiation and perpetuation of liver injury. The aim of this study was to clarify the association between dietary iron and liver injuries in rats. Liver injury was initiated by the administration of thioacetamide or ligation of the common bile duct in rats fed a control diet (CD) or iron-deficient diet (ID). In the acute liver injury model induced by thioacetamide, serum levels of aspartate aminotransferase and alanine aminotransferase, as well as hepatic levels of lipid peroxide and 4-hydroxynonenal, were significantly decreased in the ID group. The expression of 8-hy-droxydeoxyguanosine and terminal deoxynucleotidyl transferase bi-otin-dUTP nick-end labeling positivity showed a similar tendency. The expression of interleukin-1 and monocyte chemotactic protein-1 mRNA was suppressed in the ID group. In liver fibrosis induced by a