2009 年 44 巻 1 号 p. 85-94
In dietary iron overload, excess hepatic iron promotes liver damage. The aim was to attenuate free radical-induced liver damage using vitamins. Four groups of 60 Wistar rats were studied: group 1 (control) was fed normal diet, group 2 (Fe) 2.5% pentacarbonyl iron (CI) followed by 0.5% Ferrocene, group 3 (Fe + V gp) CI, Ferrocene, plus vitamins A and E (42× and 10× RDA, respectively), group 4 (Fe – V gp) CI, Ferrocene diet, minus vitamins A and E. At 20 months, glutathione peroxidase (GPx), superoxide dismutase (SOD), Oxygen Radical Absorbance Capacity (ORAC), Ames mutagenicity test, AST, ALT and 4-hydroxynonenal (4-HNE) immunohistochemistry were measured. 8OHdG levels of the Fe + V and Fe – V groups were 346 ± 117 and 455 ± 151, ng/g w.wt, respectively. Fe + V and Fe – V differences were significant (p<0.005). A positive correlation between DNA damage and mutagenesis existed (p<0.005) within the iron-fed gps. AST levels for Fe + V and Fe – V groups were 134.6 ± 48.6 IU and 202.2 ± 50.5 IU, respectively. Similarly, ALT levels were 234.6 ± 48.3 IU and 329.0 ± 48.6 IU, respectively. However, Fe – V and Fe + V groups transaminases were statistically insignificant. 4-HNE was detected in Fe + V and Fe – V gp livers. Vitamins A and E could not prevent hepatic damage.