Ascorbic acid does not increase the oxidative stress induced by dietary iron in C3H mice

Abstract

Iron is a potent prooxidant that can induce lipid peroxidation. Ascorbic acid, a potent antioxidant, has prooxidant effects in the presence of iron in vitro. We investigated whether ascorbic acid and iron co-supplementation in ascorbic acid-sufficient mice increases hepatic oxidative stress. C3H/He mice were fed diets supplemented with iron to 100 mg/kg diet or 300 mg/kg diet with or without ascorbic acid (15 g/kg diet) for 3 wk. Liver iron concentration, malondialdehyde (MDA), glutathione (GSH), glutathione S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) were measured. High dietary iron increased liver iron concentrations slightly (P < 0.05), whereas it dramatically increased hepatic MDA (P < 0.0001). Ascorbic acid increased MDA but only in mice fed the low-iron diet (P < 0.05). The high-iron diet reduced GPx (P < 0.0001), CAT (P < 0.0005), SOD (P < 0.05), and GST (P < 0.005) activities regardless of ascorbic acid supplementation. In contrast, ascorbic acid reduced GPx (P < 0.0001) and CAT (P < 0.05) activities only in mice fed the low-iron diet. In conclusion, ascorbic acid supplementation can have prooxidant effects in the liver. However, ascorbic acid does not further increase the oxidative stress induced by increased dietary iron.