Antioxidant status and lipid peroxidation in hereditary haemochromatosis

Hereditary haemochromatosis is characterized by iron overload that may lead to tissue damage. Free iron is a potent promoter of hydroxyl radical formation that can cause increased lipid peroxidation and depletion of chain-breaking antioxidants. We have therefore assessed lipid peroxidation and antioxidant status in 15 subjects with hereditary haemochromatosis and age/sex matched controls. Subjects with haemochromatosis had increased serum iron (24.8 (19.1–30.5) vs. 17.8 (16.1–19.5) μmol/l, p = 0.021) and % saturation (51.8 (42.0–61.6) vs. 38.1 (32.8–44.0), p = 0.025). Thiobarbituric acid reactive substances (TBARS), a marker of lipid peroxidation, were increased in haemochromatosis (0.59 (0.48–0.70) vs. 0.46 (0.21–0.71) μmol/l, p = 0.045), and there were decreased levels of the chain-breaking antioxidants alpha-tocopherol (5.91 (5.17–6.60) vs. 7.24 (6.49–7.80) μmol/mmol cholesterol, p = 0.001), ascorbate (51.3 (33.7–69.0) vs. 89.1 (65.3–112.9), p = 0.013), and retinol (1.78 (1.46–2.10) vs. 2.46 (2.22–2.70) μmol/l, p = 0.001). Patients with hereditary haemochromatosis have reduced levels of antioxidant vitamins, and nutritional antioxidant supplementation may represent a novel approach to preventing tissue damage. However, the use of vitamin C may be deleterious in this setting as ascorbate can have prooxidant effects in the presence of iron overload.