ANTIOXIDANT STATUS AND LIPID-PEROXIDATION IN HEREDITARY HEMOCHROMATOSIS

Hereditary haemochromatosis is characterised by iron overload that may lead to tissue damage. Free iron is a potent promoter of hydroxyl rad ical formation that can cause increased lipid peroxidation and depleti on of chain-breaking antioxidants. We have therefore assessed lipid pe roxidation and antioxidant status in 15 subjects with hereditary haemo chromatosis and age/sex matched controls. Subjects with haemochromatos is had increased serum iron (24.8(19.1-30.5) vs. 17.8(16.1-19.5) mu mo l/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(0.21-0.7I) mu mol/l, p = 0.045), and there were decreas ed levels of the chain-breaking antioxidants alpha-tocopherol (5.91(5. 17-6.60) vs. 7.24(6.49-7.80) mu mol/mmol cholesterol, p = 0.001), asco rbate (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) mu mol/l, p = 0.001). Patients with hereditary haemochromatosis have reduced levels of antioxidant vitami ns, and nutritional antioxidant supplementation may represent a novel approach to preventing tissue damage. However, the use of vitamin C ma y be deleterious in this setting as ascorbate can have prooxidant effe cts in the presence of iron overload.