469 - Implications of Altered Trace Minerals and Iron Trafficking Proteins on Oxidant Stress in Thalassemia

Abstract

Thalassemia (THAL) patients have a genetic anemia causing incomplete erythropoiesis and iron overload, possibly leading to cardiomyopathy and diabetes. Plasma zinc (Zn) and Copper (Cu) deficiency are also observed in some patients with THAL, however, these effects are not as well characterized. It has been suggested that oxidative stress can be caused by increased labile plasma iron (LPI), and decreased serum Zn and Cu levels, however this is unproven. LPI can initiate peroxidation releasing malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE). Thus, we hypothesized that that a functional Zn or Cu deficiency can increase oxidative stress and that changes in the levels of key iron trafficking proteins, such as soluble transferrin receptor (sTfR) or hemopexin (HPX) would also affect oxidative stress. 39 subjects with informed consent were enrolled (29 patients with THAL and 10 healthy controls). LPI was measured using dihydrorhodamine 123. Both MDA and 4-HNE were measured using N-methyl-2-phenylindole. Iron trafficking proteins were measured by MRM mass spectrometry. Trace mineral levels were assessed by ICP spectroscopy. Plasma levels of the iron trafficking proteins, transferrin, HPX and haptoglobin (HAP) were all decreased in THAL patients (P