%0 Journal Article
%T Plasma Levels of Aminothiols, Nitrite, Nitrate, and Malondialdehyde in Myelodysplastic Syndromes in the Context of Clinical Outcomes and as a Consequence of Iron Overload
%A Kristyna Pimkov¨¢
%A Leona Chrastinov¨¢
%A Ji£¿¨ª Suttnar
%A Jana £¿tikarov¨¢
%A Roman Kotl¨ªn
%A Jaroslav £¿erm¨¢k
%A Jan Evangelista Dyr
%J Oxidative Medicine and Cellular Longevity
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/416028
%X The role of oxidative stress in the initiation and progression of myelodysplastic syndromes (MDS) as a consequence of iron overload remains unclear. In this study we have simultaneously quantified plasma low-molecular-weight aminothiols, malondialdehyde, nitrite, and nitrate and have studied their correlation with serum iron/ferritin levels, patient treatment (chelation therapy), and clinical outcomes. We found significantly elevated plasma levels of total, oxidized, and reduced forms of cysteine , homocysteine , and cysteinylglycine and significantly depressed levels of total and oxidized forms of glutathione and nitrite in MDS patients compared to healthy donors. Moreover, total and oxidized cysteinylglycine and nitrite differed significantly between the analyzed MDS subgroups with different clinical classifications. Malondialdehyde levels in plasma correlated moderately with both serum ferritin levels and serum free iron levels and were significantly higher in patients with iron overload. The other analyzed compounds lacked correlation with iron overload (represented by serum iron/ferritin levels). For the first time our results have revealed significant differences in the concentrations of plasma aminothiols in MDS patients, when compared to healthy donors. We found no correlation of these parameters with iron overload and suggest the role of oxidative stress in the development of MDS disease. 1. Introduction Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematological disorders, characterized by ineffective hematopoiesis and a high risk of transformation into acute myeloid leukemia (AML). Although the origin of MDS development is not fully understood, it has been determined that oxidative stress plays an important role in the initialization and disease progression of MDS [1]. One of the suggested mechanisms causing oxidative stress in MDS is attributed to a non-transferrin-bound iron (NTBI or free iron), which has been found in higher levels in the early stages of MDS patients receiving frequent red blood cell (RBC) transfusions [2]. Several studies have found elevated levels of oxidative stress markers (reactive oxygen species) and reduced levels of antioxidants (reduced glutathione (GSH)) in MDS patients and their correlation with serum ferritin levels [3, 4]. However, increased oxidative stress was revealed, even in the patients not receiving transfusions [5]. The presence of several other oxidative stress markers has been described in patients with established MDS, independent of iron or ferritin levels [6¨C8]. Oxidative
%U http://www.hindawi.com/journals/omcl/2014/416028/