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首页> 外文期刊>Journal of Biotechnology and Biodiversity >Deferoxamine and deferasirox action in erythrocytes of patients with transfusion-dependent anemia, under “in vitro” oxidative stress
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Deferoxamine and deferasirox action in erythrocytes of patients with transfusion-dependent anemia, under “in vitro” oxidative stress

机译:在“体外”氧化应激下,输血依赖性贫血患者的红细胞中的去铁胺和去铁胺作用

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Patients with sickle cell anemia and thalassemia can have transfusional iron overload and oxidative stress. This study aimed to evaluate the action of iron chelators deferoxamine (DFO) and deferasirox (DFX) in the erythrocyte oxidative metabolism. In this cross-sectional, descriptive study were analyzed blood samples , collected between January and June 2011, obtained from 10 normal individuals and 31 patients with thalassemia or sickle cell anemia, being 19 under DFO or DFX treatment, attended at HEMEPAR. Erythrocytes were incubated with oxidizing agents’ tBHP and AAPH. It were carried out determinations of methemoglobin, reduced glutathione (GSH), thiobarbituric acid reactive substances (TBARS), glucose 6-phosphate dehydrogenase (G6-PD) activity, and hemolysis, with analysis of variance (one and two ways) and Tukey test (p Baseline values of parameters analyzed did not present significant differences between normal and patient erythrocytes under treatment. After oxidative stress, it was observed significant changes, but equally in all groups, for methemoglobin, GSH, and G6-PD, however indicating partial protection against oxidation for TBARS and hemolysis. Iron chelates showed no protection in normal erythrocytes, in vitro, against methemoglobin formation, GSH decrease or reduction on G6-PD activity, however partial protection against TBARS formation or induced hemolysis, under oxidative stress, was observed. The results suggest that iron chelates DFO and DFX can promote partial protection of erythrocytes against oxidative stress, both in pathological conditions of iron overload or by oxidation in vitro , mainly for TBARS parameters and hemolysis.
机译:镰状细胞性贫血和地中海贫血患者可出现输血铁超负荷和氧化应激。这项研究旨在评估铁螯合剂去铁胺(DFO)和去铁胺(DFX)在红细胞氧化代谢中的作用。在此横断面,描述性研究中,分析了2011年1月至2011年6月期间从10名正常人和31名地中海贫血或镰状细胞性贫血患者(其中19例接受DFO或DFX治疗)中采集的血液样本,这些患者参加了HEMEPAR。将红细胞与氧化剂的tBHP和AAPH孵育。进行了高铁血红蛋白,还原型谷胱甘肽(GSH),硫代巴比妥酸反应性物质(TBARS),6-磷酸葡萄糖脱氢酶(G6-PD)活性和溶血的测定,并进行了方差分析(一种和两种方法)和Tukey检验(p所分析参数的基线值在治疗的正常和患者红细胞之间没有显着差异。在氧化应激后,观察到高铁血红蛋白,GSH和G6-PD的显着变化,但在所有组中均相同,但表明部分保护在体外,正常血液中的铁螯合物对高铁血红蛋白的形成,GSH的降低或对G6-PD活性的降低均无保护作用,但是在氧化应激下,对TBARS的形成或诱导的溶血却有部分保护作用。结果表明,在病理学中,铁螯合物DFO和DFX可以促进红细胞对氧化应激的部分保护。 l铁超载或体外氧化的条件,主要用于TBARS参数和溶血作用。

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