Selenium Supplementation to Chronic Kidney Dieae Patient on Hemodialyi ha no Effect on Superoxide Dimutae Activity and Malonyldialdehyde Concentrationin Blood

Reearch Article

Autin Therapeutic. 2014;1(2): 7.

Selenium Supplementation to Chronic Kidney Dieae Patient on Hemodialyi ha no Effect on Superoxide Dimutae Activity and Malonyldialdehyde Concentration in Blood

Zachara BA1,2*, Gromadzinka J1, Waowicz W1, Swiech R3 and Zbrog Z3

1Departament of Toxicology and Carcinogenei, Nofer Intitute of Occupational Medicine, Poland

2Higher School of Health Science, Bydgozcz, Poland

3B Braun Avitum Dialyi Center, Lodz, Poland

*Correponding author: BA Zachara, Departament of Toxicology and Carcinogenei, Nofer Intitute of Occupational Medicine, Lodz, 33/67 Nowodworka St, 85120 Bydgozcz, Poland

Received: September 20, 2014; Accepted: November 07, 2014; Publihed: November 11, 2014

Abtract

Background: Hemodialyi (HD) i the mot common form of treating patient in the End-Stage Renal Dieae (ESRD). The mot common approach to meauring the effect of oxidative tre ha been to meaure the activity of Glutathione Peroxidae (GSH-Px), Superoxide Dimutae (SOD) and the product of lipid peroxidation &ndah; Malonyldialdehyde (MDA). In Chronic Kidney Dieae (CKD) patient&rquo; Selenium (Se) level in blood i frequently lower than in healthy ubject and it decreae gradually with the progre of the dieae.

Aim: The aim of our tudy wa to examine whether the adminitration of Se to patient on HD alter the activity of GSH-Px and SOD in red blood cell and the level of MDA in plama.

Patient and Method: Our tudy involved 3 group of ubject: 1) 52 CKD nondialyzed patient, 2) patient in ESRD upplemented for 3 month with Se-rich yeat, 200 μg/day (n = 30) or placebo (n = 28) and 3) 52 healthy ubject. The GSH-Px and SOD activitie in red blood cell hemolyate and lipid peroxidation product [expreed a Thiobarbituric Acid Reactive Subtance (TBARS)] in plama were aayed.

Reult: GSH-Px activity in RBC wa ignificantly lower in nondialyzed CKD patient a compared with control group, but wa even more reduced in patient on HD. SOD activity in red blood cell wa ignificantly lower in patient in ESRD than in the healthy ubject and in the nondialyzed patient. Se upplementation to the HD patient ha no effect on the change in SOD activity. TBARS level in plama in patient on HD wa ignificantly higher than in the control group and in nondialyzed patient. Se adminitration did not reduce thi level.

Concluion: Se upplementation to patient on HD ha no effect on the activity of SOD in red blood cell and doe not prevent lipid peroxidation.

Keyword: Chronic kidney dieae; Hemodialyi; Selenium upplementation; Superoxide dimutae; Malonyldialdehyde

Introduction

Oxidative tre i defined a an imbalance between prooxidant and antioxidant in favor of the oxidant, potentially leading to damaging biological ytem [1,2]. Oxidative tre i preent and it marker can be meaured in both healthy people and thoe with variou clinical diorder [3]. Oxidative tre ha been linked with damaged protein, DNA, lipid in cell membrane (mainly unaturated fatty acid; PUFA) and carbohydrate [3], and thu lead to the progreion of everal dieae including cardiovacular dieae, cancer, Chronic Kidney Dieae (CKD) and other [4]. Mot importantly, oxidative tre i believed to promote the endothelial dyfunction and atherocleroi and, therefore, cardiovacular complication [5]. Free radical formed during oxidative tre are alo reponible for DNA damage and, a a conequence, for cancer development [6-8]. Long period of Hemodialyi (HD) treatment are linked to DNA damage due to oxidative tre [9]. The relationhip between DNA damage and cancer development ha been widely documented [10].

Hemodialyi i the mot common form of treatment for End-Stage Renal Dieae (ESRD) patient, and i aociated with coniderable mortality due to cardiovacular dieae and cancer [11,12]. The mot common approach to the meaurement of oxidative tre and free radical ha been to meaure the product of lipid peroxidation and PUFA oxidation &ndah; the level of Malonyldialdehyde (MDA) [13], a well a the activity of antioxidant enzyme. The body&rquo; defene againt lipid peroxidation include the enzyme: uperoxide dimutae (SOD; EC 1.15.1.1), glutathione peroxidae (GSH-Px; EC 1.11.1.9) and catalae (CAT; EC 1.11.1.6) [3]. Thee enzyme detroy dangerou product of oxygen metabolim.

Superoxide dimutae play a central role in catalyzing the pontaneou dimutation of uperoxide (O2·-) into oxygen and hydrogen peroxide [14]. Thu, they are an important antioxidant defene in nearly all cell expoed to oxygen. Hydrogen peroxide i then detroyed by GSH-Px and CAT [15].

Selenium (Se) i an eential trace element required in microgram amount by all mammal. It i incorporated in the form of Selenocyteine (Sec) into 25 elenoprotein [16]. Enzymatic activity ha been aigned to 12 of thee elenoprotein, and ome of them have antioxidant activitie [17]. GSH-Px i the mot extenively characterized elenoprotein, being found in Red Blood Cell (RBC) and cytool of nearly all tiue of mammal, bird and everal other organim. It i called claical GSH-Px (cGSH-Px or GSH-Px1) [18-20]. Five ioform of GSH-Px have been identified [21], two are preent in the blood: GSH-Px 1 preent in red blood cell and GSHPx 3 preent in plama. Both have a tetrameric form and contain one elenium per ubunit (or four gram atom of Se per mole of enzyme) in the form of Sec [22-24].

Zinc (Zn) i incorporated in the catalytic ite of everal hundred metaloprotein [25]. Copper (Cu) i an eential element for all living organim, erving a a cofactor for many important metaloprotein and enzyme [26]. Cu and Zn form the active ite of one of the form of SOD &ndah; Cu2+/Zn2+ SOD (called SOD 1), preent in cytool and red blood cell [27]. Concentration of Se and Zn in blood plama of CKD patient are decreaed [28,29] but the tatu of copper doe not eem to be influenced by CKD [30].

The aim of thi tudy wa to determine the activity of SOD and GSH-Px in RBC, the level of Zn, Cu and MDA concentration in plama of HD patient upplemented for 3 month with 200 μg of Se per day.

Material and Method

Patient and control

A 3-month, randomized double-blind, placebo-controlled trial wa carried out. The tudy involved 3 group of ubject. Group 1 compried of 52 of CKD nondialyzed patient in different tage of the dieae (creatinine level: 1. 00 &ndah; 10.99 mg/dL; mean: 5.16 mg/ dL); group 2: 58 CKD patient in ESRD (creatinine level: 4.20 &ndah; 16.60 mg/dL; mean: 9.43 mg/dL) on regular HD, divided into 2 ubgroup: 30 patient upplemented with 200 μg Se/day in the form a high- Se yeat tablet (produced by Pharma Nord, Bioelenium, Denmark) for 3 month, and 28 patient upplemented with placebo tablet containing identical yeat with no added Se (Pharma Nord). The patient were dialyzed 3 time a week for 4 hour. Group 3 conited of 52 healthy ubject. The tudy wa approved by the Intitute Ethic Committee for Medical Reearch (No. 18/2003) and all the participant gave their written conent.

Method

Blood ample were drawn from all the participant into vacutainer tube containing lithium heparin a an anticoagulant. From the healthy control and the patient with CKD not on dialyi, blood wa taken once, and from the patient undergoing dialyi, three time: before tarting the tudy and after 1 and 3 month of tablet upplementation. Blood wa centrifuged (+4o C, 5 000 r.p.m., 10 min), the plama wa harveted and tored at &ndah;20oC until analyi. The red blood cell were wahed three time with an exce of chilled 0.9% aline olution and were then hemolyzed by freezing and thawing and centrifuged again. Hemoglobin wa meaured by the routine cyanmethemoglobin method. Creatinine concentration wa determined by routine laboratory method uing Jaffy reaction (a kit produced by Cormay, Lublin, Poland). SOD activity in RBC hemolyate wa determined according to the method of Beauchamp and Fridovich [31] and wa expreed in U/g Hb. The GSH-Px activity in red cell hemolyate wa aayed by the coupled method of Paglia and Valentine [32] uing tert-butyl hydroperoxide a a ubtrate. One unit of the enzyme activity wa expreed a 1 mol NADPH oxidized/ min/g Hb of hemolyate (U/g Hb). Lipid peroxidation in the plama wa monitored by determining the end product of lipid peroxidation &ndah; malonyldialdehyde &ndah; decribed by Waowicz et al [33]. The value were expreed a Thiobarbituric Acid Reactive Subtance (TBARS)in nmol/mL. The concentration of Zn and Cu were meaured by flame atomic aborption pectrometry [34] uing Pye Unicam SP9 800 apparatu. The accuracy of the method wa checked with erum reference material (Seronorm, Nycomed, lot 704121).

Statitical analyi

Comparion of the level under tudy were made by multivariate analyi of variance [35] at three time point (before the tudy, one month and three month after tudy). When ignificant difference were found between the group, the difference were teted at all time point. The tet were baed on Shapiro-Wilk&rquo; tatitic, ignificance being et at 0.05. All tatitic were conducted uing the STATA 9 package.

Reult

GSH-Px activity in RBC wa ignificantly lower in the patient with CKD not on dialyi (P < 0.02) a compared with the control, but wa even more reduced in the patient on HD (P < 0.0001) (Figure 1). Dialyi treatment led to an increae in GSH-Px activity in both ubgroup, however the increae in activity wa much higher (P < 0.0001) in the ubgroup upplemented with Se in comparion with the placebo group (P < 0.005).

Figure 1: GSH-Px activity in RBC of the healthy control, the CKD nondialyzed patient and the patient on hemodialyi upplemented with placebo (white column) and elenium (dark column). Statitic: a, the CKD patient v. control, P < 0.02; b, the HD 0 (both ubgroup taken together) v. the control and the nondialyzed CKD patient, P < 0.0001; c, HD 3 v. HD 0 (upplemented with placebo), P < 0.005; d, HD 3 v. HD 0 (upplemented with Se), P < 0.0001.

    

    
    

    

    Figure 1:  GSH-Px activity in RBC of the healthy control, the CKD nondialyzed patient and the patient on hemodialyi upplemented with placebo (white column) and elenium (dark column). Statitic: a, the CKD patient v. control, P < 0.02; b, the HD 0 (both ubgroup taken together) v. the control and the nondialyzed CKD patient, P < 0.0001; c, HD 3 v. HD 0 (upplemented with placebo), P < 0.005; d, HD 3 v. HD 0 (upplemented with Se), P < 0.0001.
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SOD activity in RBC of the nondialyzed patient with CKD did not differ from the activity in the healthy control. In the dialyzed patient, at the baeline (both ubgroup taken together), SOD activity wa lower only by 8.5% compared with control (P < 0.02) (Figure 2). Hemodialyi lead to a mall reduction in enzyme activity in both ubgroup, but after 3 month, thee value were not ignificantly different from the activity found at HD 0. It hould be emphaized that elenium upplementation to the patient on HD had no effect on the change in the activity of thi enzyme.

Figure 2: SOD activity in RBC of the healthy control, the nondialyzed CKD patient and the patient on hemodialyi upplemented with placebo (white column) and elenium (dark column). Statitic: a, the HD 0 (both ubgroup) v. the control and the nondialyzed CKD patient, P < 0.02; b, HD 3 v. HD 0, P = 0.1 (NS).

    

    
    

    

    Figure 2: SOD activity in RBC of the healthy control, the nondialyzed CKD patient and the patient on hemodialyi upplemented with placebo (white column) and elenium (dark column). Statitic: a, the HD 0 (both ubgroup) v. the control and the nondialyzed CKD patient, P < 0.02; b, HD 3 v. HD 0, P = 0.1 (NS).
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Zinc concentration in plama of the nondialyzed CKD patient and the patient on HD wa ignificantly lower compared with the healthy control (P < 0.0001) (Figure 3). In the dialyzed patient the concentration wa lower than in the nondialyzed (P < 0.05). In the placebo group it did not change during the 3 month tudy. In the dialyzed patient Se upplementation led to a gradual increae in the concentration of Zn, which after 3 month had reached a valueignificantly higher compared with the HD 0 (P < 0.01).

Figure 3: Zinc concentration in plama of the healthy control, the nondialyzed CKD patient and the patient on hemodialyi upplemented with placebo (white column) and elenium (dark column). Statitic: a, the CKD nondialyzed patient and the HD 0 (both ubgroup taken together) v. the control, P < 0.0001; b, HD 0 (both ubgroup) v. CKD, P < 0.05; c, HD 3 (+Se) v. HD 0 (+Se), P < 0.01. 

    

    
    

    

    Figure 3: Zinc concentration in plama of the healthy control, the nondialyzed CKD patient and the patient on hemodialyi upplemented with placebo (white column) and elenium (dark column). Statitic: a, the CKD nondialyzed patient and the HD 0 (both ubgroup taken together) v. the control, P < 0.0001; b, HD 0 (both ubgroup) v. CKD, P < 0.05; c, HD 3 (+Se) v. HD 0 (+Se), P < 0.01.
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Copper concentration in plasma in all groups was nearly the same and ranged from 1.27 to 1.37 mg/L (Figure 4). The values in both subgroups remained constant during the course of the dialysis.

Figure 4: Copper concentration in plasma of the healthy controls, the nondialyzed CKD patients and the patients on hemodialysis supplemented with placebo (white columns) and selenium (dark columns). Statistics: There were no statistical differences between the groups..

    

    
    

    

    Figure 4: Copper concentration in plasma of the healthy controls, the nondialyzed CKD patients and the patients on hemodialysis supplemented with placebo (white columns) and selenium (dark columns). Statistics: There were no statistical differences between the groups.

Plasma MDA concentration in the nondialyzed CKD patients did not differ from the values found in the control group, but was significantly higher in the patients on HD (Figure 5). The administration of Se for a period of three months to the dialyzed patients had no effect on the change in the concentration of MDA.

Figure 5: TBARS concentration in plasma of the healthy controls, the nondialyzed CKD patients and the patients on hemodialysis supplemented with placebo and selenium. Statistics: a, HD 0 (both subgroups taken together) vs. the healthy controls and the nondialyzed CKD patients, P< 0.05.

    

    
    

    

    Figure 5:  TBARS concentration in plasma of the healthy controls, the nondialyzed CKD patients and the patients on hemodialysis supplemented with placebo and selenium. Statistics: a, HD 0 (both subgroups taken together) vs. the healthy controls and the nondialyzed CKD patients, P< 0.05.

Discussion

Reactive oxygen species have been implicated in the pathogenesis of a broad variety of tissue injuries in various disease states. This is mainly mediated by peroxidation of lipids, injury of nucleic acids (mainly DNA) and proteins [36,37]. The first line of defense against ROS is SOD. There are some studies which have shown decreased activity of red blood cell SOD and GSH-Px in CKD patients and suggest that hemodialysis can produce oxidative stress which leads to lipid peroxidation [3,38]. The decreased activity of red blood cell SOD and GSH-Px in the dialyzed patients found in our study is in accordance with the above observations. Our and other studies have shown that the patients with CKD and especially those on HD have significantly lower Se concentration in blood components and lower GSH-Px activity in plasma [28,29,39-42].

GSH-Px reduces hydrogen peroxide and all organic hydroperoxides [43]. In this study we demonstrated that RBC GSHPx activity in nondialyzed patients with CKD is significantly lower compared with healthy subjects. Results of this study correspond to our previous study [44] and to the observations of many other authors [3,36,45-48]. However, studies of several other authors presented conflicting results on the red cell GSH-Px activity in the CKD patients [29,49-51].

Red blood cell GSH-Px is synthesized during erythropoiesis, and is not dependent on kidney function [52] therefore it is not clear why in these patients its activity is reduced. It seems very likely that the main reason for this is selenium deficiency [29,39,42,53].

Montazerifar et al [3] have shown that in the dialyzed patients RBC GSH-Px and SOD activity was more than two times lower compared with the controls and decreased markedly (by about 50% and 33%, respectively) after HD (P < 0.0001). The authors believe that dialysis reduces the antioxidant defense of the organism.

There is a dearth of publications on the effect of Se supplementation to CKD patients.

In the literature there is no clear opinion concerning the administration of selenium to patients on HD. Some authors suggest that Se should be administered to these patients [54-56], although it has little or no effect on the GSH-Px activity in plasma [42,57]. Due to the antioxidant properties of Se incorporated in some other selenoenzymes, it has been suggested that supplementation of this element might be of benefit and efficacious in reducing cardiovascular complications in uremic patients [58]. Koenig et al [36] believe that Se supplementation improves the oxygen radical scavenger system and increases selenium concentration in blood and the activity of selenium dependent GSH-Pxs in other tissues. Thus, Se should be considered for micronutrient supplementation in patients on chronic HD therapy.

Our group studied the effect of Se supply on plasma GSH-Px protein level in plasma [39] and on protection of DNA against ROS in lymphocytes in the patients on HD [9]. In a few studies conducted by other authors, the patients on HD were administered with different preparations and doses of Se and for different periods of time. For this reason, the results presented differ widely from each other.

In our study, RBC GSH-Px activity, in the patients on HD receiving Se for three months rose from 18.4 to 25.1 U/g Hb (P < 0.0001). Koenig et al [36] supplemented intravenously to the dialyzed patients with 400 μg sodium selenite three times a week for eight weeks and have shown that RBC GSH-Px activity rose significantly (from 16.5 to 24.2 U/g Hb; P < 0.001). The authors believe that based on the conclusions presented above, Se should be administered to the CKD patients.

Superoxide dismutase plays a major role in protecting the cells against oxidative stress

This occurs in the patients on HD and is linked to the acceleration of tissue damage in ESRD [59]. SODs work in conjunction with CAT and GSH-Pxs to diminish the harmful effects of ROS [60]. The activity of SOD varies among tissues. The highest levels are seen in the liver, kidney and spleen [37]. Vaziri et al [61] have shown that in rat kidney tissue with surgically induced CKD, Cu/Zn SOD activity was significantly lower (by 55%) compared to sham operated rats.

Studies on the activity of SOD in RBCs in the patients on HD have provided different results. Our results have shown that in the nondialyzed CKD patients RBC Cu2+/Zn2+ SOD activity was the same as in the control group but was significantly lower in the patients on HD. Results of our study are fully consistent with the observationsof Ceballos-Picot et al [40] who have also shown that the activity of this enzyme was the same as in the controls and was not affected by the progression of renal failure, but in the patients on HD the activity was significantly lower (P < 0.001). Similar to our results Atamer et al [62] did not find significant difference in RBC SOD activity between the CKD patients and the control group. Koca et al [63] showed that, similarly to our results, SOD activity in red blood cells in the dialyzed patients is significantly lower than in the healthy controls. Prolonged exposure to HD (up to 11 years) had no effect on the SOD activity.

Our study has shown that dialysis had little effect on the RBC SOD activity: After three-month treatment the activity decreased insignificantly in both subgroups [by 11% (controls) and 9% (+Se)]. Se supplementation to the HD patients had no effect on the activity of this enzyme. Quite different results were obtained by Koenig et al [36] and Mimic-Oka et al [49]. Koenig’s group has shown that in the CKD patients on HD, SOD activity in RBCs was significantly higher (P < 0.001) than in the control group. With regard to the administration of Se to the dialyzed patients, the results obtained by these authors are consistent with the data of our study: during Se administration RBC SOD activity decreased slightly and rose 4 weeks after the end of supplementation. On the contrary, Mimic-Oka et al [49] found that in all stages of CKD SOD activity in red blood cells increased from 43% (early stages) to 81% (ESRD) compared with the healthy controls. The authors argue that augmentation of erythrocyte SOD activity, which serves a key function in the elimination of ROS, in the CKD patients probably, provides significant protection for red blood cells against exogenous and endogenous oxidant metabolites accumulating in the blood in chronic renal insufficiency. In another experiment Mimic-Oka et al [64] studied the SOD activity in plasma of nondialyzed CKD patients and those on HD and have shown that in the early stages of the disease enzyme activity did not differ from the control group, but in the ESRD and in the patients on HD it was significantly (P < 0.001) higher that in the control group. The authors believe that the gradual increase in the activity of SOD in plasma of the HD patients together with the fall in plasma GSH-Px activity may result in an accumulation of H2O2 and other hydro peroxides.

Several studies on the erythrocyte SOD activity presented by other authors [47,48,65,66] have reported lower values in patients on HD. Low values of the activity was accompanied by significantly reduced concentrations of Cu and Zn. Richard et al [47] showed also a high, statistically significant (P < 0.02) correlation between RBC SOD and Zn (r = 0.58) and SOD and Cu (r = 0.60). Mimic-Oka et al [67] demonstrated that in the patients on HD red blood cell SOD was significantly lower (P < 0.001) compared to the control group and nondialyzed patients. The dialysis did not affect the activity of this enzyme.

According to most studies, the patients with CKD have reduced plasma concentration of Zn and during dialysis this concentration does not change significantly [cf 68]. The results of our study confirm these observations. In Se supplemented subgroup Zn concentration increased significantly in comparison to the baseline. The results of our observation are consistent with the data of other authors [41,69- 72], who have also shown statistically lower levels of this element compared with the healthy subject.

Our study has shown that the concentration of Cu in the plasma of patients with CKD and on dialysis did not differ from the values of the control group. Se supply to the dialyzed patients had no effect on plasma concentration of Cu. Our results are consistent with the data of Agenet et al [73] who did not show differences in the concentration of Cu in plasma and RBC among the dialyzed patients and the control group; the process of dialysis did not affect the change of these levels. Several authors [28,63,71,72] have shown higher levels of plasma/ serum Cu in the patients on HD.

Oxidative stress increased lipid peroxidation [74]. Thiobarbituric acid reactive substances are naturally present in biological specimens and include lipid hydroperoxides and aldehydes (mainly MDA) concentration which increases as a response to oxidative stress [75].

Studying the concentration of MDA in blood components in patients on HD most authors found significantly higher values of this compound compared with the healthy subjects. Martin-Mateo et al [46] have shown that in HD patients the baseline concentration of MDA in RBCs before dialysis was higher by 31% compared with the controls and after HD the concentration increased significantly (P < 0.001) by about 40%. Ozden et al [43] have shown that MDA concentration in plasma increased significantly after HD (P < 0.0001) by 67% compared to pre-HD values. Koca et al [63] showed that the concentration of MDA in plasma of patients on dialysis was nearly two times higher than in the control group, and during dialysis (up to 11 years) it further increased significantly.

However, Samouilidou and Grapsa [76] showed that in the patients treated with HD and Peritoneal Dialysis (PD) plasma MDA levels were significantly higher than in the control group, but after HD – contrary to the above mentioned authors – the concentration was significantly reduced. Paul et al [48] did not find any differences in plasma MDA levels between the HD patients and the control group, while the RBCs MDA concentrations were significantly higher in those patients.

Several studies have shown that administration of certain antioxidant compounds to the dialyzed patients prevented the oxidation of PUFAs. The most often used antioxidants in the dialyzed patients are vitamins E and C, sometimes selenium.

The results of our study showed that selenium supplementation to the dialyzed patients has no effect on lipid per oxidation – TBARS concentration in plasma after 3-month supplementation of the element did not differ from the baseline values and was the same as in the placebo group.

Our results are in some way similar to the data published by Koenig et al [36] who supplemented the patients on chronic HD with sodium selenite and observed that MDA level was only temporarily decreased during Se supplementation, but returned to the restudy level after 8 weeks. In their study [36] MDA concentration in the patients before dialysis was profoundly elevated compared with the normal controls (1.68 vs. 0.36 mmol/L plasma; P < 0.001). Also Ardalan et al [77], who supplemented the patients on HD (two times a week) with capsules containing 600 μg Se (sodium selenide) and 400 IU vitamin E found no difference in the concentration of MDA in the serum before and after the completion of the study.

Recently, Salehi et al [78] has shown that administration of 200 μg Se per day (selenium yeast) to the HD patients for a period of 12 weeks resulted in the concentration of MDA in the serum being significantly (P < 0.001) lower compared to the placebo group. The baseline concentration of MDA in both groups was the same. Also El-Demerdash and Nasr [79] have recently shown that Se supplementation (200 μg/kg BW/day for 30 days) to rats caused a significant decrease in the level of TBARS and an increase in SOD and GSH-Px activity in serum. The question about supplementation of antioxidants to the HD patients is open although there are some positive data regarding the use of moderate and safe selenium supplementation to those patients. In our experimental studies we have shown that administration of Se to the patients on HD stimulates the activity of GSH-Px in erythrocytes [42]. It has also been shown that Se administration to mammals induces the synthesis of GSHPx 1 in other tissues [20,80]. Se has a negligible effect on the activity of GSH-Px in plasma, does not induce the synthesis of this enzyme in the kidneys [39] but prevents DNA damage in lymphocytes [9]. Some authors recommend that the impaired kidney function can be improved by Se administration in the CKD patients, particularly in the patients on HD [36,78,81,82]. Zima et al [83] suggest that in the dialyzed patients Se supply may be beneficial (increasing glutathione peroxidase activity, immunostimulatory properties, cardioprotective effect, for the chronic renal failure patients. Supplementation with a trace element may be indicated when its depletion was unequivocally documented and when there is evidence of the positive effects of this element on the quality of life of the dialyzed patients.

In conclusion, our results suggest that Se supplementation to patients on HD increases the activity of GSH-Px in red blood cells but has no effect on the activity of SOD in these cells. Se administration has no effect on the reduction of MDA concentration in plasma.

Acknowledgement

This study was partly financed by the State Committee for Scientific Research Committee (KBN), Warsaw, Poland (Grant No. 2 P05D 097 27). Thanks are due to Mr. Sven Moesgaard, Pharma Nord, Denmark, for supplying us with selenium rich-yeast and placebo used in this study.

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Citation: Zachara BA, Gromadzinska J, Wasowicz W, Swiech R and Zbrog Z. Selenium Supplementationto Chronic Kidney Disease Patients on Hemodialysis has no Effect on Superoxide Dismutase Activity and Malonyldialdehyde Concentration in Blood. Austin Therapeutics. 2014;1(2): 7. ISSN:2472-3673