Marker Of Protein Oxidation Research Articles

Behaviour of protein carbonyl groups in juvenile myocardial infarction

Acute myocardial infarction (AMI) is accompanied by oxidative stress, and protein oxidation is among the consequences of oxidative stress. We examined the plasma concentration of protein carbonyl groups (PC), a marker of protein oxidation, in a group of young subjects with AMI (45 men and 5 women; mean age 40.4 ± 4.8 yrs). We found a significant increase of PC (p < 0.001) in comparison with normal controls. No difference was observed between patients with AMI characterized by elevated ST segment and those without elevation of ST segment. There was no correlation between the ejection fraction and PC in the whole group nor in the subgroups of STEMI and non-STEMI patients. Subdividing the whole group of AMI patients according to the number of risk factors and the number of stenosed coronary vessels, the difference in PC level was not statistically significant among the subgroups. This study showed an increased protein oxidation in young subjects with recent AMI. Further investigation is needed to ascertain whether this can be a target of therapeutic intervention.

Comparative Effects of Roystonea Regia (D-004) and Saw Palmetto Lipid Extracts On Blood Oxidative Variables in Men with Benign Prostate Hyperplasia (BPH)

Background: Lipid extracts of Roystonea regia (D-004) and saw palmetto (SP) fruits have been shown to prevent experimentally-induced prostate hyperplasia in rodents, and to produce antioxidant effects in experimental and clinical studies. OBJECTIVE: To compare the effects of D-004 and SP extracts on the International Prostate Symptoms Score (IPSS) and plasma oxidative variables in men with benign prostate hyperplasia (BPH) METHODS: This randomized, double-blind study was conducted in patients with moderate BPH. Forty-eight eligible subjects (average age: 65 years) were randomised to D-004 (320 mg/day) or SP (320 mg/day) capsules for 8 weeks. Decrease on IPSS was the primary efficacy variable. Oxidative markers were secondary outcomes. Data were analysed as per Intention to treat. RESULTS: D-004 and SP significantly decreased mean IPSS values by 33.9% (p<0.0001) and 24.4% (p<0.001), respectively, as compared to baseline. D-004 (p<0.0001) reduced plasma malondialdehyde (MDA) (32.6%), protein-linked carbonyl groups (CG) (25.2%) and increased (p<0.0001) catalase (CAT) activity. SP treatment lowered (p<0.0001) MDA (28.2%), CG (23.4%) and raised (p<0.0001) CAT activity. Effects on oxidative variables were similar in both groups. D-004, not SP, significantly lowered (p<0.05) prostate specific antigen (PSA) values. Both treatments were well tolerated. Only 2 SP-treated patients withdrew from the study. No adverse experiences were reported. CONCLUSIONS. Treatment with D-004 or SP (320 mg/day) for 8 weeks decreased significantly IPSS values in patients with moderate BPH, the effect of D-004 being the better, but further studies should confirm this result. Both treatments favourably and similarly modified plasma MDA (lipid peroxidation marker), GC (protein oxidation marker) and CAT activity.

Concentration dependent effect of calcium on brain mitochondrial bioenergetics and oxidative stress parameters

Mitochondrial dysfunction following traumatic brain and spinal cord injury (TBI and SCI) plays a pivotal role in the development of secondary pathophysiology and subsequent neuronal cell death. Previously, we demonstrated a loss of mitochondrial bioenergetics in the first 24 h following TBI and SCI initiates a rapid and extensive necrotic event at the primary site of injury. Within the mitochondrial derived mechanisms, the cross talk and imbalance amongst the processes of excitotoxicity, Ca2+ cycling/overload, ATP synthesis, free radical production and oxidative damage ultimately lead to mitochondrial damage followed by neuronal cell death. Mitochondria are one of the important organelles that regulate intracellular calcium (Ca2+) homeostasis and are equipped with a tightly regulated Ca2+ transport system. However, owing to the lack of consensus and the link between downstream effects of calcium in published literature, we undertook a systematic in vitro study for measuring concentration dependent effects of calcium (100–1000 nmols/mg mitochondrial protein) on mitochondrial respiration, enzyme activities, reactive oxygen/nitrogen species (ROS/RNS) generation, membrane potential (ΔΨ) and oxidative damage markers in isolated brain mitochondria. We observed a dose- and time-dependent inhibition of mitochondrial respiration by calcium without influencing mitochondrial pyruvate dehydrogenase complex (PDHC) and NADH dehydrogenase (Complex I) enzyme activities. We observed dose-dependent decreased production of hydrogen peroxide and total ROS/RNS species generation by calcium and no significant changes in protein and lipid oxidative damage markers. These results may shed new light on the prevailing dogma of the direct effects of calcium on mitochondrial bioenergetics, free radical production and oxidative stress parameters that are primary regulatory mitochondrial mechanisms following neuronal injury.

Neuroprotective Effect of 17β Estradiol on Membrane Fluidity in Ageing Rat Brain

Oxidants and fluidity of membrane lipids are known to play a major role in ageing and age related neurodegenerative diseases. In the present study, authors observed the in vitro effect of Tachykinin neuropeptide NKB, Amyloid Beta (25-35) and combined NKB and Aβ (25-35) on membrane fluidity, oxidative modification and protein surface hydrophobicity of proteins on 17β estradiol (E2) treated ageing female rat brain synaptosomes of 3 months (young), 12 months (adult) and 24 months (old) age groups. Authors found that membrane fluidity of synaptosomes decreased in ageing rat brain. Similarly, Aβ (25–35) decreased the membrane fluidity in ageing rat. These effects of ageing and Aβ (25–35) on membrane fluidity were restored by NKB and combined NKB+Aβ (25–35) with estradiol. The tryptophan fluorescence was used as a sensitive marker of protein oxidation. Tryptophan fluorescence significantly decreased in estradiol treated synaptosomes of ageing rats. To evaluate the effect of oxidative stress on membrane and protein conformation, fluorescent probe ANS was used. A decrease in ANS fluorescence in estradiol treated synaptosomes of ageing rats indicated that estradiol is associated with significant conformational changes and surface hydrophobicity of membranes and proteins. In contrast these changes were not detected with NKB and Aβ in estradiol treated synaptosomes. The present findings suggest that treatment with NKB along with estradiol restores age- and Aβ-induced alterations and demonstrating a possible beneficial role of NKB and estradiol in preventing some of the age related changes in the brain.

Oxidative stress markers, alpha-fetoprotein and alpha-fetoprotein-L3 levels of alcohol dependent subjects

As one of the most important social problems around the world, alcohol addiction damages the body by causing fatty liver and can lead to hepatitis, cirrhosis, and even hepatocellular carcinoma. In the present study we investigated the relationship between oxidative stress and liver cancer risk in alcohol dependent patients using some noninvasive pro- and antioxidant markers. We also examined the relative value of individual markers and their relationship with liver tumor markers including alpha-fetoprotein (AFP) and AFP-L3. Serum samples were collected from age-matched males who are in either healthy control or alcohol dependent groups. The effect of alcohol dependence on the serum proteins including ceruloplasmin and prealbumin, oxidative stress markers, AFP and AFP-L3 levels were evaluated. In the alcohol dependent group, the levels of lipid peroxidation end-product malondialdehyde and protein oxidation marker protein carbonyl were significantly higher than the control group. Similarly, serum ceruloplasmin, prealbumin, AFP and AFP-L3 levels were found to be slightly higher in the alcohol dependent group. However, superoxide dismutase enzyme activities were significantly lower in the alcohol dependent group than in the control group. These results showed that AFP-L3 tends to correlate positively with alcohol consumption. Further studies including higher number of study subjects will be needed to demonstrate a potential statistical significance of increased AFP-L3 levels in alcohol dependent subjects and may contribute to determining the relations between alcohol dependance and liver cancer risk.

Interplay between protein carbonylation and nitrosylation in plants

ROS and reactive nitrogen species (RNS) are key regulators of redox homeostasis in living organisms including plants. As control of redox homeostasis plays a central function in plant biology, redox proteomics could help in characterizing the potential roles played by ROS/RNS-induced posttranslational modification in plant cells. In this review, we focus on two posttranslational modifications: protein carbonylation (a marker of protein oxidation) and protein S-nitrosylation, both of which having recently emerged as important regulatory mechanisms during numerous fundamental biological processes. Here, we describe the recent progress in proteomic analysis of carbonylated and nitrosylated proteins and highlight the achievements made in understanding the physiological basis of these oxy/nitro modifications in plants. In addition, we document the existence of a relationship between ROS-based carbonylation and RNS-based nitrosylation thus supporting the finding that crosstalk between cellular signaling stress pathways induced by ROS and RNS could be mediated by specific protein modifications.

Modulation of age‐related changes in oxidative stress markers and energy status in the rat heart and hippocampus: a significant role for ozone therapy

Oxidative stress emerges as a key player in the ageing process. Controlled ozone administration is known to promote an oxidative preconditioning or adaptation to oxidative stress. The present study investigated whether prophylactic ozone administration could interfere with the age-related changes in the heart and the hippocampus of rats. Four groups of rats, aged about 3 months old, were used. Group 1 (Prophylactic ozone group) received ozone/oxygen mixture by rectal insufflations (0.6 mg/kg) twice/week for the first 3 months, then once/week till the age of 15 months. Group 2 (Oxygen group) received oxygen as vehicle for ozone in a manner similar to group 1. Group 3 (Aged control group) was kept without any treatment until the age of 15 months. A fourth group of rats (Adult control group) was evaluated at 3 months of age to provide baseline data. Ozone alleviated age-associated redox state imbalance as evidenced by reduction of lipid and protein oxidation markers, lessening of lipofuscin deposition, restoration of glutathione levels in both tissues and normalization of glutathione peroxidase activity in the heart tissue. Ozone also mitigated age-associated energy failure in the heart and the hippocampus, improved cardiac cytosolic Ca(2+) homeostasis and restored the attenuated Na(+) , K(+) -ATPase activity in the hippocampus of aged rats. These data provide new evidence concerning the anti-ageing potential of prophylactic ozone administration.

In vitro effects of nitric oxide donors on apoptosis and oxidative/nitrative protein modifications in ADP-activated platelets

Nitric oxide (NO) is an important physiological signaling molecule. However, when produced in excessive amounts, NO can also have toxic effects. The aim of this study is to investigate the effects of exogenous- and endogenous-derived NO on oxidative modifications of proteins and apoptosis in activated platelets. Washed platelets were incubated with L-arginine or nitroso-glutathione (GSNO) in the presence of adenosine diphosphate (ADP). After incubation, caspase-3 activity, phosphatidylserine (PS) externalization and the potential of mitochondrial membrane as markers of apoptosis were measured. In addition, the alterations in protein carbonylation (PCO) and nitrotyrosine (NT) formation as markers of protein oxidation were examined. Platelet activation with ADP (20 µM) significantly increased PCO and NT levels and apoptotic events. After incubation with L-arginine, platelet NO production increased significantly. This L-arginine-induced increase caused decreases in formerly increased PCO and NT levels associated with ADP-induced platelet activation. Stimulation of NO production with L-arginine protected platelets from apoptosis. GSNO caused an increase in protein NT levels. Despite this change, GSNO was effective in inhibition of P-selectin expression, platelet aggregation, protein carbonylation and apoptosis. The results suggest that L-arginine and GSNO-mediated NO leads to the inhibition of key apoptotic processes including caspase-3 activation, PS exposure and low mitochondrial membrane potential in washed platelets. The inhibitory effect of platelet clearance of L-arginine and GSNO may be a novel useful therapeutic property in clinical application.

385 A Double Blind, Randomized Controlled Trial on the Resuscitation of Preterm Infants with 30% Versus 65% Oxygen at Birth

BackgroundResuscitation of term infants at birth with 100% oxygen increases oxidative stress with concomitant deleterious effects. Optimal levels for preterm infants are unknown. We hypothesized that resuscitation of preterms with...

Urinary Bromotyrosine Measures Asthma Control and Predicts Asthma Exacerbations in Children

SH Wedes, W Wijia, SAA Comhair. J Pediatr. 2011;159(2):248–255 To determine the usefulness of urinary bromotyrosine, a marker of eosinophil-catalyzed protein oxidation, in monitoring asthma control and predicting future exacerbations. There were 57 people enrolled from the Cleveland Clinic with a diagnosis of asthma between the ages of 5 and 21 years. Recruitment occurred from July to September 2006 and follow-up from August to November 2006. …

The involvement of serotonin metabolism in cigarette smoke-induced oxidative stress in rat lung in vivo

Recently, we have reported the dysregulation of circulating serotonin (5-hydroxytryptamine, 5-HT) homeostasis in patients with chronic obstructive pulmonary disease (COPD). An increase in metabolism of 5-HT has been reported to induce oxidative stress via monoamine oxidase (MAO)-dependent pathway. The present study aimed at investigating the effect of cigarette smoke exposure on the systemic circulation and local airway 5-HT levels as well as MAO-mediated oxidative pathway using a cigarette smoke-exposed rat model. Male Sprague-Dawley rats (150–200 g) were exposed to either sham air or 4% (v/v, smoke/air) cigarette smoke for 1 hour daily for 56 consecutive days. Sera, bronchoalveolar larvage (BAL) and lung tissues were collected 24 hours after the last exposure. We found a significant reduction in the reduced glutathione (rGSH) and an elevation in advanced oxidation protein products (AOPP), a protein oxidation marker, in the lung of cigarette smoke-exposed group (p < 0.05). A significant increase in 5-HT was found in serum (p < 0.05), but not in the BAL or lung, after cigarette smoke exposure. MAO-A activity was significantly elevated in the lung of cigarette smoke-exposed group (p < 0.05). Furthermore, increased superoxide anion levels were found in lung homogenates of cigarette smoke-exposed rats after incubation with 5-HT (p < 0.05), which was positively associated with the increase in MAO-A activity (r = 0.639, p < 0.05). Our findings supported the presence of GSH disruption and protein oxidation in the lung after cigarette smoke exposure. The metabolism of 5-HT by MAO-A in the lung enhanced cigarette smoke-induced superoxides, which might contribute to the pathogenesis of COPD.

Oxidación de proteínas y lípidos en cerebro de cobayos durante la exposición a grandes alturas (4540 m)

El objetivo del presente estudio fue evaluar el efecto del tiempo de exposición a grandes alturas sobre la oxidación de proteínas y lípidos en el tejido cerebral de cobayos. Se utilizaron cincuenta cobayos nativos del nivel del mar: 10 permanecieron en su hábitat (Lima, 150 m) sirviendo de control, y cuarenta fueron trasladados a Morococha, 4540 m, y sacrificados los días 1, 3, 7 y 14 después de su arribo. Se determinaron: la actividad de fosfolipasa A2 (FLA2), los niveles de hidroperóxidos lipídicos (LOOH) y malondialdehído (TBARS), como marcadores de la oxidación de lípidos; nivel de grupos carbonílicos (GC), como marcadores de la oxidación de proteínas; y la actividad de las enzimas antioxidantes superóxido dismutasa (SOD), catalasa (CAT) y glutatión peroxidasa (GPx). La actividad de FLA2 aumentó hasta el tercer día. Se encontró niveles de LOOH, TBARS y GC incrementados al primer día; LOOH mostró tendencia a disminuir durante el experimento; TBARS mantuvo sus niveles altos y GC disminuyó por debajo del nivel de control al tercer día. Las actividades de las enzimas antioxidantes, GPx y CAT, incrementaron desde el primer día; la actividad de SOD aumentó hasta el tercer día y disminuyó posteriormente. Se concluye que la exposición a grandes alturas influye directamente en el proceso de oxidación de lípidos y proteínas. La disminución de los niveles de GC podría deberse a la activación del sistema proteolítico, que degradaría las proteínas dañadas por las EROs (especies reactivas del oxígeno). La exposición a la altura influye además en la actividad de las enzimas antioxidantes, especialmente GPx, por su importante rol en la detoxificación de LOOH.

Is reproduction costly? No increase of oxidative damage in breeding bank voles

According to life-history theory, investment in reproduction is associated with costs, which should appear as decreased survival to the next reproduction or lower future reproductive success. It has been suggested that oxidative stress may be the proximate mechanism of these trade-offs. Despite numerous studies of the defense against reactive oxygen species (ROS) during reproduction, very little is known about the damage caused by ROS to the tissues of wild breeding animals. We measured oxidative damage to lipids and proteins in breeding bank vole (Myodes glareolus) females after rearing one and two litters, and in non-breeding females. We used bank voles from lines selected for high maximum aerobic metabolic rates (which also had high resting metabolic rates and food intake) and non-selected control lines. The oxidative damage was determined in heart, kidneys and skeletal muscles by measuring the concentration of thiobarbituric acid-reactive substances, as markers of lipid peroxidation, and carbonyl groups in proteins, as markers of protein oxidation. Surprisingly, we found that the oxidative damage to lipids in kidneys and muscles was actually lower in breeding than in non-breeding voles, and it did not differ between animals from the selected and control lines. Thus, contrary to our predictions, females that bred suffered lower levels of oxidative stress than those that did not reproduce. Elevated production of antioxidant enzymes and the protective role of sex hormones may explain the results. The results of the present study do not support the hypothesis that oxidative damage to tissues is the proximate mechanism of reproduction costs.

Protein glutathionylation in cellular compartments: A constitutive redox signal

Glutathione provides means of regulating protein function by the process of glutathionylation. Despite the role of oxidative stress biomarkers assumed recently by glutathionylated proteins in human diseases, so far no information is available on the intracellular distribution of glutathionylated proteins in human cell lines. In this study, we combined the specificity of monoclonal antibody labeling for protein-bound glutathione (GS-Pro) with the ability of confocal microscopy to localize molecules with high spatial resolution. We performed immunofluorescence analysis on dermal fibroblasts, both in steady state than in proliferative conditions, and on in situ extracted matrix samples. For the first time, we report the compartmentalization of constitutively glutathionylated proteins in different subcellular districts and we found a tight association between glutathione, nuclear lamina, and cytoskeleton. In proliferating cells, total GS-Pro fluorescence increases in the early phases of growth and significantly drops when cells reach confluence. Interestingly, a nuclear shift of GS-Pro was observed between 6 and 48 hours after plating, becoming homogeneous with the cytoplasm when growth slows. The ability to visualize a detailed intracellular distribution of this critical marker of protein oxidation may provide an additional tool to highlight pathways in turns ‘redox-activated’ and to identify new pathogenic pathways in human diseases.

Exceptionally old mice are highly resistant to lipoxidation-derived molecular damage

Membrane unsaturation plays an important role in the aging process and the determination of inter-species animal longevity. Furthermore, the accumulation of oxidation-derived molecular damage to cellular components particularly in the nervous and immune systems over time leads to homeostasis loss, which highly influences age-related morbidity and mortality. In this context, it is of great interest to know and discern the degree of membrane unsaturation and the steady-state levels of oxidative damage in both physiological systems from long-lived subjects. In the present work, adult (28 ± 4 weeks), old (76 ± 4 weeks) and exceptionally old (128 ± 4 weeks) BALB/c female mice were used. Brain and spleen were analysed for membrane fatty acid composition and specific markers of protein oxidation, glycoxidation and lipoxidation damage, i.e. glutamic semialdehyde, aminoadipic semialdehyde, carboxyethyl-lysine, carboxymethyl-lysine and malondialdehyde-lysine, by gas chromatography-mass spectrometry. The results showed significantly lower peroxidizability index in brain and spleen from exceptionally old animals when compared to old specimens. The higher membrane resistance to lipid peroxidation and lower lipoxidation-derived molecular damage found in exceptionally old animals was associated with a significantly lower desaturase activity and peroxisomal β-oxidation. Protein oxidation markers in brain and spleen from adult and exceptionally old animals showed similar levels, which were higher in old mice. In addition, the higher levels of the glycoxidation-derived marker observed in exceptionally old animals, as well as in adult mice, could be considered as a good indicator of a better bioenergetic state of these animals when compared to the old group. In conclusion, low lipid oxidation susceptibility and maintenance of adult-like protein lipoxidative damage could be key mechanisms for longevity achievement.

Ischemia modified albumin and carbonyl protein as potential biomarkers of protein oxidation in hemodialysis

The aim of this study was to evaluate the effect of HD on ischemia modified albumin (IMA) and protein carbonyl groups in order to investigate the role of IMA as a marker of protein oxidation. This study was conducted with 23 chronic hemodialysis patients. The serum IMA levels and protein carbonyl groups were measured immediately before hemodialysis (pre-HD) and after the end of hemodialysis (post-HD). IMA concentrations were significantly higher in post-HD than those of the pre-HD and carbonyl protein concentrations were higher in post-HD in comparison with pre-HD. A significant correlation was observed between IMA and carbonyl protein levels. The increase of IMA levels and protein carbonyl groups post-HD could be attributed to the increase of oxidative stress associated with HD, and IMA appears to be an important biomarker for assessing protein oxidation after HD.

Influence of Punica granatum L. on region specific responses in rat brain during Alloxan-Induced diabetes

ObjectiveThe present study was carried out to investigate the effects of Punica granatum peel methanolic extract (PGPE) on cerebral cortex (CC) and Hippocampus (HC) brain antioxidant defense system and markers of lipid and protein oxidation in alloxan induced diabetic rats. MethodsOral administration of PGPE (75 and 150 mg of kg body weight) for 45 days resulted in significant reduction in blood glucose levels. ResultsSupplementation of diabetic rats with PGPE showed increased activities of SOD and GPx with concomitant decrease in MDA and PC content. Region-specific changes were more evident in the HC when compared to CC. ConclusionsThe present study indicated that PGPE can ameliorate brain oxidative stress in alloxan induced diabetic rats by up regulating antioxidant defense mechanism by attenuating lipid and protein oxidation. PGPE thus may be used as a potential therapeutic agent in preventing diabetic complications in the brain.

Oxidative stress, as measured by protein oxidation, is increased in primary Sjøgren's syndrome

Objective: Oxidative stress is an imbalance between the production of reactive oxygen species (ROS) and physiological antioxidant defences. It occurs frequently in conditions characterized by immune activation and inflammation. Plasma levels of oxidized end products have never been evaluated in primary Sjøgren's syndrome (pSS). The aim of this study was to investigate the level of oxidative stress in primary Sjøgren's syndrome. As a secondary outcome, the association between oxidative stress and fatigue was explored. Methods: A cross-sectional study of 26 pSS patients was carried out. Oxidative stress was assessed using two markers of protein oxidation, protein carbonyl (PC) and advanced oxidation protein products (AOPP). Reference values for the oxidative stress markers were obtained from 15 healthy subjects. Results: AOPP and PC levels were increased in the pSS patients compared to the healthy subjects. This is a novel finding. There were no associations between oxidative stress measures and fatigue in the patients. Conclusions: Patients with pSS have increased levels of oxidative stress compared to healthy subjects.

Epigallocatechin-3-Gallate as a Potential Therapeutic Drug for TTR-Related Amyloidosis: “In Vivo” Evidence from FAP Mice Models

BackgroundFamilial amyloidotic polyneuropathy (FAP) is a neurodegenerative disease caused by the extracellular deposition of mutant transthyretin (TTR), with special involvement of the peripheral nervous system (PNS). Currently, hepatic transplantation is considered the most efficient therapy to halt the progression of clinical symptoms in FAP since more than 95% of TTR is produced by the liver. However, less invasive and more reliable therapeutic approaches have been proposed for FAP therapy, namely based on drugs acting as inhibitors of amyloid formation or as amyloid disruptors. We have recently reported that epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea, is able to inhibit TTR aggregation and fibril formation, “in vitro” and in a cellular system, and is also able to disrupt pre-formed amyloid fibrils “in vitro”.Methodology and Principal FindingsIn the present study, we assessed the effect of EGCG subchronic administration on TTR amyloidogenesis “in vivo”, using well characterized animal models for FAP. Semiquantitative immunohistochemistry (SQ-IHC) and Western blot analysis of mice tissues after treatment demonstrated that EGCG inhibits TTR toxic aggregates deposition in about 50% along the gastrointestinal tract (GI) and peripheral nervous system (PNS). Moreover EGCG treatment considerably lowered levels of several biomarkers associated with non-fibrillar TTR deposition, namely endoplasmic reticulum (ER)-stress, protein oxidation and apoptosis markers. Treatment of old FAP mice with EGCG resulted not only in the decrease of non-fibrillar TTR deposition but also in disaggregation of amyloid deposits. Consistently, matrix metalloproteinase (MMP)-9 and serum amyloid P component (SAP), both markers of amyloid deposition, were also found reduced in treated old FAP mice.Conclusions and SignificanceThe dual effect of EGCG both as TTR aggregation inhibitor and amyloid fibril disruptor together with the high tolerability and low toxicity of EGCG in humans, point towards the potential use of this compound, or optimized derivatives, in the treatment of TTR-related amyloidoses.

The effect of different doses and types of intravenous iron on oxidative stress and inflammation in hemodialysis patients

Although intravenous iron (IVI) is thought to have potential inflammatory and atherogenic effects, there are not enough studies comparing these effects in chronic hemodialysis (HD) patients. In this study, different doses and types of IVI were examined for effects on inflammation and oxidative stress. Chronic HD patients (n=101) were grouped into those not receiving IVI (group 1, n=29), those getting intermittent iron sucrose (group 2, n=25), those receiving intermittent iron dextran (group 3, n=24) and those getting a once monthly total dose of iron dextran (group 4, n=23). Malondialdehyde (MDA), advanced oxidation protein product (AOPP), C-reactive protein (CRP) and TNF-α levels were measured on days 0, 2, 7 and 28. Groups were similar regarding age, sex, hemoglobin, iron indices and total amount of IVI given monthly. Although MDA levels at days 7 and 28, AOPP levels at days 0 and 28, CRP levels at day 28 and TNF-α level at day 7 were higher than at other days, there were no significant differences between the IVI groups on statistical analysis. The different types and doses (intermittent or once monthly total dose) of IVI treatments are well tolerated without negative effects on the markers of lipid and protein oxidation and inflammatory indices in chronic HD patients.