Reduced antioxidant capacity and increased subclinical inflammation markers in prepubescent obese children and their relationship with nutritional markers and metabolic parameters

Objective: There are associations between some inflammatory and oxidative markers and obesity in adults, but whether prepubescent children of different weights also have such markers has not been studied. We investigated multiple inflammatory markers and levels of erythrocyte oxidant/antioxidant enzymes in prepubescent children of different weights.

Methods: Children aged 2–11 years were divided into three groups: 80 were underweight, 90 were obese but otherwise healthy, and 80 were healthy age- and sex-matched children of normal-weight. We analyzed inflammatory markers and the total oxidant status, total antioxidant status (TAS), and total thiol level were also determined, and the oxidative stress index was calculated as an indicator of the degree of oxidative stress.

Results: The obese group exhibited higher levels of fasting glucose, insulin, total cholesterol, triglycerides, the homeostatic model assessment of insulin resistance (HOMA-IR), and the homeostatic model assessment of β-cell function (HOMA-β), C-reactive protein (CRP), neutrophils, and neutrophil/lymphocyte ratio (NLR), as well as lower TAS and total thiol levels than the other two groups (all P?<?0.001). Moreover, TAS and total thiols were negatively correlated with age in the obese group (r?=??0.212, P?=?0.001; r?=??0.231, P?<?0.001, respectively). CRP levels in plasma were positively correlated with the body mass index (BMI), insulin and glucose levels, HOMA-IR, HOMA-β, WBC and neutrophil counts, and the NLR, and were negatively correlated with TAS and total thiol levels in the overall studied population.

Discussion: The coexistence of increased obesity-related subclinical inflammation and decreased antioxidant capacity can be observed even in prepubescence, and may eventually increase the risk of long-term vascular damage.     

Oxidative stress contributes to muscle atrophy in chronic kidney disease patients

Abstract

Objectives

Patients with chronic kidney disease have impaired muscle metabolism, resulting in muscle atrophy. Oxidative stress has previously been identified as a significant contributor to muscle atrophy in other populations, but the contribution in chronic kidney disease is unknown. The aim of this study was to investigate the association between oxidative stress, grip strength, and lean mass in patients with chronic kidney disease.

Methods

This is a cross-sectional study of 152 participants with stage 3 or 4 chronic kidney disease. Outcome measures include grip strength, lean mass, plasma total F2-isoprostanes, inflammation, peak oxygen uptake, and standard clinical measures.

Results

Thirty four (22.4%) chronic kidney disease patients had elevated oxidative stress levels (plasma F2-isoprostanes >250 pg/ml), with 82% of patients below age-predicted grip strength normative values. There was a significant negative association between plasma F2-isoprostanes and grip strength (r = ?0.251) and lean mass (r = ?0.243). There were no associations with inflammation markers. Multiple linear regression identified plasma F2-isoprostanes as a significant predictor of grip strength independent of other predictors: sex, diabetes status, body mass index, body fat percent, and phosphate (adjusted r² = 69.5, P < 0.001).

Discussion

Plasma F2-isoprostanes were independently associated with reduced strength in chronic kidney disease patients.     

Supplementation with a combination of antioxidants does not affect glycaemic control,oxidative stress or inflammation in type 2 diabetes subjects

Abstract

The present clinical trial examined the influence of a supplement, containing a combination of antioxidants extracted from fruit, berries and vegetables, on levels of plasma antioxidants (tocopherols, carotenoids and ascorbate), glycaemic control (blood glucose, HbA1c, insulin), oxidative stress biomarkers (F₂-isoprostane, malondialdehyd, nitrotyrosine, 8-oxo-7, 8-dihydro-2′-deoxyguanosine, formamidopyrimidine glycosylase sites, frequency of micronucleated erythrocytes) and inflammatory markers (interleukin-6, C-reactive protein, prostaglandin F_2α-metabolite) in type 2 diabetes. Forty subjects were randomly assigned to control, single or double dose group and completed the study. In summary, 12 weeks of antioxidant supplementation did neither affect glycaemic control nor the levels of biomarkers of oxidative stress or inflammation, despite substantially increased plasma concentrations of antioxidants. The absence of an effect may be explained by the selected study subjects with relatively well-controlled diabetes, a high intake of fruit and vegetable and levels of plasma antioxidants, biomarkers of oxidative stress and inflammatory markers comparable to those found in healthy subjects.     

Hyperglycaemia,oxidative stress and inflammatory markers

Introduction: The increasing prevalence of hyperglycaemia implicates a state of oxidative stress and inflammation. Traditional and emerging biomarkers associated with increasing hyperglycaemia were assessed to clarify their role they play in hyperglycaemia.

Results: 309 participants attending a rural diabetic screening program were categorised into control and quintile groups based upon glucose levels: 1st quintile - <4.5?mmol/L and 4th, 5th quintile - >6.1?mmol/L. Significant results were obtained for anthropometric data and biochemical markers - glucose, HbA1c and total cholesterol (P?P?P?P?Conclusion: This study provided further evidence that inflammatory and oxidative stress biomarkers may contribute to diagnostic information associated with preclinical increases in BGL. Further we have provided a unique study in the analysis of ratios of inflammatory biomarkers and correlations with increasing BGL.     

Urinary oxidative stress markers in children with autism

Abstract

Oxidative stress caused by increased production of free radicals and impaired functions of antioxidants remains as the major factor associated with the pathophysiology of many neuropsychiatric diseases.

Objective

The objective of the present study was to analyze the oxidative stress markers in urine sample since the collection of blood from these children is highly meticulous and also to evaluate whether these urinary markers can be correlated with the severity of autism.

Methods

The subjects of the study were 45 autistic children with different grades of severity (low functioning autism (LFA), medium functioning autism (MFA), and high functioning autism (HFA) according to Childhood Autism Rating Scale (CARS), n = 15 children in each group and 50 healthy children (age and sex matched). The boys and girls ratio involved in this study was 4:1, and they were of age 4–12 years. We determined the urinary levels of oxidative stress markers like thiobarbituric acid-reacting substances, lipid hydroperoxides, 4-hydroxy nonenal, protein carbonyls, sulfhydryl groups, total antioxidant capacity, total peroxide content, oxidative stress index, and also UA/Cr ratio in autistic children.

Results

The study observed a significant elevation in the level of oxidative stress markers in autistic children when compared with normal children. The level of antioxidants excreted in urine was found to be significantly low in autistic children. These findings when correlated with the degrees of severity, oxidative stress markers showed positive correlation with increasing order of severity (LFA > MFA > HFA), whereas antioxidants showed negative correlation.

Discussion

The study reveals that the urinary levels of oxidative stress markers can be considered as the measure of oxidative stress index in autistic children. The significant correlation between the severity of autism with urinary lipid peroxidation products also support the use of oxidative stress markers and antioxidants as biomarkers of autism.     

Surgical stress during operation for gastrointestinal cancer increases plasma thioredoxin levels and decreases mitochondrial membrane potential in peripheral blood lymphocytes

Abstract

Surgical stress is difficult to evaluate quantitatively. It has been reported that mitochondrial membrane potential (Δψ_m) in the peripheral blood lymphocytes (PBLs) is decreased by surgical stress. Thioredoxin (TRX), a small protein with redox-active dithiol/disulfide in the active site, is induced by a variety of oxidative stresses and secreted from the cells. Accumulating evidence shows that plasma levels of TRX are elevated in oxidative stress-associated disorders. In the present study, we examined plasma levels of TRX in cases undergoing operations for gastrointestinal cancer. Plasma levels of TRX were significantly elevated on the first postoperative day compared with the pre-operative levels. The changes in the plasma TRX levels tended to show an inverse relationship with the changes in Δψ_m in PBLs, which shows a significant decrease caused by surgical stress. Plasma TRX levels as well as Δψ_m in PBLs are valuable markers to evaluate surgical stress.     

Time course and attenuation of ischaemia-reperfusion induced oxidative injury by propofol in human renal transplantation

Abstract

Ischaemia-reperfusion injury resulting from interruption and restoration of blood flow might be related to free radical mediated oxidative stress and inflammation, and subsequently to post-surgery related complications. We studied the impact of renal transplantation on oxidative stress and inflammation by measuring F₂-isoprostanes and prostaglandin F_2α, respectively, during transplantation and post-surgery. Additionally, due to earlier observations, two dissimilar anaesthetic agents (thiopentone and propofol) were compared to determine their antioxidative capacity rather than their anaesthetic properties. Blood samples were collected before, post-intubation, immediately, 30, 60,120, 240 min, and 12 and 24 h after reperfusion. Oxidative stress and inflammatory response were detected by measuring 8-iso-PGF_2α (a major F₂-isoprostane and a biomarker of oxidative stress) and 15-keto-dihydro-PGF_2α (a major metabolite of PGF_2α and a biomarker of COX-mediated inflammatory response), respectively. Reperfusion of the transplanted graft significantly increased plasma levels of 8-iso-PGF_2α. PGF_2α metabolite levels, although elevated, did not reach statistical significance. In addition, significantly lower levels of 8-iso-PGF_2a were observed in the propofol group compared to the thiopentone group. Together, these findings underline an augmented oxidative stress activity following an inflammatory response after human renal transplantation. Furthermore, propofol a well-known anaesthetic, counteracted oxidative stress by lowering the formation of a major F₂-isoprostane.     

Pericardial Fat Volume Correlates With Inflammatory Markers: The Framingham Heart Study

The objective of this study was to determine whether systemic inflammatory and oxidative stress marker concentrations correlate with pericardial and intrathoracic fat volumes. Participants of the Framingham Offspring Study (n = 1,175, 53% women, mean age 59 ± 9 years) had pericardial and intrathoracic fat volumes assessed by multidetector computed tomography (MDCT) scans, and provided fasting blood and urine samples to measure concentrations of 14 inflammatory markers: C‐reactive protein (CRP), interleukin‐6, monocyte chemoattractant protein‐1 (MCP‐1), CD40 ligand, fibrinogen, intracellular adhesion molecule‐1, lipoprotein‐associated phospholipase A₂ activity and mass, myeloperoxidase, osteoprotegerin, P‐selectin, tumor necrosis factor‐α, tumor necrosis factor receptor‐2, and urinary isoprostanes. Multivariable linear regression models were used to determine the association of log‐transformed inflammatory marker concentrations with fat volumes, using fat volume as the dependent variable. Due to smaller sample sizes, models were rerun after adding urinary isoprostanes (n = 961) and tumor necrosis factor‐α (n = 813) to the marker panel. Upon backward elimination, four of the biomarkers correlated positively with each fat depot: CRP (P < 0.0001 for each fat depot), interleukin‐6 (P < 0.05 for each fat depot), MCP‐1 (P < 0.01 for each fat depot), and urinary isoprostanes (P < 0.01 for pericardial fat; P < 0.001 for intrathoracic fat). Even after adjusting for BMI, waist circumference (WC), and abdominal visceral fat, CRP (P = 0.0001) and urinary isoprostanes (P = 0.02) demonstrated significant positive associations with intrathoracic fat, but not with pericardial fat. Multiple markers of inflammation and oxidative stress correlated with pericardial and intrathoracic fat volumes, extending the known association between regional adiposity and inflammation and oxidative stress.     

Decreased expression of heme oxygenase is associated with depressive symptoms and may contribute to depressive and hypertensive comorbidity

Background: There is strong evidence that hypertension and depression are comorbid and oxidative stress is implicated in both pathologies. We aimed to elucidate the relationship between biochemical markers of the antioxidant-pro-oxidant equilibrium and depression in hypertension.

Methods: Blood was collected from patients diagnosed with depression, hypertension, or comorbid depression and hypertension and healthy age- and sex-matched controls. Whole blood reduced glutathione, erythrocyte superoxide dismutase (SOD-1), glutathione peroxidase (GPx-1), glutathione reductase (GR), malondialdehyde (MDA), and plasma hydrogen peroxide (H₂O₂) were assayed using spectrophotometry, and heme oxygenase (HO-1) levels were determined immunoenzymatically.

Results: Both hypertension and depression were associated with altered antioxidant-pro-oxidant profiles. Decreased GPx-1 and SOD-1 activities, increased GR activity, increased levels of GSH, and increased concentrations of MDA and H₂O₂ were observed in patients compared to controls. Inducible HO-1 was specifically decreased in patients with depression and was significantly associated with both the prevalence and severity of depressive symptoms.

Conclusions: Heme oxygenase is a biological factor that might explain the relationship between inflammation, oxidative stress, and the biological and functional changes in brain activity in depression. HO-1 is a candidate depression biomarker and provides an avenue for novel preventative and diagnostic strategies against this disease.     

Circulating and PBMC Lp-PLA2 associate differently with oxidative stress and subclinical inflammation in nonobese women (menopausal status)

Background

This study aimed to determine the association of lipoprotein-associated phospholipase A₂ (Lp-PLA₂) activity in circulation and peripheral blood mononuclear cells (PBMCs) with inflammatory and oxidative stress markers in nonobese women and according to menopausal status. Lp-PLA₂ activity, a marker for cardiovascular risk is associated with inflammation and oxidative stress.

Methodology/Principal Findings

Eighty postmenopausal women (53.0±4.05 yr) and 96 premenopausal women (39.7±9.25 yr) participated in this study. Lp-PLA₂ activities, interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β in plasma as well as in PBMCs were measured. Plasma ox-LDL was also measured. Postmenopausal women demonstrated higher circulating levels of ox-LDL and IL-6, as well as IL-6, TNF-α, and IL-1β in PBMCs, than premenopausal women. In both groups, plasma Lp-PLA₂ activity positively correlated with Lp-PLA₂ activity in PBMCs and plasma ox-LDL. In premenopausal women, Lp-PLA₂ activities in plasma and PBMCs positively correlated with IL-6, TNF-α, and IL-1β in PBMCs. In postmenopausal women, plasma ox-LDL positively correlated with PBMC cytokine production. In subgroup analysis of postmenopausal women according to plasma ox-LDL level (median level: 48.715 U/L), a significant increase in Lp-PLA₂ activity in the plasma but not the PBMCs was found in the high ox-LDL subgroup. Plasma Lp-PLA₂ activity positively correlated with unstimulated PBMC Lp-PLA₂ activity in the low ox-LDL subgroup (r = 0.627, P<0.001), whereas in the high ox-LDL circulating Lp-PLA₂ activity positively correlated with plasma ox-LDL (r = 0.390, P = 0.014) but not with Lp-PLA₂ activity in PBMCs.

Conclusions/Significance

The lack of relation between circulating Lp-PLA₂ activity and Lp-PLA₂ activity in PBMCs was found in postmenopausal women with high ox-LDL. This may indicate other sources of circulating Lp-PLA₂ activity except PBMC in postmenopausal women with high ox-LDL. We also demonstrated that circulating Lp-PLA₂ and PBMC secreted Lp-PLA₂ associate differently with markers of oxidative stress and sub clinical inflammation in nonobese women, particularly according to the menopausal states.     

Increased oxidative stress alters nucleosides metabolite levels in sickle cell anemia

Objectives: This study was conducted to assess the markers of oxidative stress, myeloperoxidase (MPO), acetylcholinesterase (AChE) and xanthine oxidase (XO) activities as well as the levels of nucleotide metabolites in sickle cell anemia (SCA) patients.

Methods: Fifteen SCA treated patients and 30 health subjects (control group) were selected. The markers of oxidative stress (levels of reactive oxygen species (ROS), plasma proteins, carbonyl content, lipid peroxidation (TBARS), total thiols (T-SH), glutathione and catalase activity), MPO, AChE and XO activities as well as the levels of nucleotide metabolites were measured in SCA patients.

Results: ROS, thiobarbituric acid-reactive substances (TBARS) and T-SH levels as well as the activities of catalase and MPO were significantly increased while glutathione level was reduced in SCA patients. Furthermore, a significant (P?P?P?P?Discussion: The altered parameters in SCA patients suggest that the generation and impairment of oxidative stress in this disease as well as antioxidant markers are contributory factors towards cellular redox homeostasis and alteration of purine metabolites.     

Plasma angiogenesis and oxidative stress markers in patients with diabetic retinopathy

Abstract

Background: Neovascularization in the retina and hyperglycaemia-induced oxidative stress are implicated in the pathogenesis of diabetic retinopathy (DR). In this study, we hypothesized that the plasma angiogenic and oxidative stress markers associated with these derangements could aid in the screening of diabetic patients who are at an increased risk of developing retinopathy.

Methods: This study included normal (n?=?148), type2 diabetes without retinopathy (DNR; n?=?148), proliferative DR (PDR; n?=?74) and non-PDR (NPDR; n?=?148) subjects. Plasma concentrations of vascular endothelial growth factor-A (VEGF-A), hypoxia-inducible factor-1α (HIF-1α), matrix metalloproteinase-9 (MMP-9), pigment epithelium-derived factor (PEDF), nitric oxide (NO), soluble receptors for advanced glycation end products (sRAGE), malondialdehyde (MDA) and protein thiols were estimated.

Results: A statistically significant increase was observed in the plasma concentrations of pro-angiogenic factors and markers of oxidative stress in both retinopathy groups. By contrast, the concentrations of anti-angiogenic factors and antioxidants were decreased significantly in these groups. Receiver operating characteristic analysis indicated that the plasma thresholds of HIF-1α and PEDF can be suitable markers in case of NPDR. However, in PDR, HIF-1α, NO, MMP-9 and PEDF showed high sensitivity and specificity.

Conclusions: The factors associated with hypoxia, matrix degradation and angiogenic inhibition play a crucial role in predicting DR.     

The biogenesis of [Fe–S] clusters: the role of the unorthodox ABC ATPase,SufC, and the wider implications for understanding iron metabolism

Abstract

Oxidative stress is the hallmark of various chronic inflammatory lung diseases. Increased concentrations of reactive oxygen species (ROS) in the lungs of such patients are reflected by elevated concentrations of oxidative stress markers in the breath, airways, lung tissue and blood. Traditionally, the measurement of these biomarkers has involved invasive procedures to procure the samples or to examine the affected compartments, to the patient's discomfort. As a consequence, there is a need for less or non-invasive approaches to measure oxidative stress. The collection of exhaled breath condensate (EBC) has recently emerged as a non-invasive sampling method for real-time analysis and evaluation of oxidative stress biomarkers in the lower respiratory tract airways. The biomarkers of oxidative stress such as H₂O₂, F₂-isoprostanes, malondialdehyde, 4-hydroxy-2-nonenal, antioxidants, glutathione and nitrosative stress such as nitrate/nitrite and nitrosated species have been successfully measured in EBC. The reproducibility, sensitivity and specificity of the methodologies used in the measurements of EBC oxidative stress biomarkers are discussed. Oxidative stress biomarkers also have been measured for various antioxidants in disease prognosis. EBC is currently used as a research and diagnostic tool in free radical research, yielding information on redox disturbance and the degree and type of inflammation in the lung. It is expected that EBC can be exploited to detect specific levels of biomarkers and monitor disease severity in response to appropriate prescribed therapy/treatment.     

Influence of gestational diabetes on the activity of δ-aminolevulinate dehydratase and oxidative stress biomarkers

Objective: This study aimed to evaluate the activity of delta-aminolevulinate dehydratase (δ-ALA-D) and oxidative stress biomarkers in pregnant women with gestational diabetes mellitus (GDM), in order to demonstrate the involvement of oxidative stress in this condition, which presents pathophysiology still undetermined.

Methods: δ-ALA-D activity, lipid peroxidation estimated as the levels of thiobarbituric acid reactive substances (TBARS), protein (P-SH) and non-protein thiol (NP-SH) content, catalase (CAT) activity and concentration of vitamin C (VIT C) in samples of pregnant women with GDM (n?=?48) and in healthy pregnant women (n?=?30), who constituted the control group.

Results: The δ-ALA-D activity was significantly lower in pregnant women with GDM compared to controls, as well as levels of thiols, VIT C and CAT activity. Lipid peroxidation was higher in GDM group.

Discussion: The results suggest that the main factor for the increase in oxidative stress and reduced δ-ALA-D activity in diabetic pregnant women is gestational hyperglycemic environment, which changed the redox balance and interfered on mechanism of the δ-ALA-D activity in relation to normoglycemic pregnant women.     

Effects of isoquinoline alkaloid berberine on lipid peroxidation,antioxidant defense system,and liver damage induced by lead acetate in rats

Objectives: Liver is considered a target organ affected by lead toxicity. Oxidative stress is among the mechanisms involved in liver damage. Here we investigated the effects of the natural alkaloid berberine on oxidative stress and hepatotoxicity induced by lead in rats.

Methods: Animals received an aqueous solution of lead acetate (500?mg Pb/l in the drinking water) and/or daily oral gavage of berberine (50?mg/kg) for 8 weeks. Rats were then weighed and used for the biochemical, molecular, and histological evaluations.

Results: Lead-induced oxidative stress, shown by increasing lipid peroxidation along with a concomitant decrease in hepatic levels of thiol groups, total antioxidant capacity, the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase, and reduced versus oxidized glutathione ratio. Berberine corrected all the disturbances in oxidative stress markers induced by lead administration. Berberine also prevented the elevated levels of enzymes (alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase) and the decrease in body weight and albumin. The protective effects of berberine were comparable with silymarin. Furthermore, berberine attenuated liver damage, shown by decreased necrosis and inflammatory cell infiltration.

Discussion: Berberine represents a potential therapeutic option against lead-induced hepatotoxicity through inhibiting lipid peroxidation and enhancing antioxidant defenses.

Conclusion: Berberine exerted protective effects on lead-induced oxidative stress and hepatotoxicity in rats.     

The common variant in the <Emphasis Type="Italic">GSTM1</Emphasis> and <Emphasis Type="Italic">GSTT1</Emphasis> genes is related to markers of oxidative stress and inflammation in patients with coronary artery disease: a case-only study

Recent studies suggest that the common variant in the GSTM1 and GSTT1 genes modifies the risk of coronary artery disease (CAD), however, it is unclear whether the risk of CAD modulated by variants in the GSTM1 and GSTT1 genes was associated with alterations of indices of oxidative stress and inflammation. Our study is an attempt to provide insight into the role of GST genetic variant and markers of oxidative stress and inflammation in CAD patients. A total of 719 Chinese CAD patients were successfully genotyped. Plasma total antioxidant status (TAOS), glutathione(GSH), C-reactive protein (CRP), fibrinogen (FIB) and white blood cell count (WBC) were determined to evaluate the oxidative stress and inflammatory response. The correlations between GSTM1/GSTT1 genotypes and alterations of indices of oxidative stress and inflammation were analyzed. We found GSTM1-0/GSTT1-0 subjects had higher CRP and FIB and lower TAOS compared to patients with wild-type GSTM1/GSTT1 genes. A stepwise elevations in age, the incidences of hypertension and diabetes mellitus, levels of FIB and the number of WBC were associated with increased number of stenosed vessels. Reductions of plasma TAOS and GSH were associated with increased number of stenosed vessels. Our results suggest that GST polymorphisms maybe modify the effect on markers of oxidative stress and inflammation in Chinese CAD patients.     

Isoprostanes,Prostaglandins and Tocopherols in Pre-eclampsia,Normal Pregnancy and Non-pregnancy

This study is designed to evaluate whether oxidative stress and inflammation are involved in severe pre-eclampsia compared to normal pregnancy and non-pregnancy. We have measured plasma and urinary levels of 8-iso-PGF_2α, a major isoprostane as an indicator of oxidative stress; plasma and urinary 15-keto-dihydro-PGF_2α, a major metabolite of cyclooxygenase-catalysed PGF_2α as an indicator of inflammatory response, and plasma -α-and -γ-tocopherol in 18 pre-eclamptic, 19 normal pregnancy and 20 non-pregnant women. Pregnant women had significantly higher levels of 8-iso-PGF_2α and PGF_2α metabolite as compared to the non-pregnancy. Levels of 8-iso-PGF_2α in the pre-eclamptic women did not differ from the normal pregnancy but PGF_2α metabolite levels were significantly higher in normal pregnancy. On the other hand, γ-tocopherol levels were significantly lower in pre-eclampsia than normal pregnancy. In contrast, the concentration of α-tocopherol was very similar between the groups. α-and γ-tocopherol levels were significantly lower in pregnancy compared to non-pregnancy. Although no direct evidence of oxidative stress and inflammatory response was observed in severe pre-eclampsia, a reduction of γ-tocopherol suggests the possible precedence of oxidative stress in this condition. Higher levels of isoprostanes and prostaglandin metabolite in late pregnancy suggest the importance of both free radicals and cyclooxygenase-catalysed oxidation products in normal biological processes of pregnancy.     

Oxidative stress is associated with decreased heart rate variability in patients with chronic kidney disease

Objectives: Elevated oxidative stress and reduced heart rate variability (HRV) is prevalent in patients with chronic kidney disease (CKD) and is associated with increased morbidity and mortality. Previous studies have identified a positive association between elevated oxidative stress and autonomic dysfunction, however this relationship has not yet been investigated in the CKD population.

Methods: Plasma was collected from 78 patients with stage 3–4 CKD (estimated glomerular filtration rate 25–60?ml/min/1.73?m²) for the assessment of oxidative stress, including plasma total F2-isoprostanes, glutathione peroxidase activity and total antioxidant capacity. Time and frequency HRV parameters were measured from a three lead electrocardiogram.

Results: Participants with elevated F2-isoprostanes had reduced HRV compared to patients with normal levels of F2-isoprostanes. A number of HRV parameters were found to be inversely correlated with F2-isoprostanes in all CKD patients, including SDNN (r?=??0.337; P?r?=??0.281, P?=?0.01), LF (r?=??0.315, P?r?=??0.288, P?=?0.01). Multiple linear regression found F2-isoprostanes to be an independent predictor of SDNN (r²?=?0.287, β?=??0.272, P?=?0.01).

Discussion: Oxidative stress is significantly and independently associated with HRV in patients with CKD. Identifying oxidative stress in the pathogenesis of autonomic dysfunction may help target therapeutic strategies.     

Multiple cryotherapy applications attenuate oxidative stress following skeletal muscle injury

Objectives: To investigate the effects of multiple cryotherapy applications after muscle injury on markers of oxidative stress.

Methods: Following cryolesion-induced skeletal muscle injury in rats, ice was applied at the injured site for 30?minutes, three times per day, on the day of injury, and for 2 days after injury. To determine the effect of the cryotherapy treatment on markers of oxidative stress, biochemical analyses were performed 3, 7, and 14 days after injury.

Results: Compared with non-treated animals, cryotherapy reduced dichlorofluorescein at 7 and 14 days post-injury and thiobarbituric acid reactive substances levels at 3 and 7 days post-injury (P?P?>?0.05), whereas non-treated groups demonstrated lower levels than the control group (P?P?P?=?0.92).

Discussion: Cryotherapy reduced the production of reactive oxygen species after muscle injury, resulting in an attenuated response of the antioxidant system. These findings suggest that using multiple cryotherapy applications is efficient to reduce oxidative stress.     

Increased circulating endothelial microparticles in children with FMF

Objective: Endothelial microparticles (EMPs) are considered as markers of endothelial dysfunction. In this study, we aimed to examine whether there is endothelial dysfunction in children with familial Mediterranean fever (FMF), hypothesizing that endothelial dysfunction would be present especially with acute-phase response in the active period of the disease.

Methods: This cross-sectional study included 65 FMF patients (41 attack free, 24 attack period) and 35 healthy controls. Circulating EMPs, serum amyloid A (SAA), and other inflammation markers were measured in all groups. Circulating EMPs were measured using flow cytometry. Study groups were compared for circulating EMP and inflammatory markers. The relationship between EMPs and the activation of the disease was evaluated.

Results: The levels of CD144⁺ and CD146⁺ EMPs in the FMF attack period group were significantly higher than those of the control group (p?p?+ and CD146⁺ EMP were significantly correlated with CRP.

Conclusions: Our results suggest that endothelial damage is present especially in the active period of the disease in children with FMF. The endothelial dysfunction becomes an overt parallel with inflammation.