On Oxidative Stress Research Articles

Pyrroloquinoline Quinone Inhibits Oxidative Stress in Rats with Diabetic Nephropathy.

BackgroundDiabetic nephropathy (DN) is one of the chronic microvascular complications of diabetes. This study focused on the protective effects of pyrroloquinoline quinone (PQQ) on oxidative stress (OS) in DN.Material/MethodsThirty Sprague Dawley rats were randomly selected for this study; 10 rats were randomly selected as the control group. The other 20 rats were established for the DN model. After establishment of the successful model, the DN model rats were randomly divided into a DN group and a PQQ group. The PQQ group was fed with a PQQ diet. Blood urea nitrogen (BUN), serum creatinine (SCr), and blood glucose levels were measured in each group, and OS-related protein expression and AMPK pathway were detected by western blot and quantitative real-time polymerase chain reaction (qRT-PCR). At the same time, we constructed a DN model by culturing NRK-52E cells with high glucose to detect the molecular mechanisms.ResultsThe kidney function of the DN group was significantly decreased, SCr and BUN levels were significantly increased, and the renal structure under the microscope was disordered, and interstitial edema was obvious. The expression of SOD1, SOD2, GPX1, and GPX3 were significantly decreased, and the level of reactive oxygen species (ROS) was significantly increased. PQQ treatment can effectively alleviate renal function, improve structural damage, and inhibit OS. In vivo, PQQ can effectively inhibit high glucose-induced OS damage and activate the AMPK/FOXO3a signaling pathway.ConclusionsPQQ improves renal structural damage and functional damage, and protects kidney cells in DN by inhibiting OS, which may be related to activating the AMPK/FOXO3a pathway.

Improvement of Oxidative Stress in Older Women Is Dependent on Resistance Training Volume: Active Aging Longitudinal Study.

Cunha, PM, Ribeiro, AS, Padilha, C, Nunes, JP, Schoenfeld, BJ, Cyrino, LT, Tomeleri, CM, Nascimento, MA, Antunes, M, Fernandes, RR, Barbosa, DS, Venturini, D, Burini, RC, Sardinha, LB, and Cyrino, ES. Improvement of oxidative stress in older women is dependent on resistance training volume: Active aging longitudinal study. J Strength Cond Res 36(4): 1141-1146, 2022-The purpose of the present study was to investigate the effects of resistance training (RT) performed with a higher versus lower training volume on oxidative stress (OS) biomarkers in older women. Thirty-eight older women (≥60 years) were randomly assigned to 1 of 2 groups: a group that performed 1 set per exercise (low volume [LV], n = 18) or 3 sets per exercise (high volume [HV], n = 20). The whole-body RT consisted of a 12-week RT program involving 8 exercises performed with sets of 10-15 repetitions maximum, 3 days per week. Advanced oxidation protein products (AOPP), total radical-trapping antioxidant parameter (TRAP), and ferrous oxidation-xylenol orange (FOX) were used as OS biomarkers. The composite Z-score of the percentage changes from pre- to posttraining of OS biomarkers according to groups was calculated. A significant main effect of time (p < 0.05) was found for AOPP (LV = -7.3% vs. HV = -12.2%) and TRAP (LV = +1.5% vs. HV = +15.5%) concentrations, without a statistical difference between the groups (p > 0.05). A significant group vs. time interaction (p < 0.001) was revealed for FOX (LV = +6.4% vs. HV = -8.9%). The overall analysis indicated higher positive changes for HV than LV (composed Z-score: HV = 0.41 ± 1.22 vs. LV = -0.37 ± 1.03; p < 0.05). Our results suggest that a greater volume of RT seems to promote superior improvements on OS biomarkers in older women.

The Effect of Smoking on Mitochondrial Biogenesis in Patients With Graves Ophthalmopathy.

To evaluate the effects of cigarette smoking on oxidative stress (OS) and mitochondrial biogenesis related parameters in patients Graves Ophthalmopathy (GO). Patients with moderate-to-severe GO according to the European Group on Graves Orbitopathy (EUGOGO) criteria were prospectively enrolled in this study. Age- and sex-matched healthy volunteers who applied to outpatient clinic due to refractive problems consisted the control group. Participants were divided into 4 groups based on their diagnosis and smoking status: group 1 (n = 30) smoker GO patients, group 2 (n = 30) nonsmoker GO patients, group 3 (n = 30) smoker healthy controls, and group 4 (n = 30) nonsmoker healthy controls. In the sera, total antioxidant status, total oxidant status and OS index values, peroxisome proliferator-activated receptor-γ coactivator 1-α, mitochondrial transcriptional factor A levels, and paraoxonase-1 enzyme activity were evaluated. Total oxidant status and OS index values were the highest in group 1 compared to other groups (p = 0.031, p = 0.042; respectively). There was no statistically significant difference in total antioxidant status and peroxisome proliferator-activated receptor-γ coactivator 1α levels among the groups (p = 0.521, p = 0.388; respectively). Paraoxonase-1 enzyme activity was the lowest in group 1 and highest in group 4 (p = 0.024). The levels of mitochondrial transcriptional factor A was the lowest in group 1 compared to other groups (p = 0.012). Cigarette smoking in GO patients seems to be a risk factor that increases OS, and therefore, it may have an unfavorable impact on the mitochondrial biogenesis.

Silencing of microRNA-517a induces oxidative stress injury in melanoma cells via inactivation of the JNK signaling pathway by upregulating CDKN1C

BackgroundMelanoma is notoriously resistant to current treatments, and less than 25% of metastatic melanoma cases respond to existing therapies. Growing evidence has shown that microRNAs (miRNAs) play a vital role in the prognosis of melanoma. MiR-517a has been implicated in many types of cancer; however, its expressional features and potential biological functions in melanoma remain unclear. The present study aimed to investigate the possible effects of miR-517a on oxidative stress (OS) in melanoma cells.MethodsmiR-517a expression in melanoma was determined using RT-qPCR. After treatment with different concentrations of H2O2, cell viability was determined in order to identify the most appropriate H2O2 concentration. Through loss and gain of function experiments, the interactions between miR-517a, the cyclin dependent kinase inhibitor 1C (CDKN1C) and the c-Jun NH2-terminal kinase (JNK) signaling pathway, as well as their roles in OS of melanoma cells were identified. Moreover, the expression of Cleaved Caspase-3, extent of ERK1/2 phosphorylation, Bax/Bcl-2 ratio, levels of T-AOC, ROS and MDA, and SOD activity were also tested. Finally, melanoma cell viability and apoptosis were detected.ResultsMiR-517a was upregulated, while CDKN1C was downregulated in melanoma tissues and cells. MiR-517a targets CDKN1C and consequently reduced its expression. Inhibition of miR-517a was shown to increase Cleaved Caspase-3 expression, Bax/Bcl-2 ratio, levels of ROS and MDA, as well as cell apoptosis but decrease extent of ERK1/2 phosphorylation, T-AOC levels, SOD activity, along with cell proliferation and mitochondrial membrane potential.ConclusionsOverall, silencing miR-517a results in upregulated CDKN1C expression, and inhibited JNK signaling pathway activation, consequently promoting OS in melanoma cells.

Impact of Oxidative Stress on Age-Associated Decline in Oocyte Developmental Competence.

Reproductive capacity in women starts to decline beyond their mid-30s and pregnancies in older women result in higher rates of miscarriage with aneuploidy. Age-related decline in fertility is strongly attributed to ovarian aging, diminished ovarian reserves, and decreased developmental competence of oocytes. In this review, we discuss the underlying mechanisms of age-related decline in oocyte quality, focusing on oxidative stress (OS) in oocytes. The primary cause is the accumulation of spontaneous damage to the mitochondria arising from increased reactive oxygen species (ROS) in oocytes, generated by the mitochondria themselves during daily biological metabolism. Mitochondrial dysfunction reduces ATP synthesis and influences the meiotic spindle assembly responsible for chromosomal segregation. Moreover, reproductively aged oocytes produce a decline in the fidelity of the protective mechanisms against ROS, namely the ROS-scavenging metabolism, repair of ROS-damaged DNA, and the proteasome and autophagy system for ROS-damaged proteins. Accordingly, increased ROS and increased vulnerability of oocytes to ROS lead to spindle instability, chromosomal abnormalities, telomere shortening, and reduced developmental competence of aged oocytes.

Vanadium and Oxidative Stress Markers - In Vivo Model: A Review.

This review article is an attempt to summarize the current state of knowledge of the impact of Vanadium (V) on Oxidative Stress (OS) markers in vivo. It shows the results of our studies and studies conducted by other researchers on the influence of different V compounds on the level of selected Reactive Oxygen Species (ROS)/Free Radicals (FRs), markers of Lipid peroxidation (LPO), as well as enzymatic and non-enzymatic antioxidants. It also presents the impact of ROS/peroxides on the activity of antioxidant enzymes modulated by V and illustrates the mechanisms of the inactivation thereof caused by this metal and reactive oxygen metabolites. It also focuses on the mechanisms of interaction of V with some nonenzymatic compounds of the antioxidative system. Furthermore, we review the routes of generation of oxygen-derived FRs and non-radical oxygen derivatives (in which V is involved) as well as the consequences of FR-mediated LPO (induced by this metal) together with the negative/ positive effects of LPO products. A brief description of the localization and function of some antioxidant enzymes and low-molecular-weight antioxidants, which are able to form complexes with V and play a crucial role in the metabolism of this element, is presented as well. The report also shows the OS historical background and OS markers (determined in animals under V treatment) on a timeline, collects data on interactions of V with one of the elements with antioxidant potential, and highlights the necessity and desirability of conducting studies of mutual interactions between V and antioxidant elements.

Effects of photobiomodulation associated with endurance running training on oxidative stress in untrained men

This study examined the effects of photobiomodulation (PBM) associated with endurance running training on oxidative stress (OS) markers in untrained men. Thirty untrained men distributed into a placebo group (PLA) or PBM group (PBMG) performed 8 weeks of running training, in which the PBMG had the LED application before all training sessions. The PBM was performed by LED application using an equipment with 56 diodes of red light (660 nm) and 48 diodes of infrared light (850 nm) with an energy dose of 60 J on each of the 5 points. The application was done in two regions of the quadriceps muscle, two regions of the biceps femoris, and one region of the gastrocnemius muscle in both legs. The assessments were performed at pre- and post-training, and the OS markers analyzed were malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH) and oxidized (GSSG). PBM associated with running training did not significantly affect the OS markers CAT, SOD, MDA, GSH, and reduced GSH/GSSG responses after training. GSSG levels decreased in the PBMG and increased in the PLA, with significant difference between the % change values (− 13.5 ± 30.3% vs. 56.3 ± 83.4%; P = 0.043). Therefore, PBM associated with endurance running training did not significantly affect CAT, SOD, MDA, reduced GSH, and reduced GSH/GSSG ratio post-training; however, the GSSG increased in PLA group and decreased in PBMG, indicating a positive effect of the PBM in this marker of OS.

Resveratrol and Quercetin Administration Improves Antioxidant DEFENSES and reduces Fatty Liver in Metabolic Syndrome Rats.

Mixtures of resveratrol (RSV) + quercetin (QRC) have antioxidant properties that probably impact on fatty liver in metabolic syndrome (MS) individuals. Here, we study the effects of a mixture of RSV + QRC on oxidative stress (OS) and fatty liver in a rat model of MS. Weanling male Wistar rats were separated into four groups (n = 8): MS rats with 30% sucrose in drinking water plus RSV + QRC (50 and 0.95 mg/kg/day, respectively), MS rats without treatment, control rats (C), and C rats plus RSV + QRC. MS rats had increased systolic blood pressure, triglycerides, insulin levels, insulin resistance index homeostasis model (HOMA), adiponectin, and leptin. The RSV + QRC mixture compensated these variables to C values (p < 0.01) in MS rats. Lipid peroxidation and carbonylation were increased in MS. Total antioxidant capacity and glutathione (GSH) were decreased in MS and compensated in MS plus RVS + QRC rats. Catalase, superoxide dismutase isoforms, peroxidases, glutathione-S-transferase, glutathione reductase, and the expression of Nrf2 were decreased in MS and reversed in MS plus RVS + QRC rats (p < 0.01). In conclusion, the mixture of RSV + QRC has benefic effects on OS in fatty liver in the MS rats through the improvement of the antioxidant capacity and by the over-expression of the master factor Nrf2, which increases the antioxidant enzymes and GSH recycling.

DIET-INDUCED PREDIABETES: EFFECTS ON OXIDATIVE STRESS AND INFLAMMATORY BIOMARKERS AS AGENTS FOR VASCULAR COMPLICATIONS IN RENAL FUNCTION

Ponte Academic JournalFeb 2019, Volume 75, Issue 2 DIET-INDUCED PREDIABETES: EFFECTS ON OXIDATIVE STRESS AND INFLAMMATORY BIOMARKERS AS AGENTS FOR VASCULAR COMPLICATIONS IN RENAL FUNCTIONAuthor(s): Andile Khathi ,Mluleki Luvuno, Musa MabandlaJ. Ponte - Feb 2019 - Volume 75 - Issue 2 doi: 10.21506/j.ponte.2019.2.9 Abstract:Studies in our laboratory have shown that prolonged ingestion of a high fat high carbohydrate diet (HFHC) results in the development of pre-diabetes that is characterized by moderate hyperglycaemia. However, the effects of moderate hyperglycaemia, as seen in a HFHC-diet induced pre-diabetes rat model on renal function have not fully been characterized. Therefore, we investigated the changes in renal function on a HFHC diet-induced prediabetes rat model through the evaluation of markers of inflammation and oxidative stress. Animals were randomly assigned to the following diets ad libitum during experimentation: standard rat chow (ND+H2O) and high-fat high-carbohydrate supplemented with fructose (HFHC+Fructose). We measured glycosylated haemoglobin (HbA1c), lipid profile, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx1), tumor necrosis factor-alpha (TNF-α), interlukin-6 (IL-6), aldosterone concentration and mean arterial pressure. An increase in HbA1c, triglyceride (TG) and LDL-cholesterol concentration in the HFHC+Fructose diet group that occurred in parallel to an increase in MDA concentration and a decrease in SOD and GPx1 concentration was observed. This change was accompanied by an increase in TNF-α, IL-6, aldosterone concentration and mean arterial pressure. Therefore, the presence of high HbA1c, TG and LDL-cholesterol concentration that co-exists with elevated MDA concentration and lower anti-oxidant concentration suggests potential damage in renal tissue due to oxidative stress. High TNF-α and IL-6 concentration increases the risk for inflammation and development of vascular complications as evidenced by the increase in mean arterial pressure and aldosterone concentration. Altogether, chronic ingestion of the HFHC+Fructose diet increase apoptotic markers that induce glycation of proteins, dyslipidemia, oxidative stress, inflammatory condition and high blood pressure. Therefore, early management of these markers during prediabetes may prevent the onset of kidney dysfunction and circumvent development of vascular complications. Download full text:Check if you have access through your login credentials or your institution Username Password

Clinical observation of the reduced glutathione in the treatment of diabetic chronic kidney disease

Diabetic chronic kidney disease (CKD) has become the main cause of death in diabetic patients, but its pathogenesis has not yet been clear. To investigate the effects of reduced glutathione (GSH) on oxidative stress (OS), angiogenesis factors and lymphocyte subsets in diabetic CKD patients. A total of 130 subjects were retrospectively studied. The subjects were divided into the control group (45 cases), treatment group (45 cases, treated with reduced GSH), and a healthy control group (40 cases). The levels of superoxide dismutase (SOD), advanced oxidation protein products (AOPP), malondialdehyde (MDA), endostatin (ES), and vascular endothelial growth factor (VEGF), and the percentages of lymphocyte subsets were detected. After treatment, the indexes of OS and angiogenesis and the percentage of CD3- CD19+ B cells were obviously decreased, and the percentages of T cell subsets and natural killer (NK) cell subsets were markedly increased in the treatment group compared with the control group. AOPP was positively correlated with angiogenesis indexes, MDA and CD3- CD19+ B cells, and negatively correlated with SOD and other lymphocyte subsets. SOD was inversely associated with angiogenesis indexes and MDA, and positively associated with lymphocyte subsets. Moreover, MDA had a positive correlation with angiogenesis indexes, B and T cell subsets, and a negative correlation with NK cell subsets. AOPP, MDA, SOD, VEGF, CD3+ T cells, CD3+ CD8+ T cells, CD3- CDl6+ CD56+ NK cells, and CD3- CDl6+ CD56+ NK T cells were the risk factors of diabetic CKD. GSH could inhibit OS and abnormal angiogenesis, and improve cellular immune response in CKD patients.

Aging and Hyperglycemia Intensify Dyslipidemia-Induced Oxidative Stress and Inflammation in Rats: Assessment of Restorative Potentials of ALA and EPA + DHA.

Effect of aging and hyperglycemia on oxidative stress (OS) and inflammation in dyslipidemic conditions has not been elucidated. Hence, in this study, we assessed the implications of aging, hyperglycemia, and also the dietary effect of n-3 fatty acids (α-linolenic acid (ALA) and eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA)) on OS and inflammation in dyslipidemic rats. Dyslipidemia was induced in young and aged rats by feeding high-fat lard (HFL) diet. Diabetes was induced in young dyslipidemic rats by administering streptozotocin 30days after the induction of dyslipidemia. Experimental groups received diets containing canola oil (HF + CNO) and fish oil (HF + FO) as a source of ALA and EPA + DHA respectively. After 60days of feeding rats with their respective diets, OS and inflammatory markers in serum were assessed. Dyslipidemia caused significant (p < 0.05) increase in OS (lipid peroxidation, nitric oxide, and protein carbonyl), pro-inflammatory cytokine (CRP, IL-1β, MCP-1, and TNF-α), and eicosanoid (PGE2, LTB4, and LTC4) level in serum of both young and aged rats. Aged dyslipidemic rats presented significantly (p < 0.05) higher level of these markers compared to young dyslipidemic rats. Hyperglycemia onset further augmented OS and inflammatory markers in young dyslipidemic rats significantly (p < 0.05). Administration of n-3 fatty acids downregulated the serum markers of OS and inflammation in all the three experimental models. Thus, aging and hyperglycemia onset intensified dyslipidemia-induced OS and inflammation. Dietary preformed EPA + DHA presented larger restorative potentials than precursor ALA in countering OS and inflammation in all the three experimental models.

Mechanisms of synergistic neurotoxicity induced by two high risk pesticide residues – Chlorpyrifos and Carbofuran via oxidative stress

Multi-component pesticide residues, especially pesticide residues with synergistic toxicity, are a serious threat to food safety. With risk assessment, we found that Chlorpyrifos (CPF) and Carbofuran (CBF) are 2 pesticide residues with highest risk for Actinidia chinensis planch. The results showed CPF and CBF have a synergistic neurotoxicity on neural cell SK-N-SH. The toxicity was partly depending on oxidative stress (OS) and had effects on cell apoptosis and cell cycle arrest. Furthermore, the toxicity remained on long-term low-dose condition.

The effect of periodontal therapy on oxidative stress biomarkers: A systematic review.

To systematically review the literature about the effect of periodontal treatment on oxidative stress (OxS) biomarkers. Three databases (PubMed, EMBASE, and Scopus) were searched up to February 2018. Clinical trials with a follow-up of at least 6weeks after mechanical periodontal treatment were included. Due to the high heterogeneity among the units and indices of measurements used in the studies, a meta-analysis was not performed. Overall, 3,199 studies were retrieved, of which 20 were included. Four studies were randomized clinical trials (RCT), and 16 studies were non-RCTs. The most common OxS biomarkers used were 8-hydroxydeoxiguanosine (8-OHdG), total oxidant status (TOS), and total antioxidant status (TAS). After treatment, most of the studies reported a decrease in 8-OHdG concentration in the gingival crevicular fluid (GCF) and saliva. In addition, the salivary concentration of this biomarker was similar to periodontally healthy patients. Periodontal therapy was effective in reducing TOS in GCF, saliva, and serum in most studies. TAS, however, responded inconsistently to the periodontal intervention. Periodontal therapy reduces the levels of OxS biomarkers, even to values similar to those found in periodontally healthy individuals. Additional RCTs are warranted, as the information is mainly based on nonrandomized studies.

Adipose tissue-derived free fatty acids initiate myeloid cell accumulation in mouse liver in states of lipid oversupply.

Accumulation of myeloid cells in the liver, notably dendritic cells (DCs) and monocytes/macrophages (MCs), is a major component of the metainflammation of obesity. However, the mechanism(s) stimulating hepatic DC/MC infiltration remain ill defined. Herein, we addressed the hypothesis that adipose tissue (AT) free fatty acids (FFAs) play a central role in the initiation of hepatic DC/MC accumulation, using a number of mouse models of altered FFA supply to the liver. In two models of acute FFA elevation (lipid infusion and fasting) hepatic DC/MC and triglycerides (TGs) but not AT DC/MC were increased without altering plasma cytokines (PCs; TNFα and monocyte chemoattractant protein 1) and with variable effects on oxidative stress (OxS) markers. However, fasting in mice with profoundly reduced AT lipolysis (AT-specific deletion of adipose TG lipase; AAKO) failed to elevate liver DC/MC, TG, or PC, but liver OxS increased. Livers of obese AAKO mice that are known to be resistant to steatosis were similarly protected from inflammation. In high-fat feeding studies of 1, 3, 6, or 20-wk duration, liver DC/MC accumulation dissociated from PC and OxS but tracked with liver TGs. Furthermore, decreasing OxS by ~80% in obese mice failed to decrease liver DC/MC. Therefore, FFA and more specifically AT-derived FFA stimulate hepatic DC/MC accumulation, thus recapitulating the pathology of the obese liver. In a number of cases the effects of FFA can be dissociated from OxS and PC but match well with liver TG, a marker of FFA oversupply.

Agave fructans and oligofructose decrease oxidative stress in brain regions involved in learning and memory of overweight mice

Obesity is currently a public health problem worldwide. Recently, non-reducing carbohydrates, that include β(2→1) and β(2→6) linkages in their structure, have been of particular interest in the field of obesity because they are involved in lipid metabolism. Some of these are agave fructans (AF) and oligofructose (OF). In this study, we evaluated both AF and OF on oxidative stress (OS) markers in the brain of overweight mice (OM). AF and OF decreased TBARS levels and carbonyls at different levels in hippocampus (HP), frontal cortex (FC) and cerebellum (CB) of OM. The results indicated that fructans may have anti-oxidative potential and can be used as an alternative treatment for the prevention of the consequences of this pathology.

THE IMPACT OF ANTIOXIDANTS ON OXIDATIVE STRESS AND ORAL LESIONS: A REVIEW

THE IMPACT OF ANTIOXIDANTS ON OXIDATIVE STRESS AND ORAL LESIONS: A REVIEW

Impact of alcohol and cigarette smoking consumption in male fertility potential: Looks at lipid peroxidation, enzymatic antioxidant activities and sperm DNA damage.

Alcohol intake and cigarette smoking are the major lifestyle factors with negative impact on fertility. We were interested to evaluate the negative impact of these factors on oxidative stress (OS), enzymatic antioxidant activity (EAO) of spermatozoa and on its DNA damage. This study included 108 male infertile patients with normal range of sperm conventional parameters but with unexplained infertility in assisted reproductive technologies programme. Firstly, OS was analysed based on lipid peroxidation (MDA) and EAO which included catalase (CAT), superoxide dismutase (SOD) and glutathione reductase (GR). Secondly, we evaluated DNA fragmentation by TUNEL assay and chromatin decondensation by aniline blue colouration. The whole lot was divided into four groups: control (nonalcoholic and nonsmoker patients), alcohol group, smoking group and alcohol-smoking group. The results showed, in three last groups compared to control an increased CAT, SOD and GR activities with high MDA level especially in smoking and alcohol-smoking group. The latter showed the highest values of DNA fragmentation and chromatin decondensation (31% and 39%) to exceed DNA damage normal range. Indeed, smoking and alcohol intake lead to increase EAO due to long-term unbalanced antioxidant/oxidation ratio with high OS which cause consequently sperm DNA damage calling in need by urgency to change the lifestyle behaviour.

Effects of separate and concurrent supplementation of Nano-sized clinoptilolite and Nigella sativa on oxidative stress, anti-oxidative parameters and body weight in rats with type 2 diabetes

ObjectivesThe objective of this study was to investigate the effects of separate and concurrent supplementation of natural nano-sized clinoptilolite (NCLN) and Nigella sativa (NS) on oxidative stress (OS), anti-oxidative parameters and body weight (BW) in high-fat-diet (HFD)/streptozotocin (STZ)-induced diabetic rats. MethodsIn this experimental study, 42 male Wistar rats were divided into diabetic (n=36) and non-diabetic (n=6) groups. The diabetic group (DG) was fed with a HFD for one month, then injected with intra-peritoneal single dose STZ (35 mg/kg BW). The DG was divided into 4 subgroups: [1] control (DC), [2] NS 1%/food, [3] NCLN 2%/food, [4] NS 1%/food + NCLN 2%/food. At the end of the 7th week, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPX) levels and total antioxidant capacity (TAC) were measured. ResultsThe MDA level was decreased in the NCLN (p = 0.011) and NCLN+NS (p = 0.007) groups compared to the DC group. The GPX level increased in the NS and NCLN groups compared to the DC group (p = 0.014 and p = 0.034). In addition, the level of TAC demonstrated increase in the untreated DG and NS groups, as compared to the normal control (NC) group (pDC = 0.031 and pNS = 0.024). Moreover, in the NS+NCLN group, the level of SOD decreased in comparison to the NS and NCLN groups (p < 0.01). At the end of the 7th week, BW decreased in the diabetic subgroups in comparison to the NC group. Treatment with NS and/or NS+NCLN insignificantly prevented severe weight loss in the fifth week of the treatment. ConclusionsAccording to results, separate supplementation of NS and NCLN was more beneficent on anti-oxidative parameters than concurrent supplementation of NS and NCLN.

Association of lipid peroxidation and antioxidant status with metabolic syndrome in Iranian healthy elderly women.

The interconnection between aging and metabolic syndrome (MetS) and their effect on oxidative stress (OxS) status lacks adequate information. Additionally, the age-related changes of antioxidant defenses and OxS in senior women with MetS in comparison to healthy senior women are not yet established. We analyzed the correlation between oxidative defense status and OxS with MetS components. Through further examination of MetS and aging, we aimed to determine their independent effects on OxS and oxidative defense status. This community-based cross-sectional study was conducted in the rural area of Babol, Iran. A total of 75 women of ≥60 years of age with MetS along with 89 women with similar conditions without the MetS, serving as the control group, were studied. Blood glucose, lipid profile, malondialdehyde (MDA) and total antioxidant capacity (TAC) were determined. Data were analyzed using multiple linear regression, ANOVA and independent t-tests. MDA and TAC levels independently showed a significant correlation with triglyceride (TG), waist circumference, fasting blood glucose and high-density lipoprotein cholesterol (HDL-C). As suggested by the standardized B (0.810, -0.783, P<0.001; -0.052, P<0.001, 0.047, P<0.01), TG followed by HDL-C were the most strongly correlated factors with MDA and TAC. Furthermore, MetS and age were independent risk factors for antioxidant activity reduction and OxS. However, MetS had a much higher predictive power than age (standardized B 0.573 for MetS and 0.376 for age, P<0.001). Aging and MetS, both lead to OxS, but the impact of MetS on this disorder was far greater than the effect of age. However, their cumulative effects can lead to a worsening of the situation. Therefore, early diagnosis and treatment of MetS, especially in the elderly can prevent any adverse impact of MetS.

Omega-3 Fatty Acid Supplementation is Associated With Oxidative Stress and Dyslipidemia, but Does not Contribute to Better Lipid and Oxidative Status on Hemodialysis Patients

The aim of the study was to explore the effects of n-3 polyunsaturated fatty acids (PUFA) supplementation in physiological doses on oxidative stress (OS) and dyslipidemia in patients on hemodialysis (HD). Randomized, double-blind, controlled, experimental trial. A total of 88 HD patients ≥18years old and on HD for at least 6months. A total of 43 patients received 1.28g/day of n-3 PUFA, and 45 other patients received soybean oil for 12weeks. Both oil supplements were vitamin E standardized. Routine tests, lipid profile, advanced oxidation protein products, isoprostanes, vitamins C and E, total antioxidant capacity, serum fatty acids, and adverse effects were evaluated. Supplementation was not able to alter lipid or OS profiles. There was an increase in the serum n-3 PUFA levels (eicosapentaenoic acid: +116%; docosahexaenoic acid: +100%) and an improvement in the n-6/n-3 ratio (-49%) in the supplemented group. Associations between n-3 PUFA and improvement in isoprostane and advanced oxidation protein product and HDL were observed. Treatment was well tolerated. Although the n-3 PUFA supplementation was associated with lower concentrations of isoprostane and advanced oxidation protein product and higher HDL levels, it was not sufficient for the improvement of highly prevalent risk factors, such as OS and dyslipidemia in HD patients.