Neopterin in inflammation and oxidative stress.

Introduction: Few studies have reported on the association between a systematic consumption of organic diet and human health effects. Pesticides, commonly used in conventional, but not in organic agriculture, could lead to generation of reactive oxygen species, indicative of oxidative stress and inflammatory responses. We aimed to evaluate the literature on the association between organic diet and biomarkers of inflammation, oxidative stress and antioxidant capacity. Methods: Using PubMed, we searched for peer-reviewed articles that examined the influence of organic diet interventions in altering key biomarkers of oxidative stress, inflammation and antioxidant capacity in human studies; in-vitro and animal studies were excluded. Results: Only 9 relevant human studies were identified. Some of the biomarkers assessed in these articles were vitamins, cytokines, malondialdehyde and C-reactive protein. For most biomarkers, no statistically (p>0.05) significant differences were observed between conventional and organic diet interventions. In three crossover studies, organic diet resulted in significant (p<0.05) changes for markers of antioxidant capacity (vitamin B12, carotenoids, flavonols, total plasma antioxidant capacity), inflammatory biomarkers (tumor necrosis factor-alpha, interleukin-6 and -1) and for biomarkers of oxidative stress (protein oxidation). Conclusions: The small number of existing studies and their heterogeneity did not provide us with solid evidence on the association of organic diet with biomarkers of oxidative stress and inflammation. Randomized controlled human trials with sufficient power and long enough windows of monitoring exposures and biomarkers of effect should be implemented.

Aronia berry polyphenol consumption reduces plasma total and low-density lipoprotein cholesterol in former smokers without lowering biomarkers of inflammation and oxidative stress: a randomized controlled trial

Cigarette smoking is strongly associated with the development of cardiovascular disease (CVD). However, evidence is limited as to whether smokeless tobacco (ST) use is associated with CVD. Using data from 4347 adults in the Population Assessment of Tobacco and Health Study (2013-2014), we compared geometric mean concentrations of CVD-related harm biomarkers and biomarkers of exposure among exclusive ST users and exclusive cigarette smokers-in relation to recent nicotine exposure-and never tobacco users, adjusting for age, sex, race/ethnicity, income, body mass index, and CVD. Biomarker levels among exclusive ST users who were former established cigarette smokers were compared with exclusive cigarette smokers. Compared with cigarette smokers, ST users had significantly higher concentrations of total nicotine equivalents (TNE) but lower concentrations of inflammatory (high-sensitivity C-reactive protein, interleukin-6, intercellular adhesion molecule, fibrinogen) and oxidative stress (8-isoprostane) biomarkers (all p < .05). Biomarker levels among ST users were similar to never smokers. ST users who were former cigarette smokers had lower levels of inflammatory and oxidative stress biomarkers and biomarkers of exposure (cadmium, lead, 1-hydroxypyrene, acrylonitrile, and acrolein), compared with cigarettes smokers (p < .05), despite having higher TNE levels (p < .05). Among cigarette smokers, but not among ST users, inflammatory biomarkers and TNE were highly correlated. ST use is not associated with increases in biomarkers of CVD-related harm and exposure, compared with never smokers, despite exposure to nicotine at levels higher than those observed among cigarette smokers. These findings support the concept that increases in CVD risk among cigarette smokers is caused primarily by constituents of tobacco smoke other than nicotine. Despite having higher levels of nicotine and compared with exclusive cigarette smokers, exclusive ST users (including those who were former cigarette smokers) had significantly lower concentrations of inflammatory and oxidative stress biomarkers, comparable to levels observed among never tobacco users. These findings suggest that increases in CVD risk among cigarette smokers is caused primarily by tobacco constituents other than nicotine and that switching to ST is likely associated with lower CVD risk.

Protective effects of atorvastatin and quercetin on isoprenaline-induced myocardial infarction in rats

Several studies have shown the effects of pomegranate on oxidative stress and inflammation biomarkers, while some studies showed no effects of pomegranate on these biomarkers. Therefore, we aimed to evaluate the effects of pomegranate consumption on C-reactive protein (CRP), interlukin-6 (IL-6), tumor necrosis factor α (TNF-α), total antioxidant capacity (TAC), and malondialdehyde (MDA) in adults. A systematic literature search was performed using databases, including PubMed, Web of Science, and Scopus, up to May 2023 to identify eligible randomized controlled trials (RCTs). Heterogeneity tests of the included trials were performed using the I2 statistic. Random effects models were assessed based on the heterogeneity tests, and pooled data were determined as the weighted mean difference with a 95% confidence interval. Of 3811 records, 33 eligible RCTs were included in the current study. Our meta-analysis of the pooled findings showed that pomegranate consumption significantly reduced CRP (WMD: -0.50mg/l; 95% CI -0.79 to -0.20; p = 0.001), IL-6 (WMD: -1.24ng/L 95% CI -1.95 to -0.54; p = 0.001), TNF-α (WMD: -1.96pg/ml 95%CI -2.75 to -1.18; p < 0.001), and MDA (WMD: -0.34nmol/ml 95%CI -0.42 to -0.25; p < 0.001). Pooled analysis of 13 trials revealed that pomegranate consumption led to a significant increase in TAC (WMD: 0.26mmol/L 95%CI 0.03 to 0.49; p = 0.025). Overall, the results demonstrated that pomegranate consumption has beneficial effects on oxidative stress and inflammatory biomarkers in adults. Therefore, pomegranate can be consumed as an effective dietary approach to attenuate oxidative stress and inflammation in patients with cardiovascular diseases. CRD42023406684.

Linkage of hypoalbuminemia, inflammation, and oxidative stress in patients receiving maintenance hemodialysis therapy

Introduction: Although several meta-analyses support the positive effect of coenzyme Q10 (CoQ10) on biomarkers of oxidative stress and inflammation, the results of some other studies reject such effects.Methods: Therefore, in this umbrella meta-analysis, we performed a comprehensive systematic search in such databases as Web of Science, PubMed, Scopus, Embase, and Google Scholar up to January 2023.Results: Based on standardized mean difference analysis, CoQ10 supplementation significantly decreased serum C-reactive protein (CRP) (ESSMD = −0.39; 95% CI: 0.77, −0.01, p = 0.042) and malondialdehyde (MDA) (ESSMD = −1.17; 95% CI: 1.55, −0.79, p < 0.001), while it increased the total antioxidant capacity (TAC) (ESSMD = 1.21; 95% CI: 0.61, 1.81, p < 0.001) and serum superoxide dismutase (SOD) activity (ESSMD = 1.08; 95% CI: 0.37, 1.79, p = 0.003). However, CoQ10 supplementation had no significant reducing effect on tumor-necrosis factor-alpha (TNF- α) (ESSMD = −0.70; 95% CI: 2.09, 0.68, p = 0.320) and interleukin-6 (IL-6) levels (ESSMD = −0.85; 95% CI: 1.71, 0.01, p = 0.053). Based on weighted mean difference analysis, CoQ10 supplementation considerably decreased TNF-α (ESWMD = −0.46, 95% CI: 0.65, −0.27; p < 0.001), IL-6 (ESWMD = −0.92, 95% CI: 1.40, −0.45; p < 0.001), and CRP levels (effect sizes WMD = −0.28, 95% CI: 0.47, −0.09; p < 0.001).Discussion: The results of our meta-analysis supported the alleviating effects of CoQ10 on markers of inflammation cautiously. However, CoQ10 had antioxidant effects regarding the improvement of all the studied antioxidant and oxidative stress biomarkers.Systematic Review Registration:https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=323861, identifier CRD42022323861

Oxidative stress and inflammatory biomarkers in normal and preeclamptic pregnancies

Inflammation and oxidative stress contribute to the progression of chronic diseases, and the volume of research in this area is rapidly expanding. Various dietary indices have been developed to determine the overall inflammatory or oxidative stress potential of a diet; however, few have been validated in cardiometabolic disease populations. This review aimed to explore the association between dietary indices and biomarkers of inflammation and oxidative stress in adults with cardiometabolic conditions. Four databases were systematically searched for literature in any language (Embase, CINAHL, CENTRAL and MEDLINE) with 12,286 deduplicated records identified. Seventeen studies of adults with metabolic syndrome, cardiovascular disease, type 2 diabetes, non-alcoholic fatty liver disease or chronic kidney disease were included. Fourteen studies were observational studies, one study was a clinical trial, and one was a randomised controlled trial. Four dietary indices were reported on with most studies (n11) reporting on the dietary inflammatory index. The most reported biomarker was C-reactive protein. The findings were narratively synthesised. Results were inconclusive due to the heterogeneity of dietary indices and their use, disease states and biomarkers reported. Only one study reporting on the dietary inflammatory index assessed all 45 parameters. Observational studies, particularly retrospective designs (n7), are subject to recall and selection biases, potentially presenting overestimated results. Further research is required to determine the relationship between dietary indices and biomarkers of inflammation and oxidative stress in cardiometabolic disease populations. Future research should be prospective, utilise rigorous research methods, assess the full range of index parameters, and examine biomarkers the tool was developed for.

Temporal changes in biomarkers of oxidative stress and inflammation in pigs after intravenous administration of E. coli lipopolysaccharide.

Our previous study showed major changes in biomarkers on quitting compared to the smoking state. They reflected a decrease in inflammation, endothelial activation, and oxidative stress, as well as an improved lipid profile. Nicotine replacement therapy (NRT) is effective to increase the rate of successful quitting, but healthcare professionals may have concerns to prescribe this first-line smoking cessation treatment because its effect on inflammation and related processes is controversial. The present study assessed the influence of NRT on biomarkers of inflammation, endothelial function, oxidative stress, and lipids, in people who quit smoking. Sixty-five subjects who daily smoke cigarettes were recruited and followed on quitting. Thirty-five quit using NRT and thirty quit without NRT. Biomarkers of inflammation, endothelial function, oxidative stress, and lipids were quantified at baseline when actively smoking and after cessation in the presence of NRT or not. Changes in biomarkers on quitting did not differ according to the treatment used. No difference was found when comparing participants who were exposed to NRT and those who were not. These results may indicate that NRT has no effect on inflammation, endothelial function, oxidative stress, and lipids, when used as a medication aid for quitting smoking. This study provides new evidence to support the safety profile of NRT products regarding the biomarkers of endothelial function, oxidative stress, inflammation, and lipids.

Introduction: Combustible tobacco smoking is strongly associated with the development of cardiovascular disease (CVD). However, evidence is limited as to whether smokeless tobacco (ST) use is associated with CVD. Methods: Using data from 4347 adults in the Population Assessment of Tobacco and Health Study (2013-2014), we compared geometric mean concentrations of CVD-related harm biomarkers and biomarkers of exposure among current exclusive ST product users and exclusive cigarette smokers—in relation to nicotine exposure—and never tobacco users, adjusting for age, sex, race/ethnicity, income, BMI and CVD. Biomarker levels among exclusive ST users who were former established cigarette smokers were examined and compared to levels among exclusive cigarette smokers. Results: Compared to cigarette smokers, ST users had significantly higher concentrations of total nicotine equivalents (TNE) but lower concentrations of inflammatory (high-sensitivity C-Reactive-Protein, interleukin-6, intercellular adhesion molecule, fibrinogen) and oxidative stress (8-isoprostane) biomarkers (all P&lt;0.05). Biomarker levels among ST users were similar to never smokers. Exclusive ST users who were former cigarette smokers had lower levels of inflammatory and oxidative stress biomarkers and biomarkers of exposure (including cadmium, lead, 1-hydroxypyrene, acrylonitrile and acrolein), compared to cigarettes smokers (p&lt;0.05), despite having higher TNE levels (P&lt;0.05). In cigarette smokers, but not among ST users, inflammatory biomarkers and TNE were highly correlated. Conclusions: ST use is not associated with increases in biomarkers of CVD-related harm and exposure, compared to never smokers, despite exposure to nicotine at levels higher than those observed among cigarette smokers. These findings support the concept that increases in CVD risk among cigarette smokers is caused primarily by constituents of tobacco smoke other than nicotine.

Background: Tocotrienols have hypocholesterolemic, anti-inflammatory, and anti-cancer properties. Clinical studies using tocotrienol-rich fraction (TRF) from palm oil yielded inconsistent results with regards to its efficacy due to presence of tocopherols in TRF mixture. Objectives: The impact of tocopherol-free δ-tocotrienol on inflammatory and oxidative stress biomarkers, plasma cytokines/proteins, their gene expression, and microRNAs was studied in hypercholesterolemic subjects. Design: Hypercholesterolemic (n=31; serum cholesterol >5.2 mmol/L) subjects were enrolled in the study. All hypercholesterolemic subjects were given increasing doses of δ-tocotrienol (125, 250, 500, 750 mg/d) plus AHA Step-1 diet for 4 weeks each during a 30 week study period. Serum nitric oxide (NO), C-reactive protein (CRP), malondialdehyde (MDA), δ-glutamyl-transferase (δ-GT), total antioxidant status (TAS), cytokines/proteins, cDNA, and microRNAs were determined. Results: All concentrations of δ-tocotrienol reduced serum levels of NO, CRP, MDA, δ-GT. The most effective dose (250 mg/d) decreased serum NO (40%), CRP (40%), MDA (34%), δ-GT (22%) significantly (P<0.001), while TAS levels increased 22% (P<0.001). The 500 mg/d and 750 mg/d doses were less effective in improving oxidative stress compared to the 250 mg/d dose. Inflammatory plasma cytokines (resistin, IL-1α, IL-12, IFN-γ) were reduced 15-17% (P<0.05-0.01), while cardiac angiogenic fibroblast growth factor-b (FGF-b) and platelet-derived growth factor (PDGF) were decreased by 11% and 14% (P<0.05-0.01), respectively, with 250 mg/d δ-tocotrienol treatment. Similar results were obtained for cytokine gene expression. Several plasma miRNAs (miRNA-16-1, miRNA-125a, miRNA-133, miRNA-155, miRNA-223, miRNA-372, miRNA-10b, miRNA-18a, miRNA-214) associated with cardiovascular disease and cancer were modulated by δ-tocotrienol treatment. Conclusions: In a dose-dependent study of 125-750 mg/d, δ-tocotrienol maximally reduced inflammation and oxidative stress parameters with a 250 mg/d dose in hypercholesterolemic subjects, and may be a potential therapeutic alternative natural product for the maintenance of health during aging process.

Novel biomarkers of inflammation and oxidative stress might enhance the early recognition, management, and clinical outcomes of patients with rheumatic diseases (RDs). We assessed the available evidence regarding the pathophysiological role of neopterin, the oxidation product of 7,8-dihydroneopterin, a pteridine generated in macrophages activated by interferon-γ, by conducting a systematic review and meta-analysis of studies reporting its concentrations in biological fluids in RD patients and healthy controls. We searched electronic databases for relevant articles published between inception and 31 August 2023. The risk of bias and the certainty of evidence were assessed using the Joanna Briggs Institute Critical Appraisal Checklist and the Grades of Recommendation, Assessment, Development and Evaluation Working Group system, respectively. In 37 studies, when compared to healthy controls, RD patients had significantly higher concentrations of neopterin both in plasma or serum (standard mean difference, SMD=1.31, 95% CI 1.01 to 1.61; p<0.001; moderate certainty of evidence) and in the urine (SMD=1.65, 95% CI 0.86 to 2.43, p<0.001; I2 = 94.2%, p<0.001; low certainty of evidence). The results were stable in sensitivity analysis. There were non-significant associations in meta-regression and subgroup analysis between the effect size and age, male to female ratio, year of publication, sample size, RD duration, C-reactive protein, erythrocyte sedimentation rate, specific type of RD, presence of connective tissue disease, analytical method used, or biological matrix investigated (plasma vs. serum). By contrast, the effect size was significantly associated with the geographical area in studies assessing serum or plasma and with the type of RD in studies assessing urine. Pending additional studies that also focus on early forms of disease, our systematic review and meta-analysis supports the proposition that neopterin, a biomarker of inflammation and oxidative stress, can be useful for the identification of RDs. (PROSPERO registration number: CRD42023450209). PROSPERO, identifier CRD42023450209.

Comparison Effect of Atorvastatin (10 versus 80 mg) on Biomarkers of Inflammation and Oxidative Stress in Subjects With Metabolic Syndrome