Oxidative Stress In Individuals Research Articles

Monocyte-lymphocyte ratio predicts cardiovascular diseases death in individuals with type 2 diabetes.

Previous studies have shown higher cardiovascular mortality risk with higher monocyte-lymphocyte ratio levels in general population. However, the levels of oxidative stress in individuals with type 2 diabetes are higher than those in the general population, which may affect the link between monocyte-to-lymphocyte ratio and cardiovascular disease deaths. And the association between the monocyte-to-lymphocyte ratio and mortality risk in people with type 2 diabetes still be unknown. This study aimed to investigate the prognostic significance of monocyte-to-lymphocyte ratio in type 2 diabetes. This analysis involved 2,954 individuals with type 2 diabetes from the National Health and Nutrition Examination Survey 1999-2010. The National Death Index records through December 31, 2019, was used to determine all-cause and cardiovascular mortality. The prognostic roles were determined using Cox regression models, restricted cubic spline analysis, and time-dependent receiver operating characteristic curve analysis. During an average follow-up period of 12.4 years, a total of 1,007 deaths occurred, while 252 were due to cardiovascular disease. An elevated monocyte-to-lymphocyte ratio level exhibited a significant dose-response relationship with an increased risk of all-cause mortality (1.34 [95% CI 1.12, 1.60] for all-cause mortality [Ptrend = 0.001]). The multivariable-adjusted HR was 1.81 (95% CI 1.25, 2.63) (Ptrend = 0.001) for cardiovascular mortality indicating a U-shaped relationship (Pnonlinear = 0.013). The results of this study indicate a U-shaped relationship between the monocyte-to-lymphocyte ratio and cardiovascular mortality in individuals with diabetes. Both very low and high monocyte-to-lymphocyte ratio monocyte-to-lymphocyte ratio values were found to be associated with increased cardiovascular mortality risk.

Antioxidative effects of N-acetylcysteine in patients with β-thalassemia: A quick review on clinical trials.

Several studies have highlighted the potent antioxidant properties of N-acetyl cysteine (NAC). This review aimed to assess the impact of NAC on oxidative stress biomarkers in patients with β-thalassemia. The review included articles published before 2024 that investigated the effects of NAC on oxidative stress in individuals with β-thalassemia. A comprehensive search was conducted across various databases, including Scopus, PubMed, Web of Science, Trip, and CENTRAL. Only English-language clinical trials were considered for inclusion in this review. Besides, the number needed to treat (NNT) was calculated based on the included studies. Ninety-nine articles were retrieved from electronic databases, and after a thorough review, eight articles were selected for comprehensive text analysis. The highest dose of NAC administered was 10 mg/kg/day (equivalent to 600 mg/day) over a period of 3-6 months. All the studies assessing the impact of NAC on oxidative stress indicators in β-thalassemia patients demonstrated positive effects during the 3-month follow-up period. Most estimated NNTs fell into 1-5, suggesting significant clinical therapeutic value in this context. The current potency of NAC alone appears to be effective in ameliorating oxidative stress in patients with β-thalassemia major. While a 3-month duration seems adequate to demonstrate the antioxidant properties of NAC in this population, larger and well-designed clinical trials are warranted. Current clinical evidence possesses a high risk of bias.

Exploring causal associations of antioxidants from supplements and diet with attention deficit/hyperactivity disorder in European populations: a Mendelian randomization analysis.

Antioxidants from both supplements and diet have been suggested to potentially reduce oxidative stress in individuals with ADHD. However, there is a lack of studies utilizing the Mendelian randomization (MR) method to explore the relationship between dietary and supplemental antioxidants with ADHD. This study employed two-sample mendelian randomization. Various specific antioxidant dietary supplements (such as coffee, green tea, herbal tea, standard tea, and red wine intake per week), along with diet-derived circulating antioxidants including Vitamin C (ascorbate), Vitamin E (α-tocopherol), Vitamin E (γ-tocopherol), carotene, Vitamin A (retinol), zinc, and selenium (N = 2,603-428,860), were linked to independent single nucleotide polymorphisms (SNPs). Data on ADHD was gathered from six sources, comprising 246,888 participants. The primary analytical method utilized was inverse variance weighting (IVW), with sensitivity analysis conducted to assess the robustness of the main findings. In different diagnostic periods for ADHD, we found that only green tea intake among the antioxidants was significantly associated with a reduced risk of ADHD in males (OR: 0.977, CI: 0.963-0.990, p < 0.001, FDR = 0.065), with no evidence of pleiotropy or heterogeneity observed in the results. Additionally, a nominal causal association was found between green tea intake and childhood ADHD (OR: 0.989, 95% CI: 0.979-0.998, p = 0.023, FDR = 0.843). No causal relationships were detected between the intake of other antioxidant-rich diets and ADHD. Our study found a significant inverse association between green tea intake and male ADHD, suggesting that higher green tea consumption may reduce ADHD risk in males. Further research is needed to explore optimal doses and underlying mechanisms.

Glucose Load Following Prolonged Fasting Increases Oxidative Stress- Linked Response in Individuals With Diabetic Complications.

Prolonged catabolic states in type 2 diabetes (T2D), exacerbated by excess substrate flux and hyperglycemia, can challenge metabolic flexibility and antioxidative capacity. We investigated cellular responses to glucose load after prolonged fasting in T2D. Glucose-tolerant individuals (CON, n = 10) and individuals with T2D with (T2D+, n = 10) and without (T2D-, n = 10) diabetes complications underwent oral glucose tolerance test before and after a 5-day fasting-mimicking diet. Peripheral blood mononuclear cell (PBMC) resistance to ex vivo dicarbonyl methylglyoxal (MG) exposure after glucose load was assessed. Markers of dicarbonyl detoxification, oxidative stress, and mitochondrial biogenesis were analyzed by quantitative PCR, with mitochondrial complex protein expression assessed by Western blotting. T2D+ exhibited decreased PBMC resistance against MG, while T2D- resistance remained unchanged, and CON improved postglucose load and fasting (-19.0% vs. -1.7% vs. 12.6%; all P = 0.017). T2D+ showed increased expression in dicarbonyl detoxification (mRNA glyoxalase-1, all P = 0.039), oxidative stress (mRNA glutathione-disulfide-reductase, all P = 0.006), and mitochondrial complex V protein (all P = 0.004) compared with T2D- and CON postglucose load and fasting. Citrate synthase activity remained unchanged, indicating no change in mitochondrial number. Mitochondrial biogenesis increased in T2D- compared with CON postglucose load and fasting (mRNA HspA9, P = 0.032). T2D-, compared with CON, exhibited increased oxidative stress postfasting, but not postglucose load, with increased mRNA expression in antioxidant defenses (mRNA forkhead box O4, P = 0.036, and glutathione-peroxidase-2, P = 0.034), and compared with T2D+ (glutathione-peroxidase-2, P = 0.04). These findings suggest increased susceptibility to glucose-induced oxidative stress in individuals with diabetes complications after prolonged fasting and might help in diet interventions for diabetes management.

Hypothalamus-pituitary-adrenal axis in patients with post-traumatic stress disorders and related to oxidative stress.

The study involves the effect of hypothalamus-pituitary-adrenal hormones disorders, and related to oxidative stress in individuals with PTSD to those in the healthy group after they experience a specific event that results in a congenital illness or limb loss. Obtaining serum samples from males exclusively in cases where psychiatrists have determined that the men have experienced psychological damage brought on by a particular tragedy, and testing the men for hypothalamus-pituitary-adrenal axis and oxidative stress parameters in comparison to healthy participants. It was observed that there was a notable rise in cortisol levels (5.60±0.93) at 4 pm compared with healthy control (3.43±0.64) resulting from the stimulating effect of the pituitary gland, and this increase has a role in raising levels of oxidative stress in patients total oxidant status (1.08±0.13) compared with control (0.70±0.10). High oxidative stress may lead to increased prolactin levels and decreased testosterone levels. Transmission of incorrect chemical signals from the central nervous system has a role in causing disturbances in hormonal levels of the hypothalamus and its associated glands, and thus an imbalance in the metabolic rate due to high cortisol. Also, high levels of prolactin hormones play a role in a significant decrease in testosterone levels.

Potential Role of Dipeptidyl Peptidase-4 in Regulating Mitochondria and Oxidative Stress in Cardiomyocytes.

Oxidative stress causes mitochondrial damage and bioenergetic dysfunction and inhibits adenosine triphosphate production, contributing to the pathogenesis of cardiac diseases. Dipeptidyl peptidase 4 (DPP4) is primarily a membrane-bound extracellular peptidase that cleaves Xaa-Pro or Xaa-Ala dipeptides from the N terminus of polypeptides. DPP4 inhibitors have been used in patients with diabetes and heart failure; however, they have led to inconsistent results. Although the enzymatic properties of DPP4 have been well studied, the substrate-independent functions of DPP4 have not. In the present study, we knocked down DPP4 in cultured cardiomyocytes to exclude the effects of differential alteration in the substrates and metabolites of DPP4 then compared the response between the knocked-down and wild-type cardiomyocytes during exposure to oxidative stress. H2O2 exposure induced DPP4 expression in both types of cardiomyocytes. However, knocking down DPP4 substantially reduced the loss of cell viability by preserving mitochondrial bioenergy, reducing intracellular reactive oxygen species production, and reducing apoptosis-associated protein expression. These findings demonstrate that inhibiting DPP4 improves the body's defense against oxidative stress by enhancing Nrf2 and PGC-1α signaling and increasing superoxide dismutase and catalase activity. Our results indicate that DPP4 mediates the body's response to oxidative stress in individuals with heart disease.

Effects of Polyphenol-Rich Foods on Lipids and Oxidative Stress Status in Patients with Hyperlipidemia: A Systematic Review of Randomized Controlled Trials.

Hyperlipidemia has been demonstrated to be an autonomous predictor of numerous cardiovascular and cerebrovascular ailments, and research indicates that polyphenols have preventive and therapeutic effects on hyperlipidemia. Nevertheless, the impact of polyphenol-rich foods on blood lipids and oxidative stress status in patients with hyperlipidemia remains inconclusive. To examine the impact of polyphenol-rich foods on lipid levels and oxidative stress in individuals with hyperlipidemia. To retrieve papers published from the establishment of the database through October 9, 2023, eight databases were searched: the Chinese National Knowledge Infrastructure, the China Biomedical Literature Database, the Wanfang Database, the China Science and Technology Journal Database, PubMed, the Cochrane Library, Embase, and the Web of Science. The quality of include studies was assessed using the Cochrane Risk of Bias in Randomized Trials tool, v2. The study involved 13 surveys encompassing 640 patients diagnosed with hyperlipidemia. The scope of the food surveys included 12 commonly consumed food groups and medicinal and food homologous substances. All 13 studies reported the effects of polyphenol-rich foods on blood lipids, with significant improvements observed in blood lipid levels for 9 types of foods. Eight studies examined the impact on oxidative stress, and six foods demonstrated a significant reduction in oxidative stress levels. The observed effects were found to be influenced by factors such as dosage, duration of intervention, and gender. Foods abundant in polyphenols play a crucial role in the prevention and treatment of hyperlipidemia by counteracting oxidative stress and regulating metabolic disorders. The confirmation of certain positive effects by several studies notwithstanding, discrepancies in results arise from various factors, necessitating further large-scale, prospective, well-designed randomized controlled studies to address this issue.

Evaluation of adiponectin serum levels and their association with oxidative stress in individuals with type 2 diabetes mellitus in Iraq

Evaluation of adiponectin serum levels and their association with oxidative stress in individuals with type 2 diabetes mellitus in Iraq

Mitochondrial Dysfunction due to Novel COQ8A Variation with Poor Response to CoQ10 Treatment: A Comprehensive Study and Review of Literatures.

COQ8A plays an important role in the biosynthesis of coenzyme Q10 (CoQ10), and variations in COQ8A gene are associated with primary CoQ10 deficiency-4 (COQ10D4), also known as COQ8A-ataxia. The current understanding of the association between the specific variant type, the severity of CoQ10 deficiency, and the degree of oxidative stress in individuals with primary CoQ10 deficiencies remains uncertain. Here we provide a comprehensive analysis of the clinical and genetic characteristics of an 18-year-old patient with COQ8A-ataxia, who exhibited novel compound heterozygous variants (c.1904_1906del and c.637C > T) in the COQ8A gene. These variants reduced the expression levels of COQ8A and mitochondrial proteins in the patient's muscle and skin fibroblast samples, contributed to mitochondrial respiration deficiency, increased ROS production and altered mitochondrial membrane potential. It isworthnotingthat the optimal treatment for COQ8A-ataxia remains uncertain. Presently, therapy consists of CoQ10 supplementation, however, it did not yield significant improvement in our patient's symptoms. Additionally, we reviewed the response of CoQ10 supplementation and evolution of patients in previous literatures in detail. We found that only half of patients could got notable improvement in ataxia. This research aims to expand the genotype-phenotype spectrum of COQ10D4, address discrepancies in previous reviews regarding the effectiveness of CoQ10 in these disorders, and help to establish a standardized treatment protocol for COQ8A-ataxia.

Role Of Lncrna In Alzheimer’s Diseases

Long noncoding RNA (lncRNA) are a family of RNA molecules with over 200 nucleotides in size. They cannot code for proteins but still have biological activities. lncRNAs are abundantly expressed in the pathogenic process of neurological diseases like Alzheimer’s. The lncRNA EBF3-AS is more expressed in the brains of older Alzheimer's disease patients called late onset Alzheimer’s disease. NAT-Rad18, a lncRNA over synthesized in specific areas of the brain in AD rats. The lncRNA n336694 targets miR-106b which increases its expression. MiR-106b leads to apoptosis markers in cells. oxidative stress-induced injury to the neurons is caused by the lncRNA SOX21-AS1. The lncRNA-ATB is involved in AD pathophysiology and reducing its expression helps with oxidative stress-induced injury. lncRNA MEG3 inhibits inflammatory injury and oxidative stress in individuals suffering from AD. The increase of lncRNA 17A in cerebral tissues of AD patients affects Aβ secretion. BACE1-AS suppression reduces Aβ and BACE1 levels and inhibits tau protein phosphorylation (3). The lncRNA BC200, also known as BCYRN1 upregulates Aβ production through BACE1 modulation which leads to AD pathogenesis. NEAT1 regulates the miR-124/BACE1 axis and plays a role in AD development. Reduced SORL1 expression increases neurotoxic Aβ formation in AD brains. LRP1-AS negatively regulates systemic Aβ clearance during AD progression. GAS5 regulates insulin signaling, neuronal survival, tau phosphorylation, and neuroinflammation. MAGI2-AS3-miR-374b-5p axis modulates neuroinflammation and neurotoxicity caused by Aβ fragment. Upregulation of WT1-AS inhibits the miR-375/SIX4 axis, OSI, and neuronal apoptosis in AD. BDNF-AS is found to be important in AD though the mechanism has yet to be determined. This review study aims to enhance comprehension of the disease progression of Alzheimer's disease (AD) in relation to various long non-coding RNAs (lncRNA).

The Comparative Study of Physical Exercise Towards Brain Natriuretic Peptide (BNP) and Malondialdehyde (MDA) as Oxidative Stress Markers in Rattus Novergicus Wistar Strain Rats

Background: Physical exercise has an effect on biological functions, namely a positive effect in terms of cell repair and a negative effect, namely inhibiting or damaging cells. Strenuous physical exercise can increase muscle injury and oxidative stress in individuals who are not conditioned or are not used to physical exercise. In addition, oxidative stress also plays a role in chronic fatigue syndrome. This occurs because the speed of energy demand exceeds the speed and ability of the oxygen transport system to supply oxygen to the mitochondria. The heart muscle is a muscle that has a major role in physical exercise. Oxidative stress plays an important role in the pathogenesis of myocardial infarction. Objectives: The purpose of this research is to determine the difference between aerobic and anaerobic exercise in the formation of free radicals. The formation of free radicals can be predicted by measuring levels of malondialdehyde (MDA) and Brain Natriuetic Peptide (BNP). Methods: The design used in this study was an experimental study in vivo with a pretest-posttest design with a comparison group. The subjects of this study were 28 male Wistar rats, Rattus novergicus, which were divided into 6 treatment groups and 1 comparison group. The data is taken by doing treadmill physical exercise with a speed of 20m / minute for aerobics and 35m / minute for anaerobics. Different tests of average MDA and BNP levels were used using independent t-tests, ANOVA, and post hoc. Result: The results showed a decrease in MDA and BNP levels in the aerobic treatment group and an increase in anaerobic compared to the comparison group. The analysis showed that there was a significant difference between the aerobic group for 1 day, 3 times a week, and 7 days, respectively, with p 0.05. Conclusion: It can be concluded that aerobic and anaerobic physical exercise performed 1 day, 3 times a week, and 7 consecutive days can increase the antioxidant defence system so that oxidative stress decreases, which is indicated by a decrease in MDA and BNP levels.

Roxyscan: A Novel Method to Assess Red Blood Cell Resilience to Oxidative Stress in Sickle Cell Disease

Background: Red blood cells (RBCs) are biconcave-shaped cells with viscoelastic membranes that are optimally adapted for oxygen delivery and gas exchange during their normal lifespan of 120 days. Reactive oxygen species (ROS) continuously challenge the viability of RBCs. Despite an arsenal of compounds to protect the RBC, including Glutathione (GSH), Vitamin E, superoxide dismutase (SOD) and Catalase, damage can easily be inflicted that will disrupt cellular deformability, structure, and membrane properties. The susceptibility to oxidative stress in individuals with Sickle Cell Disease (SCD) is believed to be linked to multiple factors. These include the release of heme and iron during hemolysis, inflammation processes, and a reduction in antioxidant defenses. Methods:Susceptibility of RBCs to oxidative stress was assessed with the RoxyScan. This novel application of the Lorrca MaxSis (RR Mechatronics) measures rheological behavior of RBCs in response to cumene hydroperoxide (CuHP, 100 µM) exposure during continuous shear (30 Pa). For this we used the Lorrca's peristaltic pump and suction needle, directing the blood and CuHP to the instrument's cup and mixing them for 30 seconds (s) before starting the run. Deformability of RBCs (EI, elongation index) was measured over time. PoX is defined as the time where a 10% decrease in EI is reached. EI start: EI t=0. EI final: EI t=1600s, ΔEI (EIstart-EIfinal). RoxyScan measurements were performed on blood samples from 16 adult SCD patients (HbSS, HbS/β0 or HbS/β+) and 19 healthy controls (HC). Outcome measurement PoX (calculated from curve fitted data) was correlated to laboratory parameters from complete blood count (Cell Dyn Sapphire, Abbott), RBC sickling tendency (Point of Sickling, PoS, as assessed by oxygen gradient ektacytometry on the Lorrca MaxSis), and levels of HbF/HbS (Tosoh G8). Results:RBCs from untreated HC show a stable EI over time (Fig 1A). Upon exposure to CuHP a similar decrease in EI is seen in 19 HC (Fig 1A), mean decrease 0.055, range (0.017 to 0.10). The mean and median calculated PoX in HC is 1723s and 1702s respectively. In contrast, SCD RBC showed an earlier and more pronounced decrease in EI in response to CuHP exposure (representative example, Fig 1A). Comparing the PoX between HC and SCD revealed significant differences: mean PoX HC: 1723s (SD 329s), SCD: 725s (SD 472s), ***p&amp;lt;0.0001, indicating that SCD RBCs are more susceptible to oxidative stress. Correlating PoX to routine laboratory parameters identified a correlation with Hb levels (***p=0.002), inverse correlation with reticulocyte count (***p=0.0014) and hemoglobin distribution width (HDW, ***p&amp;lt;0.001) (Fig 1B). Similarly strong inverse correlations were found for EI start and EI end (***p&amp;lt;0.001) (Fig 1B). PoX also showed an inverse correlation with red cell distribution width (RDW, ns p=0.07) and mean corpuscular volume (MCV, ns p=0.77). Interestingly, PoX showed a significant inverse correlation with PoS (***p=0.004), indicating that SCD RBCs which are more susceptible to oxidative stress tend to sickle at a higher oxygen tension. PoX showed no significant correlations with HbS/HbF levels (Fig 1B). Conclusion: In this study we demonstrate the applicability of the RoxyScan as a novel method to assess RBC resilience to oxidative stress. When applied to SCD, RBCs show an earlier and more pronounced response to oxidative stress than RBCs from HC. The inverse correlation of PoX, the major outcome parameter of this technique, with reticulocyte count could indicate a generally increased susceptibility to oxidative stress due to a higher level of hemolysis. The correlation with Hb levels affirms this. PoX showed other strong and significant correlations with routine laboratory parameters, such as HDW, implying that the greater variability in hemoglobin content is associated with higher susceptibility to oxidative stress. On a functional level, it is interesting to find strong correlations of PoX with PoS, showing a direct link between RBC sickling tendency and ability to withstand oxidative stress. On the other hand, HbS and HbF levels did not correlate significantly to PoX. Overall, our study highlights the potential use of the RoxyScan and its associated biomarkers in the analysis of the RBC's response to oxidative stress. Further research is in progress to investigate the clinical applicability of this new technique.

Investigating the relationship between COVID-19 and total oxidative stress and antioxidant capacity in individuals

Free oxygen radicals are effective in the development and progression of viral infections. The aim of this study was to evaluate the levels of oxidative stress in individuals who have been diagnosed with COVID-19, a viral disease nowadays. The study was carried out between March 2021 and June 2021. Blood samples of 50 patients who applied to Medipol University Faculty of Medicine with suspected COVID-19 infection, whose clinical and molecular diagnoses were corrected and were taken for routine evaluations, were included in this study. In the healthy group, 50 serum samples taken before the COVID-19 pandemic were used. Total antioxidant status (TAS) and total oxidant status (TOS) levels were measured, and the data collected were then statistically compared. The TAS level in the COVID-19 group (1.470±0.269) was lower than the healthy group TAS level (1.491±0.286), but it was not statistically significant (p&gt;0.05). The TOS level in COVID-19 group was 13.962 (3.02±36.35) while it was low as 7.925 (1.19±15.03) in the healthy group. The high TOS value in the COVID-19 group was found to be statistically significant compared to the healthy group (p

A simple dietary intervention to reduce inflammation and oxidative stress in individuals with metabolic syndrome

Abstract Funding Acknowledgements Type of funding sources: None. Background Approximately 25% of the world's population have metabolic syndrome and those diagnosed have a two-fold risk of developing cardiovascular disease. Inflammation and oxidative stress are responsible for the pathogenesis of metabolic syndrome. Diets with a high intake of vegetables containing carotenoids, a type of antioxidants, are associated with reduced levels of inflammation and oxidative stress, yet interventions to increase vegetable intake have been difficult to adapt. We conducted a randomized controlled trial of a simple dietary antioxidant intervention to reduce the levels of inflammation and oxidative stress. Purpose To examine the effect of a simple dietary antioxidant intervention on levels of inflammation and oxidative stress in persons with metabolic syndrome. Methods A total of 93 individuals with metabolic syndrome (mean age 61 ± 12 years old, 71% female) were enrolled. The intervention group received an 11.5-ounce serving of 100% carotenoid-rich vegetable juice to consume once per day for 30 days. The control group maintained their normal dietary pattern for 30 days. Adherence to the intervention was measured with Veggie Meter®, a validated reflection spectroscopy approach to assess skin carotenoid levels. Inflammation and oxidative stress were measured by plasma levels of high-sensitivity C-reactive protein (CRP) and malondialdehyde (MDA) at baseline and one-month post intervention. Two-way repeated measures analysis of variance was used to compare the group means over time. Log-transformation was applied as necessary for the variables with skewed distribution. Results There was no significant interaction between treatment and time on skin carotenoid levels, (respectively, P=0.214). There was a statistically significant increase of skin carotenoid levels in the intervention group alone (220 vs 264 in pre and post intervention, respectively, P=0.002). Change in mean CRP levels did not differ between control and intervention groups (P=0.520). Similarly, change in mean MDA did not significantly differ between two groups (P = 0.450). Conclusion A simple and easy to adapt, 1-month dietary antioxidant intervention did not change levels of inflammation and oxidative stress in individuals with metabolic syndrome, potentially due to the short-term treatment. Future interventions with dietary antioxidants should be implemented for longer time periods to fully assess the impact on inflammation and oxidative stress.

A Novel Functional Refined Olive Oil, Enhanced with Orange Peel Extract, Modulates Postprandial LDL-Cholesterol Responses in Individuals at Cardiometabolic Risk: A Pilot Randomized, Controlled, Cross-Over Nutritional Intervention

Olive oil, as the main source of polyphenols in the Mediterranean diet pattern, is mentioned to show remarkable postprandial bioactivity, contributing to the reduction of cardiometabolic risk factors. In recent years, the consumption of refined olive oil, instead of other olive oil classes, led to a reduced intake of polyphenols from the usual diet. This controlled, human nutritional intervention investigated whether the enhancement of refined olive oil with orange peel extract may modulate postprandial lipemia, glycemia, and oxidative stress in individuals at cardiometabolic risk. In a cross-over framework, 21 participants aged 30–65 years, who met the eligibility criteria, received a fat and carbohydrate meal of mashed potatoes, homogenized with refined olive oil (50 mL) or the functional olive oil, enhanced with 10% orange peel extract, intervening a washout week. Blood draws were performed in fasting, 30 min, 1.5 h, and 3 h after the meal intake. Plasma lipids, glucose, uric acid, and total plasma antioxidant capacity, according to the FRAP method, were measured at each timepoint. A significant reduction of LDL-cholesterol was observed, 1.5 h and 3 h after the functional meal intake, compared to non-significant changes after the control meal (p &lt; 0.05). No other statistically significant interactions were detected to the remaining biomarkers (p &gt; 0.05). Further investigation is needed for safer conclusions about the postprandial modulation of cardiometabolic risk factors by the functional olive oil enhanced with orange peel extract.

The effect of nutritional interventions reducing oxidative stress on behavioural and gastrointestinal problems in autism spectrum disorder.

Although the exact cause of autism spectrum disorder (ASD), which is a neurodevelopmental disorder, is not known, it is thought that environmental factors are also effective in addition to genetic risk factors. Studies are showing an increase in oxidative stress markers and a decrease in some antioxidant enzymes in individuals with autism. This study aims to try to explain the effect of nutritional interventions that reduce oxidative stress on behavioural and gastrointestinal problems in ASD based on a literature review. All relevant studies from 2000 to 2021 were identified through a systematic search in the PubMed and Web of Science databases by using key search terms. A systematic search of the electronic databases resulted in a total of 3235 potential articles, and data were extracted from 24 studies. There were 9 clinical trials and 15 animal studies. Most studies find statistically significant results for nutritional supplementation compared with placebo ASD symptoms. Most studies on the interventions of nutritional supplements that reduce oxidative stress in individuals with ASD have found improving effects on ASD symptoms, and no serious side effects have been observed. However, more interventional studies are needed to determine the precise effects of oxidative stress-reducing nutritional supplementation.

Neuroinflammation and Oxidative Stress in Individuals Affected by DiGeorge Syndrome

DiGeorge syndrome (DGS) is a rare genetic disease caused by microdeletions of the 22q11.2 region (DGS1). A haploinsufficiency at 10p level has been proposed also as a DGS cause (DGS2). Clinical manifestations are variable. The most frequent features are thymic hypoplasia or aplasia with consequent immune deficiency, cardiac malformations, hypoparathyroidism, facial and palatine abnormalities, variable degrees of cognitive impairment and psychiatric disorders. The specific aim of this descriptive report is to discuss the correlation between oxidative stress and neuroinflammation in DGS patients with microdeletions of the 22q11.2 region. The deleted chromosomic region maps various genes involved in mitochondrial metabolisms, such as DGCR8 and TXNRD2, that could lead to reactive oxygen species (ROS) increased production and antioxidant depletion. Furthermore, increased levels of ROS in mitochondria would lead to the destruction of the projection neurons in the cerebral cortex with consequent neurocognitive impairment. Finally, the increase in modified protein belonging to the family of sulfoxide compounds and hexoses, acting as inhibitors of the IV and V mitochondria complex, could result in direct ROS overproduction. Neuroinflammation in DGS individuals could be directly related to the development of the syndrome's characteristic psychiatric and cognitive disorders. In patients with psychotic disorders, the most frequent psychiatric manifestation in DGS, Th-17, Th-1 and Th-2 cells are increased with consequent elevation of proinflammatory cytokine IL-6 and IL1β. In patients with anxiety disorders, both CD3 and CD4 are increased. Some patients with autism spectrum disorders (ASDs) have an augmented level of proinflammatory cytokines IL-12, IL-6 and IL-1β, while IFNγ and the anti-inflammatory cytokine IL-10 seem to be reduced. Other data proposed that altered synaptic plasticity could be directly involved in DGS cognitive disorders. In conclusion, the use of antioxidants for restoring mitochondrial functionality in DGS could be a useful tool to protect cortical connectivity and cognitive behavior.

Plasma biomarkers of endothelial function, inflammation and oxidative stress in individuals with non-freezing cold injury.

What is the central question of this study? Are biomarkers of endothelial function, oxidative stress and inflammation altered by non-freezing cold injury (NFCI)? What is the main finding and its importance? Baseline plasma [interleukin-10] and [syndecan-1] were elevated in individuals with NFCI and cold-exposed control participants. Increased [endothelin-1] following thermal challenges might explain, in part, the increased pain/discomfort experienced with NFCI. Mild to moderate chronic NFCI does not appear to be associated with either oxidative stress or a pro-inflammatory state. Baseline [interleukin-10] and [syndecan-1] and post-heating [endothelin-1] are the most promising candidates for diagnosis of NFCI. Plasma biomarkers of inflammation, oxidative stress, endothelial function and damage were examined in 16 individuals with chronic NFCI (NFCI) and matched control participants with (COLD, n=17) or without (CON, n=14) previous cold exposure. Venous blood samples were collected at baseline to assess plasma biomarkers of endothelial function (nitrate, nitrite and endothelin-1), inflammation [interleukin-6 (IL-6), interleukin-10 (IL-10), tumour necrosis factor alpha and E-selectin], oxidative stress [protein carbonyl, 4-hydroxy-2-nonenal (4-HNE), superoxide dismutase and nitrotyrosine) and endothelial damage [von Willebrand factor, syndecan-1 and tissue type plasminogen activator (TTPA)]. Immediately after whole-body heating and separately, foot cooling, blood samples were taken for measurement of plasma [nitrate], [nitrite], [endothelin-1], [IL-6], [4-HNE] and [TTPA]. At baseline, [IL-10] and [syndecan-1] were increased in NFCI (P<0.001 and P=0.015, respectively) and COLD (P=0.033 and P=0.030, respectively) compared with CON participants. The [4-HNE] was elevated in CON compared with both NFCI (P=0.002) and COLD (P<0.001). [Endothelin-1] was elevated in NFCI compared with COLD (P<0.001) post-heating. The [4-HNE] was lower in NFCI compared with CON post-heating (P=0.032) and lower than both COLD (P=0.02) and CON (P=0.015) post-cooling. No between-group differences were seen for the other biomarkers. Mild to moderate chronic NFCI does not appear to be associated with a pro-inflammatory state or oxidative stress. Baseline [IL-10] and [syndecan-1] and post-heating [endothelin-1] are the most promising candidates for diagnosing NFCI, but it is likely that a combination of tests will be required.

Starvation and cadmium affect energy reserves and oxidative stress in individuals of Spodoptera exigua

Different factors, such as starvation and metal exposure, may affect development and cause oxidative stress in insects. Some host plants may contain a high concentration of cadmium due to their hyperaccumulating property. The negative effects of metals and hunger may be manifested by low availability of energetic substrates. This study aimed to assess whether the insect population with a history of long metal exposure may better manage metal stress or/and starvation at different developmental stages, with the use of energetic substrates. Two strains of Spodoptera exigua model organism were tested: control strain and cadmium strain (treated continuously for over 200 generations with subtoxic amounts of cadmium). The effects of different factors, individually and in combination, on the tested strains were assessed, first by determining the body weight of larvae and pupae and then by estimating the concentration of biomolecules (proteins, carbohydrates, lipids, or glycogen) in the 4th and 5th larval stages and in pupae, and the total antioxidant capacity and lipid peroxidation level in the 4th larval stage. Compared to control strain, cadmium strain individuals exhibited changes in the concentration of soluble carbohydrates and protein. This was partly related to earlier 1-day starvation. In particular, changes in carbohydrate concentration seemed to be a sensitive biomarker of metal stress, independent of the age of individuals and period of starvation. However, the increase in the total antioxidant capacity and the concentration of lipid peroxidation products in the 4th larval stage under the effect of cadmium was dependent on strain origin.

The Relationship Between Menstruation-related Symptoms And Oxidative Stress In Young Women

The symptoms associated with menstruation affect the daily lives of many premenopausal women. These symptoms are classified into two categories: premenstrual symptoms which occur during the luteal phase, and menstrual symptoms which occur during the menstrual period. Recently, oxidative stress has been shown to be associated with various gynecological diseases, but the relationship between oxidative stress and menstrual symptoms is unclear. PURPOSE: To examine the relationship between menstruation-related symptoms and oxidative stress levels in young women. METHODS: Sixteen female college students completed a menstrual distress questionnaire (MDQ)for a menstrual cycle. A blood sample was taken at four points during one menstrual cycle: menstrual period (day 2.4 ± 1.0), follicular phase (day 9.2 ± 1.0), early luteal phase (day 16.2 ± 0.9) and late luteal phase (day 22.8 ± 0.8). All participants have a regular menstrual cycle and have never taken oral contraceptives. We measured plasma reactive oxygen metabolites (Reactive Oxygen Metabolites-derived compounds: d-ROMs) and antioxidant capacity (Biological Antioxidant Potential: BAP). RESULTS: MDQ scores were highest during the menstrual period, decreased during the follicular and early luteal phases, and increased slightly during the late luteal phase (menstrual period: 31.1 ± 20.1 vs. early luteal phase: 16.4 ± 15.7, p < 0.05). The highest d-ROMs levels were observed during the menstrual period, followed by a gradual decrease during the follicular, early luteal, and late luteal phases (menstrual period: 322.2 ± 49.2 U.CARR vs. early luteal phase: 300.3 ± 32.5 U.CARR p < 0.05). The BAP level did not change during the menstrual cycle. The pain score in the MDQ was significantly higher in the menstrual period than in the early luteal phase, and its rate of change showed a weak positive association with the rate of change in d-ROMs (r = 0.30, NS). CONCLUSIONS: Pain of menstruation-related symptoms was observed to be possibly related to changes in oxidative stress in individuals. In healthy female college students, oxidative stress was the highest during the menstrual period, but the degree of oxidative stress was mild. Further studies are needed in women with severe menstruation-related symptoms, irregular menstrual cycles, and high oxidative stress status.