Markers Of Antioxidant Capacity Research Articles

131 Selenium-form effects on hepatic function and selenoprotein mRNAs in the early pregnant heifer

Abstract Selenium (Se) is an integral component of selenoproteins, with effective scavenging of harmful reactive oxygen species (ROS) by selenoproteins necessary to protect cells from oxidative stress. Due to the presence of Se-deficient soils in large portions of the US, including the southeast cow-calf producing states, grazed forages are insufficient in this trace mineral and dietary supplementation is recommended. We have investigated the effects of providing Se in an inorganic form (ISe, the industry standard) versus a 1:1 mixture (MIX) of ISe to organic Se (OSe), and have observed significant effects on luteal function, endometrial function and conceptus development. Herein, our objective was to determine the effect of form of Se on 1) clinical markers of total antioxidant capacity and liver function, and 2) the expression of mRNAs encoding selenoproteins in the liver. Following consecutive 45-d periods of Se-depletion then repletion, Angus-cross heifers were assigned to 90 d of treatment with a vitamin-mineral mix containing 35-ppm Se as ISe or MIX. Heifers were then inseminated at estrus (d 0) with serum collected at d 0, 7 and 17 to quantify albumin, beta-hydroxybutyrate (BHBA) and aspartate aminotransferase (AST). Liver samples were collected at euthanasia on d 17 (n = 6 pregnant heifers per treatment) for the quantification of the relative abundance of 25 selenoprotein mRNAs using qPCR. There was no effect of treatment on circulating albumin (P > 0.05). Hepatocyte-secreted albumin is the most prominent antioxidant in the circulation, with this result suggesting that albumin-driven redox capacity is not sensitive to the form of Se supplied to achieve a Se-adequate status. Systemic concentrations of BHBA and AST were increased (P < 0.05) in MIX- versus ISe-treated heifers at d 7 and 17 of pregnancy. Circulating BHBA is considered a primary indicator of liver function and the hepatic response to increased metabolic demands, whereas increased AST is conventionally considered a marker for liver damage. These results suggest increased demands on the liver in MIX versus ISe-treated heifers, however not at the level indicative of dysfunction or disease. Additionally, the serum concentration of urea nitrogen was quantified and determined to be reduced (P < 0.05) at estrus in MIX- versus ISe-treated heifers, indicative of form-induced changes in hepatic nitrogen metabolism. Targeted qPCR analysis to determine the effect of treatment on the abundance of encoding selenoproteins by mRNA, including the iodothyronine deiodinases, glutathione peroxidases and thioredoxin reductases, was largely unaffected by treatment, with only the abundance of mRNA encoding Selenoprotein V tending to differ (P = 0.07) with treatment. Overall, this study revealed form of Se-effects on markers of hepatic health and function, as well as blood urea nitrogen, but did not reveal form of Se-effects on the expression of hepatic selenoproteins mRNAs.

Involvement of oxidative stress in orofacial mechanical pain hypersensitivity following neonatal maternal separation in rats

Patients with persistent pain have sometimes history of physical abuse or neglect during infancy. However, the pathogenic mechanisms underlying orofacial pain hypersensitivity associated with early-life stress remain unclear. The present study focused on oxidative stress and investigated its role in pain hypersensitivity in adulthood following early-life stress. To establish an early-life stress model, neonatal pups were separated with their mother in isolated cages for 2 weeks. The mechanical head-withdrawal threshold (MHWT) in the whisker pad skin of rats received maternal separation (MS) was lower than that of non-MS rats at postnatal week 7. In MS rats, the expression of 8-hydroxy-deoxyguanosine, a marker of DNA oxidative damage, was enhanced, and plasma antioxidant capacity, but not mitochondrial complex I activity, decreased compared with that in non-MS rats. Reactive oxygen species (ROS) inactivation and ROS-sensitive transient receptor potential ankyrin 1 (TRPA1) antagonism in the whisker pad skin at week 7 suppressed the decrease of MHWT. Corticosterone levels on day 14 increased in MS rats. Corticosterone receptor antagonism during MS periods suppressed the reduction in antioxidant capacity and MHWT. The findings suggest that early-life stress potentially induces orofacial mechanical pain hypersensitivity via peripheral nociceptor TRPA1 hyperactivation induced by oxidative stress in the orofacial region.

Effects of different drying methods on physico-chemical properties, bioactive and taste substances of Cynomorium songaricum

Cynomorium songaricum is a typical edible and medicinal plant, also called Suoyang (Chinese name). The effect of different drying methods on Suoyang quality has not yet been performed. Here, four drying methods were tested, including sun drying (SD), microwave drying (MD), hot air drying (HAD), and vacuum freeze drying (VFD), to evaluate the influences of various drying methods on the physico-chemical properties, bioactive and taste substances of dried Suoyang. Results showed that VFD treated samples maintained the original cellular structure and color, and had higher textural properties, antioxidant activities, and rich flavor. In addition, a total of 980 metabolites in four kinds of dried Suoyang were detected and clustered into 9 co-response modules based on utilizing widely targeting metabolomics method and weighted metabolite co-response network analysis (WMCNA). Among the important modules, 3 key metabolites were identified as potential quality markers of overall antioxidant capacity and 30 key metabolites were identified as the main taste substances, which also might be relate to the nutritional value of dried Suoyang. This finding will provide reference for choosing proper drying method that can maintain the quality of dried Suoyang and adapt to industrial production.

Bioactive compounds from Prosopis species as potential oxidative stress and inflammation modulators: an update on mechanisms

Oxidative stress and inflammation processes are involved in most diseases and illnesses. Many herbal remedies have been shown to have anti-inflammatory and antioxidant effects, and have been used since ancient times as traditional medicine. Species of the genus Prosopis are one of these herbal remedies that grow in arid, semiarid, subtropical, and tropical areas of the world. Paste, gum, and smoke from pods and leaves of Prosopis plants are traditionally used to treat diseases related to oxidative stress and inflammation. This review aims to provide up-to-date information on Prosopis plants as oxidative stress and inflammation modulators. Relevant information was collected from researching scientific databases such as PubMed/Medline, Wiley, Web of Science and Springer. Folk medicinal applications and biologically active molecules of Prosopis spp., and its derivatives, have been collected paying attention to studies that used verified markers of oxidative stress, antioxidant capacity and inflammation. Future studies are needed to deepen more pharmacodynamic, pharmacokinetic and structure-activity relationships of phytochemicals isolated from Prosopis species.

Ranolazine exhibits anti-inflammatory and antioxidant activities in H9c2 cardiomyocytes.

The aim of this study was to evaluate the effectiveness of ranolazine on hypoxia-inducible factor-1α (HIF-1α) and oxidative stress in H9c2 cardiomyocyte cells. We have assessed the effects of increasing concentrations of methotrexate (MTX) and ranolazine on proliferation of H9c2 rat cardiomyocyte cells by MTT assay. Malondialdehyde (MDA) protein oxidation [advanced oxidation protein products (AOPPs)], lipid hydroperoxide (LOOH) and xanthine oxidase (XO) activity as oxidative stress markers and HIF-1α levels increased and total thiol (T-SH), catalase (CAT) activity and total antioxidant capacity (TAC) antioxidant capacity markers decreased in MTX-treated cells compared to control cells. Oxidative stress markers decreased, and antioxidant capacity markers increased in cells treated with ranolazine alone compared to control cells. For all parameters, we showed that the levels of oxidant, antioxidant markers and HIF-1α in cells treated with MTX and ranolazine together reached the level of the control group, and ranolazine reversed the oxidative damage caused by MTX. The cell viability increased the levels of oxidant and prooxidant markers and decreased the levels of antioxidant markers decreased in H9c2 cardiomyocytes induced by oxidative stress. These results suggest that ranolazine may protect the cardiomyocytes from MTX-induced oxidative damage. The effects of ranolazine could result from its antioxidant properties.

Relationship between Oxidative Stress and Left Ventricle Markers in Patients with Chronic Heart Failure

Oxidative stress is proposed in the literature as an important player in the development of CHF and correlates with left ventricle (LV) dysfunction and hypertrophy in the failing heart. In this study, we aimed to verify if the serum oxidative stress markers differ in chronic heart failure (CHF) patients' groups depending on the LV geometry and function. Patients were stratified into two groups according to left ventricular ejection fraction (LVEF) values: HFrEF (<40% (n = 27)) and HFpEF (≥40% (n = 33)). Additionally, patients were stratified into four groups according to LV geometry: NG-normal left ventricle geometry (n = 7), CR-concentric remodeling (n = 14), cLVH-concentric LV hypertrophy (n = 16), and eLVF-eccentric LV hypertrophy (n = 23). We measured protein (protein carbonyl (PC), nitrotyrosine (NT-Tyr), dityrosine), lipid (malondialdehyde (MDA), oxidizes (HDL) oxidation and antioxidant (catalase activity, total plasma antioxidant capacity (TAC) markers in serum. Transthoracic echocardiogram analysis and lipidogram were also performed. We found that oxidative (NT-Tyr, dityrosine, PC, MDA, oxHDL) and antioxidative (TAC, catalase) stress marker levels did not differ between the groups according to LVEF or LV geometry. NT-Tyr correlated with PC (rs = 0.482, p = 0.000098), and oxHDL (rs = 0.278, p = 0.0314). MDA correlated with total (rs = 0.337, p = 0.008), LDL (rs = 0.295, p = 0.022) and non-HDL (rs = 0.301, p = 0.019) cholesterol. NT-Tyr negatively correlated with HDL cholesterol (rs = -0.285, p = 0.027). LV parameters did not correlate with oxidative/antioxidative stress markers. Significant negative correlations were found between the end-diastolic volume of the LV and the end-systolic volume of the LV and HDL-cholesterol (rs = -0.935, p < 0.0001; rs = -0.906, p < 0.0001, respectively). Significant positive correlations between both the thickness of the interventricular septum and the thickness of the LV wall and the levels of triacylglycerol in serum (rs = 0.346, p = 0.007; rs = 0.329, p = 0.010, respectively) were found. In conclusions, we did not find a difference in serum concentrations of both oxidant (NT-Tyr, PC, MDA) and antioxidant (TAC and catalase) concentrations in CHF patients' groups according to LV function and geometry was found. The geometry of the LV could be related to lipid metabolism in CHF patients, and no correlation between oxidative/antioxidant and LV markers in CHF patients was found.

Protective effect of eicosapentaenoic acid against estradiol valerate-induced endometrial hyperplasia via modulation of NF-κB/HIF-1α/VEGF signaling pathway in rats

BackgroundEarly diagnosis and treatment of endometrial hyperplasia (EH) remains mandatory for endometrial cancer (EC) prevention. ObjectiveTo study the possible protective effect of eicosapentaenoic acid (EPA) in EH - induced by estradiol valerate (EV) in rats. Methods/materialsAdult female Wistar rats were given EV with or without EPA for 10 days. The uterine changes were evaluated by both physical (weight index) and histopathological methods. The markers of oxidative stress (Uterine malondialdehyde (MDA) and serum total antioxidant capacity (TAC) as well as serum estradiol and progesterone levels, and apoptosis (uterine caspase-3) were determined. Immunohistochemical estimations of nuclear factor kappa B (NF-κB) and vascular endothelial growth factor (VEGF) in addition to hypoxia-inducible factor 1 alpha (HIF-1α) immunoblotting were measured in uterine tissue. Key findingsEV showed significant increase in uterine weight index that is accompanied with histopatholigical evidences of EH. Such changes were associated with significant alterations in oxidative stress markers, modulation of estradiol and progesterone serum levels, an increase in HIF-1α, NF-κB and VEGF immuno-expressions and a significant decrease in caspase-3. EPA, in either dose, showed significant amelioration in uterine weight index as well as in histopathological changes. Such effect was accompanied with significant improvement in the measured hormonal levels, oxidative stress, apoptosis, and inflammatory parameters. ConclusionsEPA in the used doses provided biochemical and histopathological improvement in EV-induced EH via modulation of NF-κB/HIF-1α/VEGF signaling pathway.

γ-Glutamyl transferase as a marker of oxidative stress in pre and post-menopausal women

Introduction: Menopause is a physiologic process in women representing complete cessation of menstruation and gradual decrease of estrogen secretion. The antioxidant substances present in the body play a role in combating the oxidative stress in menopause. Since, the enzyme γ-glutamyl transferase plays an important role in the metabolism of the endogenous antioxidant reduced glutathione (GSH), it can reflect the antioxidant ability in vivo. Aim: The present study was conducted to investigate γ-glutamyl transferase as a possible marker of total antioxidant capacity (TAC) of plasma. Materials and Method: The study included 50 female volunteers, selected from medical & paramedical staff, and healthy attendants of patients as per inclusion and exclusion criteria and divided into 2 groups. Group I: Premenopausal women (n = 25); Group II: Postmenopausal women (n = 25). Venous blood samples were collected using aseptic techniques in plain vials for estimating estradiol hormone and Gamma GT and whole blood was collected in EDTA vials for the estimation of Ferric reducing ability of plasma (FRAP) which is a marker of antioxidant capacity. The data collected were analyzed using unpaired “t”-test for evaluating the level of oxidative stress in pre and post menopausal women and the variations in the levels of gamma GT in the two groups. The results were expressed as Mean ± Standard Deviation (SD). Results and Conclusion: Depressed estrogen synthesis in postmenopausal women enhanced oxidative stress and lead to deficit of total antioxidant capacity of plasma. A significant increase in serum GGT in the post-menopausal group relative to the pre-menopausal group was found which was to compensate and correct the reduced glutathione levels by increasing its biosynthesis. Thus, GGT can be used as a marker of total antioxidant capacity of plasma and oxidative stress.

Quercetin supplementation promotes recovery after exercise-induced muscle damage: a systematic review and meta-analysis of randomized controlled trials.

Quercetin (Q) is one of the most frequently consumed flavonoids in the human diet. The purpose of this systematic review and meta-analysis was to determine the effects of Q supplementation on muscle damage, muscle soreness and biochemical markers of inflammation, antioxidant capacity and oxidative stress after intense exercise. A literature search of SPORTDiscus, PubMed, Web of Science and Scopus was performed from inception to May 31, 2022. Forest plots were generated with fixed or random-effect models and standardized mean differences (SMD). Data extraction and quality assessment were performed independently by two authors. After application of the inclusion and exclusion criteria, 13 studies with a total of 249 sedentary to well-trained participants were included. For all studies there were some concerns about the risk of bias. All but one study used a supplementation dosage of 1000 mg/day. Q supplementation accelerated recovery of muscle function and significantly decreased muscle soreness 0/24 h after exercise (SMD: -1.33; p = 0.03), creatine kinase levels 24/48 h after exercise (SMD: -1.15; p = 0.02), and post-exercise oxidative stress (SMD: -0.92; p = 0.03). However, Q supplementation had no effect on IL-6 concentration. Q supplementation with a dose of 1000 mg/day for periods of more than seven days and a maximum of 12 weeks appears to be a safe and efficacious strategy to reduce muscle damage and muscle soreness, as well as to enhance recovery after intense exercise in sedentary to well-trained young men. Systematic review registration: PROSPERO CRD42021266801.

Tracking peripheral vascular function for six months in young adults following SARS-CoV-2 infection.

SARS-CoV-2 infection is known to instigate a range of physiologic perturbations, including vascular dysfunction. However, little work has concluded how long these effects may last, especially among young adults with mild symptoms. To determine potential recovery from acute vascular dysfunction in young adults (8M/8F, 21 ± 1yr, 23.5± 3.1kg⋅m-2 ), we longitudinally tracked brachial artery flow-mediated dilation (FMD) and reactive hyperemia (RH) in the arm and hyperemic response to passive limb movement (PLM) in the leg, with Doppler ultrasound, as well as circulating biomarkers of inflammation (interleukin-6, C-reactive protein), oxidative stress (thiobarbituric acid reactive substances, protein carbonyl), antioxidant capacity (superoxide dismutase), and nitric oxide bioavailability (nitrite) monthly for a 6-month period post-SARS-CoV-2 infection. FMD, as a marker of macrovascular function, improved from month 1 (3.06 ± 1.39%) to month 6 (6.60 ± 2.07%; p< 0.001). FMD/Shear improved from month one (0.10± 0.06 AU) to month six (0.18 ± 0.70 AU; p=0.002). RH in the arm and PLM in the leg, as markers of microvascular function, did not change during the 6 months (p> 0.05). Circulating markers of inflammation, oxidative stress, antioxidant capacity, and nitric oxide bioavailability did not change during the 6 months (p> 0.05). Together, these results suggest some improvements in macrovascular, but not microvascular function, over 6 months following SARS-CoV-2 infection. The data also suggest persistent ramifications for cardiovascular health among those recovering from mild illness and among young, otherwise healthy adults with SARS-CoV-2.

Red Palm Oil Ameliorates Oxidative Challenge and Inflammatory Responses Associated with Lipopolysaccharide-Induced Hepatic Injury by Modulating NF-κβ and Nrf2/GCL/HO-1 Signaling Pathways in Rats.

Lipopolysaccharide (LPS), a well-conserved cell wall component of Gram positive bacteria, exerts its toxic effects via inducing oxidative and pro-inflammatory responses. Red palm oil (RPO) is a unique natural product with a balanced ratio of saturated and unsaturated fatty acids, with reported antioxidant and anti-inflammatory effects. In this study, we assess the protective effect and mechanistic action of RPO using a lipopolysaccharide (LPS)-induced hepatic injury model. Male Wistar rats were assigned into four groups (10 animals/group): normal control (NC), RPO, LPS and RPO + LPS. Animals in the RPO and RPO + LPS groups were administered RPO (200 μL/day) for 28 days. On the 27th day of experiment, animals in LPS and RPO + LPS groups were injected with LPS (0.5 mg/kg body weight). Animals were sacrificed 24 h later, and blood and liver tissues harvested for biochemical and molecular analysis. RPO resolved hepatic histological dysfunction induced by LPS, and lowered alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and γ-glutamyl transferase activities in the serum. Hepatic malondialdehyde and conjugated dienes, as well as pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6 and TNFα were significantly diminished (p < 0.05) by RPO pre-treatment. Activity of hepatic antioxidant enzymes including superoxide dismutase, glutathione reductase, glutathione peroxidase, as well as glutathione redox status (GSH:GSSG), and markers of antioxidant capacity that decreased as a result of LPS injection were improved by RPO pre-treatment. Mechanistically, RPO up-regulated mRNA expression of redox sensitive transcription factor Nrf2 and its downstream targets GCL and HO-1, while also suppressing the expression of NFκβ and associated inflammatory protein, Iκβ kinase (IκKβ). In conclusion, this study highlights the ameliorating effects of RPO against LPS-induced hepatic injury and revealed the Nrf2/GCL/HO-1 and NFκβ signaling axis as potential contributing mechanisms.

Dexpanthenol Inhibits Inflammation and Apoptosis in LPS-Induced Acute Lung Injury by Reducing Increased VCAM-1 and Caspase-3 Expressions in Rats

This study aims to investigate the effects of Dexpanthenol (Dex), a stable alcoholic analogue of D-pantothenic acid which has anti-oxidant, antiapoptotic, and antiinflammatory properties, on lipopolysaccharide (LPS)-induced lung damage via caspase-3 (cas-3) and vascular cell adhesion molecule-1 (VCAM-1) levels. According to the experimental plan of study, thirty-two Wistar Albino species rats were distributed randomly into four groups as control, LPS (5 mg/kg, intraperitoneally (i.p), single dose), LPS (30 minutes before last Dex treatment) + Dex (500 mg/kg, i.p, for 3 days) and Dex. After six hours of LPS application, lung tissues of the rats were taken for histopathological, immunohistochemical and biochemical examinations. According to results of the study, LPS causes hyperemia, neutrophil leukocyte chemotaxis and thickened septal tissue on lung. Inducing inflammation by increasing VCAM-1 levels and triggers apoptosis by increasing cas-3 levels in lung tissue. In addition, LPS decreased total antioxidant status levels, which is a marker of anti-oxidant capacity, and increased oxidative stress index and total oxidant status values, which are indicators of oxidative stress. Dex has shown its effect by reversing all these alterations and normalizing the values. These results suggest that Dex can be used as a preservative to reduce LPS-induced acute toxicity in the lung.

Differential effects of high-altitude exposure on markers of oxidative stress, antioxidant capacity, and iron profiles.

High-altitude (HA) exposure may stimulate significant physiological and molecular changes, resulting in HA-related illnesses. HA may impact oxidative stress, antioxidant capacity, and iron homeostasis, yet it is unclear how both repeated exposure and HA acclimatization may modulate such effects. Therefore, we assessed the effects of weeklong repeated daily HA exposure (2,900-5,050 m) in altitude-naïve individuals (n = 21 individuals, 13 females, mean ± SD, 25.3 ± 3.7 yr) to mirror the working schedule of HA workers (n = 19 individuals, all males, 41.1 ± 9.4 yr) at the Atacama Large Millimeter Array (ALMA) Observatory (San Pedro de Atacama, Chile). Markers of oxidative stress, antioxidant capacity, and iron homeostasis were measured in blood plasma. Levels of protein oxidation (P < 0.001) and catalase activity (P = 0.023) increased and serum iron (P < 0.001), serum ferritin (P < 0.001), and transferrin saturation (P < 0.001) levels decreased with HA exposure in both groups. HA workers had lower levels of oxidative stress, and higher levels of antioxidant capacity, iron supply, and hemoglobin concentration as compared with altitude-naïve individuals. On a second week of daily HA exposure, changes in levels of protein oxidation, glutathione peroxidase, and nitric oxide metabolites were lower as compared with the first week in altitude-naïve individuals. These results indicate that repeated exposure to HA may significantly alter oxidative stress and iron homeostasis, and the degree of such changes may be dependent on if HA is visited naïvely or routinely. Further studies are required to fully elucidate differences in HA-induced changes in oxidative stress and iron homeostasis profiles among visitors of HA.

Arousal from Torpor Increases Oxidative Damage in the Hibernating Thirteen-Lined Ground Squirrel (Ictidomys tridecemlineatus).

AbstractDuring hibernation, especially during arousal from torpor to interbout euthermia (IBE), blood flow changes drastically. In nonhibernating mammals, similar changes during ischemia/reperfusion lead to oxidative damage. We hypothesized that suppression of mitochondrial metabolism during hibernation protects against such damage. We compared markers of oxidative damage and total antioxidant capacity in eight tissues among summer, torpid, and IBE thirteen-lined ground squirrels. Overall, summer tissue had less lipid and protein oxidative damage than tissue from the hibernation season, but DNA damage (in four tissues) and total antioxidant capacity (in all eight tissues) were similar among all groups. During torpor, when mitochondrial metabolism is suppressed, lipid damage in heart, brown adipose tissue, and small intestine was lower than IBE by as much as fivefold. By contrast, oxidative damage to protein was at least twofold higher in liver and skeletal muscle in torpor compared with IBE. Our findings suggest that arousal from torpor creates oxidative damage similar to ischemia/reperfusion injury but that this damage is repaired during IBE. These differences cannot be explained by changes in antioxidant capacity, so they are likely due to differences is reactive oxygen species production among hibernation states that may relate to the well-characterized reversible suppression of mitochondrial metabolism during torpor.

Biological Anti-TNF-α Therapy and Markers of Oxidative and Carbonyl Stress in Patients with Rheumatoid Arthritis.

Rheumatoid arthritis (RA) as a chronic inflammatory disease is associated with oxidative stress. Drugs targeting tumor necrosis factor-alpha (TNF-α) ameliorate inflammation and symptoms of RA in most patients. Whether markers of oxidative stress can be used for monitoring of treatment effects is unknown. The aim of our study was to analyze the effects of anti-TNF-α treatment on oxidative stress in plasma and saliva of patients with RA. Samples were collected from 26 patients with RA at baseline as well as 3 and 6 months after starting the anti-TNF-α treatment. Thiobarbituric acid-reacting substances (TBARS), advanced oxidation protein products (AOPP), advanced glycation end products (AGEs), and fructosamine were quantified using spectrophotometry and spectrofluorometry in plasma. TBARS were measured also in saliva. The disease activity score (DAS28) was used to assess the clinical status of patients. No significant dynamic changes were found except plasma TBARS that decreased continuously. At 6 months after starting the treatment, plasma TBARS were lower by 39% in comparison to baseline (p = 0.006). Salivary concentrations of TBARS did not reflect the dynamics in plasma. Although a trend was observed (r = 0.33), a significant correlation between plasma TBARS and DAS28 was not found. Our results indicate that anti-TNF-α treatment decreases plasma TBARS as a marker of lipid peroxidation. However, the lack of a significant correlation with DAS28 suggests that it cannot be used for monitoring of treatment. Other markers of oxidative stress and antioxidant capacity with lower biological variability should be tested in future studies.

Pinosylvin Extract Retinari™ Sustains Electrophysiological Function, Prevents Thinning of Retina, and Enhances Cellular Response to Oxidative Stress in NFE2L2 Knockout Mice.

Chronic oxidative stress eventually leads to protein aggregation in combination with impaired autophagy, which has been observed in age-related macular degeneration. We have previously shown an effective age-related macular degeneration disease model in mice with nuclear factor-erythroid 2-related factor-2 (NFE2L2) knockout. We have also shown pinosylvin, a polyphenol abundant in bark waste, to increase human retinal pigment epithelium cell viability in vitro. In this work, the effects of commercial natural pinosylvin extract, Retinari™, were studied on the electroretinogram, optical coherence tomogram, autophagic activity, antioxidant capacity, and inflammation markers. Wild-type and NFE2L2 knockout mice were raised until the age of 14.8 ± 3.8 months. They were fed with either regular or Retinari™ chow (141 ± 17.0 mg/kg/day of pinosylvin) for 10 weeks before the assays. Retinari™ treatment preserved significant retinal function with significantly preserved a- and b-wave amplitudes in the electroretinogram responses. Additionally, the treatment prevented thinning of the retina in the NFE2L2 knockout mice. The NFE2L2 knockout mice showed reduced ubiquitin-tagged protein accumulation in addition to local upregulation of complement factor H and antioxidant enzymes superoxide dismutase 1 and catalase. Therefore, the treatment in the NFE2L2 KO disease model led to reduced chronic oxidative stress and sustained retinal function and morphology. Our results demonstrate that pinosylvin supplementation could potentially lower the risk of age-related macular degeneration onset and slow down its progression.

Interactive effects of dietary quercetin nanoparticles on growth, flesh antioxidant capacity and transcription of cytokines and Aeromonas hydrophila quorum sensing orchestrating genes in Nile tilapia (Oreochromis niloticus)

Recently, the concept of incorporating natural products into nanocarriers has been intended to promote fish growth and health via modulating their stability and bioavailability. In this concern, the potential role of reformulated quercetin into nanocarriers was examined, for the first time, on Nile tilapia's performance and immunity, flesh quality and antioxidant indices and disease resistance. Five hundred fish assigned into five experimental groups with formulated diets containing quercetin nanoparticles (QT-NPs) at levels of 0, 100, 200, 300 and 400 mg/kg were challenged with Aeromonas hydrophila (A. hydrophila) after 12 weeks feeding trial. Fish final body weight gain and feed efficiency were significantly maximized in groups enriched with 300 and 400 mg/kg of QT-NPs. Significant reduction in total saturated fatty acids and an elevation in polyunsaturated fatty acids’ contents were noticed in fish fed higher QT-NPs doses. The levels of Hydrogen peroxide, reactive oxygen species and malondialdehyde, the markers of meat antioxidant capacity, were reduced by higher inclusion levels of QT-NPs. Accordingly, serum activities and transcriptional levels of GSH-Px, CAT and SOD genes were increased with elevated QT-NPs levels. Immune responses mediated by upregulation of IL-10 and TGF-β and downregulation of IL-1β, IL-8 and TNF-α mRNA levels were found to be positively affected by QT-NPs. Dietary QT-NPs downregulated the expression of ahyI and ahyR quorum sensing genes conferring protection against A. hydrophila challenge. This study concluded that supplementation of quercetin in encapsulated nanoparticles could improve its efficacy making it as a compelling approach to improve fish performance and as a promising drug candidate against A. hydrophila virulence.

The Effects of Korean Red Ginseng on Biological Aging and Antioxidant Capacity in Postmenopausal Women: A Double-Blind Randomized Controlled Study.

Postmenopausal women are vulnerable to aging and oxidative stress due to reduced estrogen. Previous studies have shown that Korean red ginseng (KRG) has beneficial effects on aging and antioxidant capacity. Therefore, we evaluated the effects of KRG on biological aging and antioxidant capacity in postmenopausal women. This study conducted a double-blinded, placebo-controlled clinical trial. The participants were randomly administered KRG or a placebo, and the following metrics were measured: mitochondria DNA (mtDNA) copy number as an indicator of biological aging and, total antioxidant status (TAS) as a marker of antioxidant capacity. Clinical symptoms of fatigue, as measured by the fatigue severity scale, were assessed before and after KRG administration. There were 63 participants, of whom 33 received KRG and 30 received a placebo. The mtDNA copy number (KRG group: 1.58 ± 2.05, placebo group: 0.28 ± 2.36, p = 0.023) and TAS (KRG group: 0.11 ± 0.25 mmol/L, placebo group: −0.04 ± 0.16 mmol/L, p = 0.011) increased and the fatigue severity scale (KRG group: −7 ± 12, placebo group: −1 ± 11, p = 0.033) decreased significantly more in the KRG group than the placebo group. KRG significantly increased the mtDNA copy number, total antioxidant status, and improved symptoms of fatigue in postmenopausal women.

Evaluation of minor steviol glycosides effect on insulin resistance, serum triglycerides, and antioxidant capacity of diabetised Wistar rats

The objective of the present work was to evaluate the effect of minor glycosides on the QUICKI index as a marker of insulin resistance, triglycerides (TG), and antioxidant capacity in Wistar rats induced with diabetes mellitus type 2 (DM2). DM2 was induced in male Wistar rats (n = 35) through streptozotocin-nicotinamide. Hyperglycaemia was confirmed two weeks later, and the subjects were divided into seven experimental groups, and each group was treated as follows: (1-5) dulcoside A, steviolbioside, rebaudioside B, C, and D (20 mg/kg, respectively); (6) metformin (180 mg/kg); and (7) standard diet, orally for four weeks. Blood sample was obtained from the tail before and after the treatment. The serum was separated after clotting by centrifugation. The included parameters namely serum triglycerides (TG) and superoxide dismutase (SOD) activity were measured before and after the treatments, then the changes were determined; and at the end of the treatment, the QUICKI index was determined. The analysis of one-way variance (ANOVA) was performed considering p &lt; 0.05. No statistically significant differences were found in any of the three variables (p &gt; 0.05); however, the rebaudioside group B had the highest QUICKI index, while the reduction of triglycerides was greater in rebaudioside D. SOD activity increased in all groups, but was higher in rebaudioside D and steviolbioside. Minor glycosides at the dose and time evaluated had no significant effects on QUICKI index, antioxidant capacity, and triglycerides concentration.

The ketogenic diet preserves skeletal muscle with aging in mice.

The causes of the decline in skeletal muscle mass and function with age, known as sarcopenia, are poorly understood. Nutrition (calorie restriction) interventions impact many cellular processes and increase lifespan and preserve muscle mass and function with age. As we previously observed an increase in life span and muscle function in aging mice on a ketogenic diet (KD), we aimed to investigate the effect of a KD on the maintenance of skeletal muscle mass with age and the potential molecular mechanisms of this action. Twelve‐month‐old mice were assigned to an isocaloric control or KD until 16 or 26 months of age, at which time skeletal muscle was collected for evaluating mass, morphology, and biochemical properties. Skeletal muscle mass was significantly greater at 26 months in the gastrocnemius of mice on the KD. This result in KD mice was associated with a shift in fiber type from type IIb to IIa fibers and a range of molecular parameters including increased markers of NMJ remodeling, mitochondrial biogenesis, oxidative metabolism, and antioxidant capacity, while decreasing endoplasmic reticulum (ER) stress, protein synthesis, and proteasome activity. Overall, this study shows the effectiveness of a long‐term KD in mitigating sarcopenia. The diet preferentially preserved oxidative muscle fibers and improved mitochondrial and antioxidant capacity. These adaptations may result in a healthier cellular environment, decreasing oxidative and ER stress resulting in less protein turnover. These shifts allow mice to better maintain muscle mass and function with age.