Concentrations Of Oxidative Stress Markers Research Articles

Characterization of lipid peroxidation processes and antioxidant defense in parturients with COVID-19

Aim. The aim of the study was to investigate the functional state of the «lipid peroxidation - antioxidant defense» system in the peripheral blood of parturients with mild and severe COVID-19.Materials and methods. This casecontrol study examined 95 parturients with confirmed COVID-19 diagnosis in the third trimester, divided into two groups based on the severity of the disease. Group 1a included parturients with severe COVID-19 (community-acquired pneumonia, n=48), while group 1b consisted of patients with mild COVID-19 (acute respiratory viral infection, n=47). The control group was composed of 45 parturients without a prior or current diagnosis of COVID-19. The average age of women in the study groups was 23.9±0.50 years, and 24.4±0.60 years in the control group (p>0.05). Peripheral venous blood served as the material for the study. Spectrophotometric methods were used to examine the concentrations of primary (diene conjugates - DC) and final (active thiobarbituric acid products - TBARS) products of lipoperoxidation. The content of 8-isoprostane, total antioxidant capacity of plasma components, and phospholipase A2 were investigated using enzymelinked immunosorbent assay (ELISA).Results. Study showed that parturients with severe COVID-19 had increased levels of phospholipase A2 by 2.1 times (p<0.001), oxidative stress markers: diene conjugate concentrations by 1.94 times (p><0.001), TBARS by 2.2 times (p><0.001), and 8-isoprostane by more than 2 times (p><0.001), along with a simultaneous decrease in the total antioxidant capacity of blood plasma components by 1.7 times (p><0.001) compared to the control group. In the group of parturients with mild COVID-19, the studied indicators changed less significantly. Conclusion. The study established the pathogenetic role of SARS-CoV-2 in disrupting the functional system of «lipid peroxidation - antioxidant defense» and the development of oxidative stress in parturients who had COVID-19 in the third trimester. A dependency of oxidative stress marker concentrations in peripheral blood on the severity of COVID-19 was identified. It was shown that COVID-19 in the third trimester of pregnancy is associated with high levels of phospholipase A2, an imbalance in the prooxidant-antioxidant system, characterized by a reduction in the level of total antioxidant capacity and an increase in oxidative modification products of biomolecules, expressed by the growth of DC, TBARS, and 8-isoprostane levels, leading to oxidative stress correlated with the severity of lung damage. Key words: COVID-19, parturients, lipid peroxidation, antioxidant defense, oxidative stress> ˂ 0.001), oxidative stress markers: diene conjugate concentrations by 1.94 times (p ˂ 0.001), TBARS by 2.2 times (p ˂ 0.001), and 8-isoprostane by more than 2 times (p ˂ 0.001), along with a simultaneous decrease in the total antioxidant capacity of blood plasma components by 1.7 times (p ˂ 0.001) compared to the control group. In the group of parturients with mild COVID-19, the studied indicators changed less significantly.Conclusion. The study established the pathogenetic role of SARS-CoV-2 in disrupting the functional system of «lipid peroxidation - antioxidant defense» and the development of oxidative stress in parturients who had COVID-19 in the third trimester. A dependency of oxidative stress marker concentrations in peripheral blood on the severity of COVID-19 was identified. It was shown that COVID-19 in the third trimester of pregnancy is associated with high levels of phospholipase A2, an imbalance in the prooxidant-antioxidant system, characterized by a reduction in the level of total antioxidant capacity and an increase in oxidative modification products of biomolecules, expressed by the growth of DC, TBARS, and 8-isoprostane levels, leading to oxidative stress correlated with the severity of lung damage.

Protein intake affects erythrocyte glutathione synthesis in healthy adults aged ≥60 years in a repeated-measures trial

BackgroundProtein recommendations for older adults are based on nitrogen balance data from young adults. Physiological studies using the indicator amino acid oxidation method suggest they need 30% to 50% more protein than current recommendations. We herein present glutathione (GSH) as a physiological estimate of protein adequacy in older adults. ObjectivesThe objective was to measure GSH kinetics in response to varying protein intakes in a repeated-measures design in healthy adults aged ≥60 y using the precursor-product method. MethodsSixteen healthy older adults (n = 8 male and n = 8 female; body mass index ≤30 kg/m2) were studied. Each received 4 of 6 protein intakes in random order (0.66, 0.8, 0.9, 1.1, 1.3 and 1.5 g⋅kg−1⋅d−1). At each intake level, participants underwent isotope infusion studies of 7 h duration following a 3-d adaptation to the test level of protein. On the fourth day, GSH fractional (FSR) and absolute synthesis (ASR) rates were quantified by measuring the incorporation of U-[13C2-15N]glycine into GSH at isotopic steady state. A mixed-effect change-point regression model was used to determine a breakpoint in FSR and ASR. Secondary outcomes included plasma concentrations of oxidative stress markers, homocysteine, 5-L-oxoproline (5-OP), and urinary sulfate. The effect of secondary outcomes on GSH kinetics was analyzed using a joint linear mixed-effect model and Tukey’s post hoc test. ResultsA protein intake of 1.08 g⋅kg−1⋅d−1 (95% confidence interval [CI]: 0.83, 1.32; Rm2 = 0.207; Rc2 = 0.671; P < 0.001) maximized GSH FSR. There was no effect of protein intake on concentrations of erythrocyte GSH, plasma homocysteine, oxidative stress markers, or 5-OP (P > 0.05). Protein intake had a positive effect on urinary sulfate excretion (P < 0.0001). ConclusionA protein intake of 1.08 g⋅kg−1⋅d−1 from a high-quality protein maximized GSH synthesis in adults ≥60 y. This lends support to data suggesting a requirement higher than the current recommendation.This study was registered at clinicaltrials.gov as NCT02971046.

MiR-26a-5p Attenuates Oxidative Stress and Inflammation in Diabetic Retinopathy through the USP14/NF-κB Signaling Pathway.

Diabetic retinopathy (DR) is an ocular disease caused by diabetes and may lead to vision impairment and even blindness. Oxidative stress and inflammation are two key pathogenic factors of DR. Recently, regulatory roles of different microRNAs (miRNAs) in DR have been widely verified. miR-26a-5p has been confirmed to be a potential biomarker of DR. Nevertheless, the specific functions of miR-26a-5p in DR are still unclear. Primary cultured mouse retinal Müller cells in exposure to high glucose (HG) were used to establish an in vitro DR model. Müller cells were identified via morphology observation under phase contrast microscope and fluorescence staining for glutamine synthetase. The in vivo animal models for DR were constructed using streptozotocin-induced diabetic C57BL/6 mice. Western blotting was performed to quantify cytochrome c protein level in the cytoplasm and mitochondria of Müller cells and to measure protein levels of glial fibrillary acidic protein (GFAP), ubiquitin-specific peptidase 14 (USP14), as well as factors associated with NF-κB signaling (p-IκBα, IκBα, p-p65, and p65) in Müller cells or murine retinal tissues. ROS production was detected by CM-H2DCFDA staining, and the concentration of oxidative stress markers (MDA, SOD, and CAT) was estimated by using corresponding commercial kits. Quantification of mRNA expression was conducted by RT-qPCR analysis. The concentration of proinflammatory factors (TNF-α, IL-1β, and IL-6) was evaluated by ELISA. Hematoxylin-eosin staining for murine retinal tissues was performed for histopathological analysis. Immunofluorescence staining was conducted to determine NF-κB p65 nuclear translocation in Müller cells. Furthermore, the interaction between miR-26a-5p and USP14 was verified via the luciferase reporter assays. HG stimulation contributed to Müller cell dysfunction by inducing inflammation, oxidative injury, and mitochondrial damage to Müller cells. miR-26a-5p was downregulated in Müller cells under HG condition, and overexpression of miR-26a-5p relieved HG-induced Müller cell dysfunction. Moreover, miR-26a-5p targeted USP14 and inversely regulated USP14 expression. Additionally, HG-evoked activation of NF-κB signaling was suppressed by USP14 knockdown or miR-26a-5p upregulation. Rescue assays showed that the protective impact of miR-26a-5p upregulation against HG-induced Müller cell dysfunction was reversed by USP14 overexpression. Furthermore, USP14 upregulation and activation of NF-κB signaling in the retinas of DR mice were detected in animal experiments. Injection with miR-26a-5p agomir improved retinal histopathological injury and weakened the concentration of proinflammatory cytokines and oxidative stress markers in the retinas of DR mice. miR-26a-5p inhibits oxidative stress and inflammation in DR progression by targeting USP14 and inactivating the NF-κB signaling pathway.

MicroRNA-195-5p Attenuates Pregnancy-Induced Hypertension by Inhibiting Oxidative Stress via OTX1/MAPK Signaling Pathway.

Pregnancy-induced hypertension (PIH) is a hypertensive disorder during pregnancy and can induce perinatal death of human infants. MicroRNA (miR)-195-5p was validated to display low expression in severe preeclampsia placentas, but the role of miR-195-5p in pregnancy-induced hypertension (PIH) has not been investigated. The study emphasized on the functions and mechanism of miR-195-5p in PIH. A reduced uterine perfusion pressure (RUPP) rat model was established to mimic PIH in vivo. Adenovirus (Ad)-miR-195-5p agomir and/or Ad-OTX1 were further injected into some model rats. RT-qPCR was conducted to assess the expression of miR-195-5p and orthodenticle homeobox 1 (OTX1) in rat placental tissues, the isolated aortic endothelial cells (AECs), and in serum samples of PIH patients. Western blot analysis was implemented to measure the protein levels of OTX1, VEGFA, and key factors involved in the MAPK signaling pathway. The concentrations of oxidative stress markers (superoxide dismutase, catalase, and lipid hydroperoxide) in AECs and placental tissues of RUPP rats were measured by corresponding kits. The binding relation between miR-195-5p and OTX1 was verified using the dual-luciferase reporter assay. Hematoxylin-eosin staining was conducted to evaluate the pathological features of rat placental tissues. MiR-195-5p was downregulated, while OTX1 was upregulated in rat placental tissues and human serum samples of PIH patients. MiR-195-5p could target OTX1 and inversely regulate OTX1 expression in AECs and rat placental tissues. In addition, miR-195-5p can negatively regulate VEGFA level. Furthermore, miR-195-5p inactivates oxidative stress and the MAPK signaling by downregulating OTX1 in AECs. In vivo experiments revealed that OTX1 overexpression reversed the protective effect of miR-195-5p overexpression on placental damage and oxidative stress. MiR-195-5p alleviates PIH by inhibiting oxidative stress via targeting OTX1 and inactivating MAPK signaling.

GW1929 (an agonist of PPARγ) inhibits excessive production of reactive oxygen species in cisplatin-stimulated renal tubular epithelial cells, hampers cell apoptosis, and ameliorates renal injury

ABSTRACT Cisplatin-induced nephrotoxicity has long been explored for development of preventative and therapeutic drugs. The current investigation focused on the renal protective effect of GW1929, an agonist for peroxisome proliferator-activated receptors gamma (PPARγ), on cisplatin-induced kidney injury. HK2 cells treated with 20 μM cisplatin and C57BL/6 mice injected with 20 mg/kg cisplatin were used as the cell model and animal model for acute kidney injury. HK2 cell viability after cisplatin or GW1929 (0–80 μM) treatment was tested using methyl thiazolyl tetrazolium assays. Flow cytometry analysis and TUNEL assays were used to measure cell apoptosis. Intracellular reactive oxygen species (ROS) level was measured through fluorescence intensities. Levels of blood urea nitrogen (BUN) and serum creatinine (SCr) were measured to evaluate the renal function of mice. For renal morphology observation and cell apoptosis assessment in vivo, hematoxylin-eosin staining and TUNEL assays were conducted. The concentrations of oxidative stress markers in renal samples were measured using colorimetric tests. It was found that GW1929 dose-dependently enhanced protein levels of PPARγ, PGC-1α and TFEB in HK2 cells. Meanwhile, intracellular ROS overproduction, the decrease in cell viability and excessive cell apoptosis mediated by cisplatin were reversed by GW1929. For in vivo experiments, GW1929 notably attenuated cisplatin-stimulated nephrotoxicity and oxidative stress while reducing BUN and Scr levels in cisplatin-challenged model mice. Moreover, GW1929 significantly dampened renal cell apoptosis in vivo. GW1929 mitigates renal tubular epithelial cell injury and renal damage by inhibiting oxidative stress and renal cell apoptosis.

PSIX-2 Effects of Diets Supplemented with Bioactive Peptides on Nutrient Digestibility, Immune Cell Responsiveness, and Fecal Characteristics, Microbiota, and Metabolites of Adult Cats

Abstract Bioactive peptides (BP) are recognized for their ability to function as antioxidants and maintain lipid stability. They may have positive health effects, including antihypertensive, anti-inflammatory, antimicrobial, osteoprotective, gut health and immunomodulatory properties. Our objective was to determine the apparent total tract digestibility (ATTD) of bioactive peptide-containing kibble diets and assess how the fecal characteristics, metabolites, and microbiota were affected in adult cats. All procedures were approved by the University of Illinois IACUC. Twelve adult cats (4-5 yr; 4.84 kg avg. BW) were used in a replicated 4x4 Latin square design (n = 12/group) and fed to maintain BW. In each experimental period, cats were allotted to one of four extruded kibble experimental diets: control (4% dried chicken), chicken (4% chicken BP), marine1 (2% marine BP), and marine2 (4% marine BP). Health was confirmed by baseline serum chemistry and complete blood count analysis. Each experimental period lasted 28 days, with a 20-day adaptation phase, 5-day fecal collection [for nutrient digestibility, microbiota, metabolites, IgA, calprotectin, lactoferrin, pH, and dry matter (DM) analysis], 2-day blood collection (for serum chemistry, complete blood count, and immune cell functionality analysis), and 1 day for transport stress testing. For transport stress, cats were transported in a vehicle in individual carriers for 45 minutes. Upon return, their behavior was evaluated using the cat stress score (CSS). Saliva samples were collected within 15 minutes to measure cortisol concentrations and blood samples were collected after 3 hours to measure concentrations of oxidative stress markers [superoxide dismutase (SOD) and malondialdehyde (MDA)] and inflammatory cytokines. Fecal microbiota data were evaluated using QIIME2. All other data were analyzed using the Mixed Models procedure of SAS, with P &amp;lt; 0.05 being considered significant. No significant differences were observed in animal health outcomes, with all cats remaining healthy within reference ranges. There were no differences in fecal characteristics, metabolites, and microbiota diversity. Cats fed the marine2 diet had a 3.61% greater (P &amp;lt; 0.05) ATTD of DM and a 2.5% greater organic matter digestibility than those fed the control diet. The relative abundance of fecal Blautia was greater (P &amp;lt; 0.05) in cats fed the control diet than those fed the chicken diet, while relative abundance of fecal Slackia was greater (P &amp;lt; 0.05) in cats fed the control diet than those fed the chicken or marine1 diets. In comparison with cats fed the marine1 diet, the relative abundances of fecal Sellimonas and Bifidobacterium were less (P &amp;lt; 0.05) in cats fed the control diet. Neither transport stress nor diet impacted the oxidative stress markers, cytokines, cortisol, or CSS. Furthermore, the diet did not affect immune cell functionality. In conclusion, including BP, in particular marine2 at 4% inclusion to feline diets may increase nutrient digestibility and modify fecal microbiota.

Oxidative stress a potent risk factor for thyroid diseases in young pregnant females.

Objective: To evaluate the potent role of oxidative stress in thyroid disease development and progression in young pregnant females during 1st and second trimesters compared with matched healthy pregnant females of the same gestational age. Study Design: Cross-sectional Comparative study. Setting: Institute of Molecular Biology and Biotechnology (IMBB), The University of Lahore, Pakistan. Samples were collected at the Punjab Institute of Nuclear Medicine (PINUM), Faisalabad, and the Department of Obstetrics at DHQ Hospital, Chiniot. Period: July 2019 to July 2021. Material &amp; Methods: Thyroid disease- comorbid pregnant women and euthyroid pregnant women were compared for serum levels of oxidative stress markers and antioxidants. The markers were evaluated between 68 healthy subjects in Group A and 43 subjects in Group B known for having thyroid diseases. Blood samples were taken under highly sterile conditions after gaining written consent from all subjects and stored at –8°c to –30°c. A spectrophotometer at 532nm was used to measure serum concentrations of oxidative stress markers. ELISA kits were used to determine serum levels of triiodothyronine, thyroxin, and thyroid-stimulating hormone. Data was analyzed using independent student t-test, multiple logistic regression, and receiver operating characteristic curve (ROC) analysis using SPSS version 25. Results: Group A and Group B had a mean age of 26.07±4.88 and 29.19±4.17 years, respectively. Pregnant women having thyroid dysfunction had decreased superoxide dismutase levels (0.05±0.01 nmol/ml) than group A (0.06±0.01). Other indicators of lipid peroxidation showed a non-significant mean difference compared between both groups (p&gt;0.05). Multiple linear regression studies revealed healthy pregnant women with a positive thyroid medication history had higher SOD levels among group B than those without antithyroid medicine, with a Beta coefficient of +0.26 and p=0.04. According to ROC curve analysis, the Superoxide Dismutase biomarker area under ROC was 67.25% at p=0.002. Thus, it may be used as a diagnostic and predictive biomarker. A cutoff value of 51.5pg/ml was proposed, at which sensitivity is 79% and specificity is 69%. It can be a diagnostic and predictive biomarker. Conclusion: The results of the current study concluded that oxidative stress can be considered a potent risk factor for the development and progression of thyroid disease in young pregnant females.

Exposure to Benzo[a]pyrene and 1-Nitropyrene in Particulate Matter Increases Oxidative Stress in the Human Body.

Polycyclic aromatic hydrocarbons (PAHs) have been reported to cause oxidative stress in metabolic processes. This study aimed to evaluate the relationship between exposure to PAHs, including benzo[a]pyrene (BaP) and 1-nitropyrene (1-NP), in the atmosphere and oxidative stress levels in the human body. This study included 44 Korean adults who lived in Cheongju, Republic of Korea. Atmospheric BaP and 1-NP concentrations and urinary 6-hydroxy-1-nitropyrene (6-OHNP), N-acetyl-1-aminopyrene (1-NAAP), and 1-hydroxypyrene (1-OHP) concentrations were measured. The oxidative stress level was assessed by measuring urinary thiobarbituric acid-reactive substances (TBARS) and 8-hydroxydeoxyguanosine (8-OHdG) concentrations. Urinary TBARS and 6-OHNP concentrations significantly differed between winter and summer. BaP exposure was significantly associated with urinary 8-OHdG concentrations in summer. However, atmospheric 1-NP did not show a significant correlation with oxidative stress marker concentrations. Urinary 1-NAAP concentration was a significant determinant for urinary 8-OHdG concentration in summer. Oxidative stress in the body increases in proportion to inhalation exposure to BaP, and more 8-OHdG is produced in the body as the amount of 1-NP, which is metabolized to 1-AP or 1-NAAP, increases.

Clinical significance of oxidative stress markers as angioinvasion and metastasis indicators in papillary thyroid cancer

Angioinvasion remains the important prognostic feature in papillary thyroid cancer (PTC) patients. Literature data indicates several markers that may be associated with oxidative stress and/or angioinvasion. Therefore, we assessed the utility of selected parameters in angioinvasion and metastasis screening in serum of PTC patients. Serum antioxidant capacity (TAC) and sirtuin 3 (SIRT3) levels were decreased (all p < 0.05) and both DNA/RNA oxidative stress damage products (DNA/RNA OSDP) and malondialdehyde (MDA) levels were increased in PTC patients with angioinvasion and metastasis (study group) when compared with PTC patients without these features (all p < 0.01). The highest screening utility in differentiation between angioinvasion and metastasis presence and absence in PTC patients was presented for DNA/RNA OSDP (AUC = 0.71), SIRT3 (AUC = 0.70), and TAC (AUC = 0.67) (all p < 0.05). Our study suggests that peripheral concentration of oxidative stress markers could be useful as angioinvasion and metastasis indicator in PTC patients.

8-Hydroxy-2'-deoxyguanosine and malondialdehyde in plasma and their association with disease severity in 20 cats with chronic kidney disease.

Oxidative stress is associated with the development and progression of chronic kidney disease (CKD) in humans. The aim of this study was to evaluate the concentrations of oxidative stress markers, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), in the plasma and urine of cats with different stages of CKD. Plasma and urine samples were collected from cats with CKD that were referred to the Veterinary Medical Center of the University of Tokyo between April 2019 and October 2022. Plasma and urine samples were collected from healthy cats (n = 6 at most), cats with stage 2 CKD (n = 8) and stage 3-4 CKD (n = 12), and cats with idiopathic cystitis (disease control, n = 5). Plasma and urine concentrations of 8-OHdG and MDA were measured using ELISA and thiobarbituric acid reactive substances assay kits, respectively. The median plasma 8-OHdG concentrations were 0.156 ng/ml (<0.125-0.210 ng/ml) in the healthy group, <0.125 ng/ml (range <0.125 ng/ml) in the idiopathic cystitis group, 0.246 ng/ml (range 0.170-0.403 ng/ml) in cats with stage 2 CKD and 0.433 ng/ml (range 0.209-1.052 ng/ml) in cats with stage 3-4 CKD. Concentrations in stage 3-4 CKD were significantly higher than those in the healthy and disease control groups. Plasma MDA concentrations were low in the healthy and disease control groups and significantly higher in cats with stage 3-4 CKD. In every cat with CKD, plasma 8-OHdG and MDA concentrations were positively correlated with plasma creatinine concentrations (8-OHdG, rs = 0.68; MDA, rs = 0.67). Urinary 8-OHdG/urinary creatinine (u-CRE) and urinary MDA/u-CRE levels did not differ significantly between the groups; however, it was difficult to evaluate them because of the small sample size. This report shows that plasma 8-OHdG and MDA concentrations increase with the severity of feline CKD. These markers may be useful for assessing oxidative stress in cats with CKD.

Punica granatum L. Extract Shows Cardioprotective Effects Measured by Oxidative Stress Markers and Biomarkers of Heart Failure in an Animal Model of Metabolic Syndrome.

Metabolic syndrome (MetS) significantly increases the risk of cardiovascular diseases (CVD), a leading cause of death globally. The presented study investigated the cardioprotective role of dietary polyphenols found in pomegranate peels in an animal model of metabolic syndrome. Zucker diabetic fatty rats (ZDF, MetS rats, fa/fa) were supplemented with polyphenol-rich pomegranate peel extract (EPP) at two dosages: 100 mg/kg BW and 200 mg/kg BW. The extract was administered for 8 weeks. The effect of ethanolic peel extract on the concentration of oxidative stress markers (CAT, SOD, MnSOD, GR, GST, GPx, TOS, SH, and MDA), biomarkers of heart failure (cTnI, GAL-3), and alternations in tissue architecture was assessed. The results showed a significant increase in SH concentration mediated via EPP supplementation (p < 0.001). Treatment with a 100 mg/kg BW dosage reduced the TOS level more efficiently than the higher dose. Interestingly, the CAT and GST activities were relevantly higher in the MetS 100 group (p < 0.001) compared to the MetS control. The rats administered EPP at a dose of 200 mg/kg BW did not follow a similar trend. No differences in the GR (p = 0.063), SOD (p = 0.455), MnSOD (p = 0.155), and MDA (p = 0.790) concentration were observed after exposure to the pomegranate peel extract. The administration of EPP did not influence the cTnI and GAL-3 levels. Histology analysis of the heart and aorta sections revealed no toxic changes in phenolic-treated rats. The findings of this study prove that the extract from pomegranate peels possesses free radical scavenging properties in the myocardium. The effect on alleviating ventricular remodeling and cardiomyocyte necrosis was not confirmed and requires further investigation.

Omega-3 fatty acids prevent nicotine withdrawal-induced exacerbation of anxiety and depression by affecting oxidative stress balance, inflammatory response, BDNF and serotonin metabolism in rats

Adolescents are known to be more vulnerable than adults to the adverse effects of nicotine dependence. In the present study, we aimed to investigate whether adolescent nicotine exposure, followed by a period of abstinence, could affect the anxiety- and depressive-like behaviors in rats. For this purpose, behavioral assessments were carried out using open field test, elevated plus maze and forced swimming test in male rats received chronic nicotine intake during adolescence followed by a period of abstinence in adulthood, compared to their control counterparts. In addition, O3 pre-treatment was done at three different doses to reveal whether it could prevent nicotine withdrawal effects. Then, animals were euthanized and the cortical concentrations of oxidative stress markers, inflammatory indices, brain-derived neurotrophic factor, serotonin and the enzymatic activity of monoamine oxidase-A were measured. Results indicated that nicotine withdrawal exacerbates the behavioral signs of anxiety through alteration of the brain oxidative stress balance, inflammatory response and serotonin metabolism. Moreover, we found that omega 3 pre-treatment significantly prevents the nicotine withdrawal-induced complications by restoration of changes in the mentioned biochemical indices. Moreover, the improving effects of O3 fatty acids were found to be dose-dependent in all experiments. Taken together, we would like to suggest the O3 fatty acids supplementation as a safe, inexpensive and effective strategy for prevention or amelioration of detrimental effects induced by nicotine withdrawal at cellular and behavioral levels.

PSXI-6 Effects of a Saccharomyces Cerevisiae Fermentation Product-Supplemented Diet on Circulating Immune Cells and Oxidative Stress Markers of Dogs

Abstract Feeding Saccharomyces cerevisiae fermentation product (SCFP) has previously altered fecal microbiota, fecal metabolites, and immune cell function of adult dogs. The objective of this study was to further measure circulating immune cell numbers and activity, antioxidant status, and oxidative stress marker concentrations of adult dogs fed SCFP in an extruded diet. Sixteen adult pointer dogs (8M, 8F; mean age = 8.35 y; mean BW = 27.13 kg) were used in a randomized crossover design study. All dogs were fed a control diet for 4 wk, then randomly assigned to the control or SCFP-supplemented diet and fed to maintain BW for 10 wk. A 6-wk washout preceded the second 10-wk experimental period with dogs receiving opposite treatments. After baseline/washout and treatment phases, pre- and post-prandial blood samples were collected. Oxidative stress and immune cell function were measured using commercial ELISA kits, circulating immune cell numbers were analyzed using flow cytometry, and mRNA expression of oxidative stress genes were analyzed using RT-PCR. Change from baseline data were analyzed using the Mixed Models procedure of SAS 9.4, with P&amp;lt; 0.05 being significant and P&amp;lt; 0.10 being trends. Changes in unstimulated lymphocytes and stimulated IFN-g secreting T-cells were lower (P&amp;lt; 0.05) in SCFP-fed dogs, while change in stimulated T cells were lower (P&amp;lt; 0.05) in control-fed dogs. The stimulated cytotoxic T cells delta trended lower (P&amp;lt; 0.10) in SCFP-fed dogs. Change in serum superoxide dismutase (SOD) concentrations were higher (P&amp;lt; 0.05) and change in catalase mRNA expression was lower (P&amp;lt; 0.05) in SCFP-fed dogs. All other immune cells, oxidative stress markers, and gene expression were unaffected by treatment. In conclusion, SCFP-fed dogs have increased SOD, which supports lower acute-inflammatory responses and aligns with some immune stimulation data.

Effects of a Saccharomyces cerevisiae fermentation product-supplemented diet on circulating immune cells and oxidative stress markers of dogs.

Feeding Saccharomyces cerevisiae fermentation product (SCFP) has previously altered fecal microbiota, fecal metabolites, and immune function of adult dogs. The objective of this study was to investigate measures of skin and coat health, changes in circulating immune cell numbers and activity, antioxidant status, and oxidative stress marker concentrations of healthy adult dogs fed a SCFP-supplemented extruded diet. Sixteen adult English Pointer dogs (8 M, 8 F; mean age = 6.7 ± 2.1 yr; mean BW = 25.9 ± 4.5 kg) were used in a randomized crossover design study. All dogs were fed a control diet for 4 wk, then randomly assigned to either the control or SCFP-supplemented diet (0.13% of active SCFP) and fed to maintain BW for 10 wk. A 6-wk washout preceded the second 10-wk experimental period with dogs receiving opposite treatments. After baseline/washout and treatment phases, skin and coat were scored, and pre and postprandial blood samples were collected. Transepidermal water loss (TEWL), hydration status, and sebum concentrations were measured (back, inguinal, ear) using external probes. Oxidative stress and immune cell function were measured by ELISA, circulating immune cell percentages were analyzed by flow cytometry, and mRNA expression of oxidative stress genes was analyzed by RT-PCR. Change from baseline data was analyzed using the Mixed Models procedure of SAS 9.4. Sebum concentration changes tended to be higher (P < 0.10; inguinal, ear) in SCFP-fed dogs than in controls. TEWL change was lower (P < 0.05) on the back of controls, but lower (P = 0.054) on the ear of SCFP-fed dogs. Delayed-type hypersensitivity response was affected by diet and time post-inoculation. Other skin and coat measures and scores were not affected by diet. Changes in unstimulated lymphocytes and stimulated IFN-γ secreting T cells were lower (P < 0.05) in SCFP-fed dogs, while changes in stimulated T cells were lower (P < 0.05) in control-fed dogs. Upon stimulation, the percentage of cytotoxic T cells delta trended lower (P < 0.10) in SCFP-fed dogs. Change in serum superoxide dismutase concentrations was higher (P < 0.05) and change in catalase mRNA expression was lower (P < 0.05) in SCFP-fed dogs. All other measurements of immune cell populations, oxidative stress markers, and gene expression were unaffected by treatment. In conclusion, our data suggest that SCFP positively impacts indicators of skin and coat health of dogs, modulates immune responses, and enhances some antioxidant defense markers.

FOXO4 alleviates hippocampal neuronal damage in epileptic mice via the miR-138-5p/ROCK2 axis.

Epilepsy (EP) is one of the most universal neurological disorders. This study investigated the mechanism of forkhead box protein O4 (FOXO4) on hippocampal neuronal damage in EP mice. Initially, the EP mouse model and the in vitro HT-22 cell model were established. EP seizures and neuronal damage in mice were assessed. FOXO4, microRNA (miR)-138-5p, and rho-associated coiled-coil containing protein kinase 2 (ROCK2) levels in hippocampal tissues or HT-22 cells were examined. The cell viability and apoptosis of HT-22 cells were determined. The concentrations of oxidative stress markers and the levels of inflammatory cytokines in hippocampal tissues or HT-22 cells were detected. We found that FOXO4 was poorly expressed in EP. FOXO4 overexpression alleviated hippocampal neuronal damage in EP mice and improved HT-22 cell viability and inhibited apoptosis, and decreased oxidative stress and inflammation in hippocampal tissue and HT-22 cells. The bindings of miR-138-5p to FOXO4 and ROCK2 were analyzed, which showed that FOXO4 promoted miR-138-5p via binding to the miR-138-5p promoter region, and miR-138-5p inhibited ROCK2 expression. Joint experiments showed that miR-138-5p suppression or ROCK2 overexpression reversed the alleviation of FOXO4 overexpression on hippocampal neuronal damage. FOXO4 inhibited ROCK2 expression via promoting miR-138-5p expression, thus alleviating hippocampal neuronal damage in EP mice.

Markers of oxidative stress in postmenopausal women with metabolic syndrome

During the postmenopausal period, there are metabolic alterations that predispose individuals to metabolic syndrome (MS), oxidative stress (OS), and the risk of developing cardiovascular diseases. We aimed to compare the concentrations of OS markers in postmenopausal women with and without MS. Malondialdehyde, carbonyl groups, and total antioxidant capacity (TAC) were quantified. We conducted a cross-sectional study: Group 1 (n = 42) included women without MS, and Group 2 (n = 58) comprised women with MS. Participants’ age was similar between groups. Glucose, insulin, the homeostasis model assessment of insulin resistance, triglycerides, uric acid, and body mass index were significantly lower in postmenopausal women without MS. OS markers were significantly lower in Group 1 vs. Group 2: malondialdehyde, 31.32 ± 14.93 vs. 40.27 ± 17.62 pmol MDA/mg dry weight (p = .01); protein carbonylation, 6325 ± 1551 vs. 7163 ± 1029 pmol PC/mg protein (p = .0003); and TAC, 1497 ± 297.3 vs. 1619 ± 278.8 pmol Trolox equivalent/mg protein (p = .041). OS markers were significantly higher in postmenopausal women with MS. Impact statement What is already known on this subject? Oxidative stress has been implicated in numerous disease processes; however, information on the relationship between oxidative stress and metabolic syndrome among postmenopausal women remains limited. What do the results of this study add? Our results indicate that in postmenopausal Mexican women, oxidative stress markers were significantly lower in those without metabolic syndrome, whereas total antioxidant capacity was higher in those with metabolic syndrome, which could be explained as an antioxidant defense mechanism capable of neutralising excess oxidative damage markers. What are the implications of these findings for clinical practice and/or further research? This study is of interest to a broad audience because it compares the concentrations of oxidative stress markers in postmenopausal women with and without metabolic syndrome. Our study could support intervention with supplements or foods rich in antioxidants as lifestyle modifications in postmenopausal women with metabolic syndrome.

Cytokine Production in Whole Blood Cells Culture of Patients with Alcohol Dependence and Autologous Plasma Oxidative Stress Markers

We studied spontaneous production of a spectrum of proinflammatory cytokines by cultured whole blood cells from men with alcohol dependence at the stage of withdrawal syndrome and oxidative stress markers (carbonylated proteins and TBA-reactive substances) in the plasma of these blood samples. Enhanced production of cytokines by blood cells and increased concentrations of oxidative stress markers in the autologous plasma were revealed in comparison with the corresponding parameters in the control (blood from healthy men). Direct correlations were found between the levels of spontaneous cytokine production by blood cells from subjects with alcohol dependence and the concentration of oxidized proteins and lipids in autologous plasma.

Pre-Operative Assessment of Micronutrients, Amino Acids, Phospholipids and Oxidative Stress in Bariatric Surgery Candidates.

Obesity has been linked to lower concentrations of fat-soluble micronutrients and higher concentrations of oxidative stress markers as well as an altered metabolism of branched chain amino acids and phospholipids. In the context of morbid obesity, the aim of this study was to investigate whether and to which extent plasma status of micronutrients, amino acids, phospholipids and oxidative stress differs between morbidly obese (n = 23) and non-obese patients (n = 13). In addition to plasma, malondialdehyde, retinol, cholesterol and triglycerides were assessed in visceral and subcutaneous adipose tissue in both groups. Plasma γ-tocopherol was significantly lower (p < 0.011) in the obese group while other fat-soluble micronutrients showed no statistically significant differences between both groups. Branched-chain amino acids (all p < 0.008) and lysine (p < 0.006) were significantly higher in morbidly obese patients compared to the control group. Malondialdehyde concentrations in both visceral (p < 0.016) and subcutaneous (p < 0.002) adipose tissue were significantly higher in the morbidly obese group while plasma markers of oxidative stress showed no significant differences between both groups. Significantly lower plasma concentrations of phosphatidylcholine, phosphatidylethanolamine, lyso-phosphatidylethanolamine (all p < 0.05) and their corresponding ether-linked analogs were observed, which were all reduced in obese participants compared to the control group. Pre-operative assessment of micronutrients in patients undergoing bariatric surgery is recommended for early identification of patients who might be at higher risk to develop a severe micronutrient deficiency post-surgery. Assessment of plasma BCAAs and phospholipids in obese patients might help to differentiate between metabolic healthy patients and those with metabolic disorders.

Datura stramonium Leaf Extract Exhibits Anti-inflammatory Activity in CCL4-Induced Hepatic Injury Model by Modulating Oxidative Stress Markers and iNOS/Nrf2 Expression.

Background Inflammation is a frequent phenomenon in the pathogenesis of hepatic disorders leading to fibrosis and cirrhosis. Phytopharmaceuticals developed from traditional medicine can provide effective therapeutic alternatives to conventional medications. Datura stramonium (DS) has reported traditional uses in inflammatory diseases. In this study, we have tried to validate its potential as a source of anti-inflammatory agents. Methods Powdered leaf part of DS was extracted using ethyl acetate (EA) to provide the extract (DSL-EA). Lymphocyte and macrophage viability and acute toxicity assays established the safety profile, while nitric oxide (NO) scavenging assay estimated the in vitro anti-inflammatory potential. Noninvasive anti-inflammatory, antidepressant, and antinociceptive activities were monitored using BALB/c mice using low and high doses (150 and 250 mg/kg). Major inflammatory studies were performed on Sprague-Dawley male rats using CCl4-induced liver injury model. Disease induction was initiated by intraperitoneal injections of CCl4 (1 mL/kg of 30% CCl4 in olive oil). The rats were divided into six groups. The anti-inflammatory potential of DSL-EA in low and high doses (150 and 300 mg/kg, respectively) was assessed through hematological, biochemical, liver antioxidant defense, oxidative stress markers, and histological studies as well as the expression of Nrf2 and iNOS. Results DSL-EA exhibited prominent in vitro NO scavenging (IC50: 7.625 ± 0.51 μg/mL) and in vivo anti-inflammatory activity in paw and anal edema models. In CCl4 model, hematological investigations revealed vasotonic effects. Liver functionality was significantly (P < 0.001 − 0.05) improved in DSL-EA-treated rats. The activity level of endogenous antioxidant enzymes in liver tissues was improved in a manner identical to silymarin. The extract reduced the percent concentration of oxidative stress markers in liver tissues. Furthermore, DSL-EA displayed restorative effects on histological parameters (H and E and Masson's trichrome staining). Immunohistochemistry studies showed marked decline in Nrf2 expression, while overexpression of iNOS was also observed in disease control rats. The damage was distinctly reversed by the extract.

A Comparison of the Antioxidant Effects Between Hydrogen Gas Inhalation and Vitamin C Supplementation in Response to a 60-Min Treadmill Exercise in Rat Gastrocnemius Muscle.

The reactive oxygen species (ROS) produced during exercise act as a double-edged sword because they may cause oxidative damage but also play a role in the signaling pathways. A supplementation of exogenous antioxidants can reduce the total amount of ROS during exercise while it may also affect the ROS’ role in the signaling pathways of mitochondrial biogenesis. It has been suggested that hydrogen gas, as an antioxidant, can selectively scavenge hydroxyl radicals but does not affect superoxide anion’s signal transduction. The aim of this study was to compare the effects of 1-h hydrogen gas inhalation 30min prior to a treadmill exercise on the key biomarkers of mitochondrial biogenesis and related signaling pathways, and the activities of endogenous antioxidant enzymes, with those of vitamin C, in the rat skeletal muscle. Eighty-one 8-week-old male Sprague–Dawley (SD) rats were randomly assigned to three interventions (exercise-only, exercise+4%H2, and exercise+vitamin C at 500mg/kg weight, with 27 rats under each intervention), and sampled at pre-, immediately post and 4h post a 60-min treadmill exercise at speed of 27m/min and flat inclination, with nine rats in each sub-group. Expression of mitochondrial biogenetic markers and related signaling molecules in gastrocnemius muscle, and concentrations of oxidative stress markers in serum were measured. Two-way ANOVA or Kruskal–Wallis analyses showed that both hydrogen inhalation and vitamin C supplementation significantly reduced serum levels of MDA immediately after exercise and AGEs 4h after exercise. The pre-exercise supplement of vitamin C significantly reduced mitochondrial complex IV concentrations and PGC-1α, NRF-1, TFAM gene expression levels compared to the pre-exercise group, but the hydrogen gas intervention did not result in a reduction in these measurements. Unlike vitamin C, hydrogen inhalation did not blunt post-exercise mitochondrial biogenetic signals, but resulted in an increase in complex IV concentration, activation of PGC-1α, and TFAM and NRF-2 gene transcription, and up-regulation of PGC-1α protein expression. The findings indicated that hydrogen gas inhalation could play the role as an effective antioxidant in response to the exercise, whilst it did not significantly affect mitochondrial biogenesis. The dose–response relationship and antioxidant effects in different types of exercise for hydrogen inhalation require further investigation.