Lower Superoxide Dismutase Levels Research Articles

Therapeutic effect and mechanism of combination therapy with ursolic acid and insulin on diabetic nephropathy in a type I diabetic rat model.

This work aims to investigate the therapeutic effect of ursolic acid (UA) plus insulin (In) on diabetic nephropathy (DN) in streptozotocin (STZ)-induced T1DM rats. The experimental groups and operational details are as follows: A total of thirty-two SD rats were divided into four groups: the DN model group (DN, n = 8), DN + In treatment group (DN + In, n = 8), DN + In + UA administration group (DN + In + UA, n = 8), and negative control group (control, n = 8). After 8 weeks, changes in renal function indices and pathological damage were assessed. Additionally, oxidative stress-, apoptosis-, and fibrosis-related proteins in kidney tissue were measured. Compared with the control group, the vehicle group showed higher levels of creatine, blood urea nitrogen, urinary protein, apoptosis, and lipid peroxidation; lower superoxide dismutase levels; more severe levels of pathological kidney damage and renal fibrosis; and a deepened degree of EMT and EndMT. Better outcomes were achieved with the combined treatment than with insulin-only treatment. The improvement of TGF-β1, phosphorylated p38 MAPK, FGFR1, SIRT3 and DPP-4 expression levels in renal tissues after combination therapy was greater than that after insulin-only treatment. This study shows that the combination of insulin and UA significantly improved the pathological changes in the renal tissue of T1DM rats, and the underlying mechanism may be related to improving apoptosis and oxidative stress by regulating p38 MAPK, SIRT3, DPP-4 and FGFR1 levels, thereby blocking TGF-β signaling pathway activation and inhibiting EMT and EndMT processes.

The role of inflammation, oxidation and Cystatin-C in the pathophysiology of polycystic ovary syndrome.

Objective:The relationship between Cystatin-C levels and inflammatory, oxidant, and antioxidant markers in polycystic ovary syndrome (PCOS) was investigated.Materials and Methods:A total of 96 participants were included in the study as PCOS (n=58) and control (n=38) groups. Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1B), interleukin 6 (IL-6), malondialdehyde (MDA), superoxide dismutase (SOD), and Cystatin-C were evaluated by ELISA method. Relationships metabolic and endocrine parameters seen in PCOS were examined. Univariate and multivariate logistic regression analyzes were performed to identify risk factors that may affect the PCOS group. Bivariate correlations were investigated by the Spearman’s correlation analysis.Results:While Cystatin-c, TNF-α, IL-1B, IL-6, MDA were found to be higher in patients with PCOS compared with the control group, SOD was found to be lower than the control group (p<0.05). In the correlation analysis, increased Cystatin-C levels were found to be associated with high IL-6 (r=0.214, p=0.037) and low SOD levels (r=-0.280, p=0.006).Conclusion:In our study, it was found that the increase in Cystatin-C levels was associated with an increase in IL-6 and a decrease in SOD. These results may bring up different treatment options to reduce cardiovascular risks for treating PCOS.

Perfluorobutanoic Acid (PFBA) Induces a Non-Enzymatic Oxidative Stress Response in Soybean (Glycine max L. Merr.).

Short-chain perfluoroalkyl substances (PFAS) are generally considered to be of less environmental concern than long-chain analogues due to their comparatively shorter half-lives in biological systems. Perfluorobutanoic acid (PFBA) is a short-chain PFAS with the most root–shoot transfer factor of all PFAS. We investigated the impact of extended exposure of soybean plants to irrigation water containing environmentally relevant (100 pg–100 ng/L) to high (100 µg–1 mg/L) concentrations of PFBA using phenotypical observation, biochemical characterization, and transcriptomic analysis. The results showed a non-monotonous developmental response from the plants, with maximum stimulation and inhibition at 100 ng/L and 1 mg/L, respectively. Higher reactive oxygen species and low levels of superoxide dismutase (SOD) and catalase (CAT) activity were observed in all treatment groups. However transcriptomic analysis did not demonstrate differential expression of SOD and CAT coding genes, whereas non-enzymatic response genes and pathways were enriched in both groups (100 ng/L and 1 mg/L) with glycine betaine dehydrogenase showing the highest expression. About 18% of similarly downregulated genes in both groups are involved in the ethylene signaling pathway. The circadian rhythm pathway was the only differentially regulated pathway between both groups. We conclude that, similar to long chain PFAS, PFBA induced stress in soybean plants and that the observed hormetic stimulation at 100 ng/L represents an overcompensation response, via the circadian rhythm pathway, to the induced stress.

Asiatic acid improves high-fat-diet-induced osteoporosis in mice via regulating SIRT1/FOXO1 signaling and inhibiting oxidative stress.

Asiatic acid can attenuate osteoporosis through suppressing adipogenic differentiation and osteoclastic differentiation. Oxidative stress enhances osteoclastic differentiation but represses osteogenic differentiation to promote osteoporosis. However, the role and mechanism of asiatic acid in osteoporosis have not been reported. Firstly, mice were fed with high-fat-diet (HFD) with or without asiatic acid for 16 weeks. Data from an automatic biochemical analyzer showed that HFD induced down-regulation of high-density lipoprotein (HDL) and an increase of serum levels of triglyceride (TG), total cholesterol (TC) and low-density lipoprotein (LDL). However, asiatic acid administration attenuated the decrease of HDL and increase of serum TG, TC and LDL in osteoporotic mice. Secondly, HFD induced high levels of malondialdehyde (MDA) and reactive oxygen species (ROS), low levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in osteoporotic mice. However, the levels of MDA, ROS, SOD and GSH-Px in osteoporotic mice were reversed by asiatic acid administration. (this section is unclear and requires revision) Asiatic acid administration reduced expression of c-telopeptide of type 1 collagen (CTX-1), enhanced alkaline phosphatase (ALP) and procollagen type 1 N-terminal propeptide (P1NP) in HFD-induced osteoporotic mice. (this section is unclear and requires revision) Thirdly, asiatic acid promoted calcium deposition in bone marrow cells and osteogenic differentiation in osteoporotic mice, but decreased ALP in bone marrow cells. Lastly, asiatic acid enhanced SIRT1 and nuclear FOXO1 (Nu-FOXO1) expression, while it reduced Acetyl FOXO1 (Ac-FOXO1) in osteoporotic mice. In conclusion, asiatic acid might inhibit oxidative stress and promote osteogenic differentiation through activating SIRT1/FOXO1 to attenuate HFD-induced osteoporosis in mice.

Evaluation of Advanced Oxidation Protein Products (AOPP) and Superoxide Dismutase (SOD) Tissue Levels in Patients with Nasal Polyps.

The aim of this study is to eveluate levels of advanced oxidation protein products (AOPP) which are thought to increase in the polyp tissue and superoxide dismutase (SOD), an antioxidant enzyme, with using specthrophotometry in polyp tissue and healthy mucosa. 30 nasal polyp patients without inflammatory disease except for nasal polyposis were included in the study. The control group consisted of 18 patients who did not have allergy, asthma, inflammatory and granulomatous disease and planned surgery due to septum deviation and concha hypertrophy. AOPP and SOD tissue levels were measured by spectrophotometry in polyp tissue specimens taken from patients with nasal polyps and concha samples taken from patients in the control group. The mean AOPP tissue level of patients in the nasal polyposis group was statistically significantly higher than the control group. (p < 0.05). The meanSODactivity level was significantly lower in the nasal polyposis group than the control group. (p < 0.05) As a result of this study, high AOPP levels in polyp tissue and low SOD levels in polyp tissue compared to healthy nasal mucosa, oxidative stress plays an important role in nasal polyp development.

Protective Effect of Poria Cocos Polysaccharides on Fecal Peritonitis-Induced Sepsis in Mice Through Inhibition of Oxidative Stress, Inflammation, Apoptosis, and Reduction of Treg Cells.

This study was conducted to investigate the potential pharmacological effects of Poria cocos polysaccharides (PCPs) on fecal-induced peritonitis (FIP) mice. Consequently, the fecal peritonitis (FP)-induced septic mice with the higher levels of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), IL-1β, malondialdehyde (MDA), myeloperoxidase (MPO), histopathological lesion and bacterial burden, and lower levels of superoxide dismutase (SOD) and glutathione (GSH). Interestingly, PCP pre-treatment reduced inflammatory cytokines and oxidative stress in plasma and spleen and improved the resistance to FIP. Inflammatory infiltration and cell death in thymus or splenic tissue were alleviated with PCP pretreatment. Furthermore, Treg cells were moderated in the spleen with PCP pre-administration. In addition, PCP pretreatment downregulated Annexin-V in the thymus of FP-induced septic mice, and apoptosis of splenic cells was dose-dependent. In conclusion, PCPs have pharmacological and biological effects on FP-induced septic mice, and its molecular mechanism is related to antioxidative, anti-inflammation, anti-apoptosis, and the reduction of Treg activity in splenic cells.

High L-Valine Concentrations Associate with Increased Oxidative Stress and Newly-Diagnosed Type 2 Diabetes Mellitus: A Cross-Sectional Study.

ObjectiveBranched-chain amino acids (BCAAs) are essential AAs which are widely used as antioxidants in patients with liver and kidney dysfunction. However, BCAAs are strongly correlated with insulin resistance (IR) and diabetes. This study aimed to evaluate the relationship among BCAAs, oxidative stress, and type 2 diabetes mellitus (T2DM) in a Chinese population.MethodsAnthropometric and biochemical examinations were performed in 816 individuals who participated in the Huai’an Diabetes Prevention Program. Serum BCAAs concentrations were measured by hydrophilic interaction chromatography-tandem mass spectrometric method. Oxidative stress was evaluated by malondialdehyde (MDA) as an index of lipid peroxidation and the superoxide dismutase (SOD) activity.ResultsA total of 816 participants were divided into three groups: normal glucose metabolism (NGM), prediabetes, and newly-diagnosed diabetes mellitus (NDM). Subjects in NDM group show higher MDA and lower SOD levels than subjects in other groups. L-Val levels positively correlated with MDA levels and negatively with SOD in NDM groups. After adjusting for T2DM risk factors, high L-Val levels were significantly associated with higher BMI, WC, FPG, increased LnTG and decreased HDL-C. L-Val was also independently associated with NDM (OR 1.06, 95% CI 1.02–1.10; P = 0.005). Furthermore, the odds ratios for NDM among participants with high L-Val (≥35.25μg/mL) levels showed a 2.25-fold (95% CI 1.11–4.57; P = 0.024) increase compared to participants with low L-Val (<27.26 μg/mL) levels after adjusting for MDA and confounding factors.ConclusionHigh serum L-Val levels are independently associated with oxidative stress, thus promoting IR and NDM. Further study should be done to clarify the mechanism.

Attenuation of hyperglycemia and amadori products by aminoguanidine in alloxan-diabetic rabbits occurs via enhancement in antioxidant defenses and control of stress.

The micro- and macro-complications in diabetes mellitus (DM) mainly arise from the damage induced by Amadori and advanced glycation end products, as well as the released free radicals. The primary goal of DM treatment is to reduce the risk of micro- and macro-complications. In this study, we looked at the efficacy of aminoguanidine (AG) to prevent the production of early glycation products in alloxan-diabetic rabbits. Type1 DM was induced in rabbits by a single intravenous injection of alloxan (90 mg/kg body weight). Another group of rabbits was pre-treated with AG (100 mg/kg body weight) prior to alloxan injection; this was followed by weekly treatment with 100 mg/kg of AG for eight weeks. Glucose, insulin, and early glycation products (HbA1C and fructosamine) were measured in control, diabetic and AG treated diabetic rabbits. The effects of hyperglycemia on superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (Gpx), reduced glutathione (rGSH), nitric oxide, lipid peroxides, and protein carbonyl were investigated. Alloxan-diabetic rabbits had lower levels of SOD, CAT, Gpx, and rGSH than control rabbits. Nitric oxide levels were considerably greater. AG administration restored the activities of SOD, CAT, Gpx enzymes up to 70–80% and ameliorated the nitric oxide production. HbA1c and fructosamine levels were considerably lower in AG-treated diabetic rabbits. The observed control of hyperglycemia and amadori adducts in alloxan-diabetic rabbits by AG may be attributed to decrease of stress and restoration of antioxidant defenses.

PATHOGENETIC ASPECTS OF METABOLIC SYNDROME IN EXPERIMENTAL ANIMALS

The aim: Was to study the state of the nitric oxide system, LPO and antioxidant system in the body of experimental animals in simulated metabolic syndrome. The aim of the study was to study the state of the nitric oxide system, lipid peroxidation and antioxidant system in the body of experimental animals in simulated MS. Materials and methods: The study was performed on 20 white male Wistar rats. Male control rats (n = 10) were fed a normal control diet. Male rats of the main group (n = 10) were fed a diet high in fat (over 60 % energy from fats) for 16 weeks, thus modeling the development of MS. The indicators of the prooxidant and antioxidant system, as well as the nitric oxide system were determined by photospectrographic method. Results: In animals with simulated MS, intensification of lipoperoxidation (statistically significantly higher level of TBA-active products 1.84 times), depletion of antioxidant protection (statistically significantly lower level of superoxide dismutase 2 times), activation of nitric oxide system (statistically significantly higher NO-synthase level 2.15 times) were found compared with intact animals. Conclusions: In animals with simulated MS, activation of lipid peroxidation processes, depletion of antioxidant protection and increased

Effect of dietary supplementation of antioxidants on growth, serum metabolites and enzymatic activities in Mandya lambs during summer

A study was conducted to assess the effect of dietary supplementation of vitamins on growth, serum metabolites and enzymatic activities in Mandya lambs during summer. Forty- eight lambs (3 months-old, average body weight 10.23 kg) were randomly allotted to four groups as control (Gr-I; basal diet), basal diet supplemented with vitamin E (Gr-II), vitamin C (Gr-III) and vitamin E @ 250 mg+ vitamin C @ 2 g (Gr-IV). The results indicated that the lambs of antioxidant supplemented groups (Gr-II, III and IV) had significantly (p<0.05) higher body weight as compared to the control after 90 days of supplementation. The average daily gain was significantly (p<0.05) higher in Gr-IV (64.44±2.34 g), followed by Gr-I (59.15±1.62 g) and Gr-II (56.66±0.15 g). Significantly (p<0.05) higher levels of glucose, total protein, albumin, triglycerides, total cholesterols and HDLcholesterol and lower levels of urea nitrogen were noticed in supplemented groups as compared to the control group. Significantly (p<0.05) lower levels of superoxide dismutase, glutathione peroxidase, catalase activities and thiobarbituric acid reactive substances (TBARS) levels were observed in supplemented groups as compared to the control. These results suggested that dietary supplementation of vitamin C and vitamin E either alone or in combination for 90 days improved growth and reduced the stress in lambs during summer.

CORRELATION OF CARDIAC BIOMARKERS WITH THE LEVELS OF SELENIUM AND ANTIOXIDANT ENZYMES IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION AND A HISTORY OF HYPERTENSION

The aim: To determine the interrelations between the levels of antioxidant enzymes, selenium and the markers of myocardial injury in patients with non-ST segment elevation myocardial infarction and a history of antecedent arterial hypertension. Materials and methods: A total of 72 patients with non-ST segment elevation myocardial infarctionwere examined (42 with antecedent hypertension - group 1; 30-without hypertension – group2). Results: Patients of group 1 were characterized by significantly higher troponin I levels (p = 0.006), creatine kinase MB levels (p=0.008) and lower levels of superoxide dismutase (p=0.005), catalase (p=0.003) and selenium (p=0.008) as compared with group 2. In both groups, the activity of superoxide dismutase had an inverse correlation with troponin I: (r = -0.46, p = 0.005) and (r = -0.38, p = 0.004), respectively. A significant inverse relationships were found between selenium levels and both markers of myocardial injury in group 1 (p≤0.009), whereas in group 2 a weak correlation was found between the levels of selenium and troponin I only (p=0.006). Conclusions: The obtained data suggest that the levels of selenium and antioxidant enzymes in blood of all patients with non-ST elevation myocardial infarction inversely correlate with cardiac biomarkers. Patients with non-ST elevation myocardial infarction and a history of hypertension have significantly lower levels of antioxidant agents, higher levels of markers of myocardial injury, and stronger connections between them, indicating the development of more significant myocardial injury.

Do smokers have a different gingival crevicular fluid cytokine/chemokine profile than nonsmokers in clinically healthy periodontal sites? A systematic review and meta-analysis

Assessing the evidence and comparing the levels of cytokines in gingival crevicular fluid (GCF) of periodontal healthy sites of smokers and nonsmokers. Seven databases were surveyed for observational studies up to April 8, 2021. Studies comparing cytokine levels on GCF in periodontally healthy sites of smokers vs. nonsmokers were included in the study. The risk of bias was evaluated using NIH (2014) tool. For meta-analyses, levels in GCF were analyzed, followed by evidence certainty assessment using the GRADE approach. Eighteen studies were included for qualitative evaluation, and eight were included in meta-analysis. Qualitatively, despite high heterogeneity and risk of bias observed among the studies, most of them presented no significant difference in the gingival crevicular cytokine fluid levels between groups. Regarding meta-analyses, interleukin-8 (IL-8) and superoxide dismutase (SOD) levels in GCF were analyzed. The significant difference was observed only in SOD levels, where heavy smokers had lower levels compared to nonsmokers (MD - 30.06 [- 40.17, - 19.96], p = 0.07, 95%CI), as well as light smokers had lower levels compared to nonsmokers (MD - 15.22 [- 16.05, - 14.39], p < 0.00001, 95%CI). No distinct GCF cytokine profiles were detected for smokers and non-smokers. However, despite the limitations observed in the included studies, lower levels of SOD were identified in smokers. Indicating a distinct GCF profile of cytokines in periodontal healthy smokers may help to understand the mechanism whereby smoking may affect the host response.

Uncoupling protein 1 knockout aggravates isoproterenol-induced acute myocardial ischemia via AMPK/mTOR/PPAR\u03b1 pathways in rats

Uncoupling protein 1 (UCP1) was found exclusively in the inner membranes of the mitochondria of brown adipose tissue (BAT). We found that UCP1 was also expressed in heart tissue and significantly upregulated in isoproterenol (ISO)-induced acute myocardial ischemia (AMI) rat model. The present study is to determine the underlying mechanism involved in the UCP1 upregulation in ISO-induced AMI rat model. The Ucp1−/− rats were generated by CRISPR-Cas9 system and presented decreased BAT volume. 2-months old Sprague Dawley (SD) wild-type (WT) and Ucp1−/− rats were treated with ISO intraperitoneally 30 mg/kg once a day for 3 consecutive days to establish AMI model. In saline group, the echocardiographic parameters, serum markers of myocardial injury cardiac troponin I (cTnI), creatine kinase isoenzyme MB (CK-MB), oxidant malondialdehyde (MDA), antioxidant superoxide dismutase (SOD) or fibrosis were comparable between WT and Ucp1−/− rats. ISO treatment induced worse left ventricle (LV) hypertrophy, myocardial fibrosis, increased higher cTnI, CK-MB and MDA and decreased lower SOD level in Ucp1−/− rats compared with that of WT rats. Ucp1−/− rats also presented lower myocardial phosphocreatine (PCr)/ATP-ratio, which demonstrated worse cardiac energy regulation defect. ISO treatment induced the phosphorylation of AMP-activated protein kinase (AMPK) activation, subsequently the phosphorylation of mammalian target of rapamycin (mTOR) inhibition and peroxisome proliferators-activated receptor α (PPARα) activation in WT rats, whereas activation of AMPK/mTOR/PPARα pathways significantly inhibited in Ucp1−/− rats. To sum up, UCP1 knockout aggravated ISO-induced AMI by inhibiting AMPK/mTOR/PPARα pathways in rats. Increasing UCP1 expression in heart tissue may be a cytoprotective therapeutic strategy for AMI.

Controlled expression of the migratory phenotype affects oxidative status in birds.

High caloric intake can increase production of reactive oxygen and nitrogen species. We examined whether the emergence of the migratory phenotype, primarily signalled by increased food intake and fuelling, is accompanied by changes in oxidative status. We induced autumn migration followed by a non-migratory wintering phase in common quails (Coturnix coturnix). We compared three markers of oxidative status - oxidative damage to lipids expressed as thiobarbituric acid reactive substances (TBARS); superoxide dismutase (SOD); and glutathione peroxidase (GPx) - between birds sampled during the migratory and non-migratory phase. We found that the emergence of the migratory phenotype was associated with: (i) higher levels of TBARS in the liver; (ii) lower levels of SOD in red blood cells and, marginally, in the liver; (iii) higher levels of GPx in the pectoral muscle; and (iv) sex-specific changes in red blood cells and liver. We found no link between food intake and variation in markers of oxidative status in any of the tissues examined, despite food intake being higher in the migratory birds. However, the increase in body mass was positively correlated with muscle GPx activity as birds entered the pre-migratory fattening phase, while the amount of decrease in body mass was negatively correlated with muscle GPx as birds transitioned to the non-migratory phase. Such correlations were absent in red blood cells and liver. Our work suggests that during the emergence of the migratory phenotype, birds might strategically displace oxidative costs on the liver in order to safeguard the pectoral muscles, which have a fundamental role in successfully completing the migratory flight.

Cytotoxic response of phagocytes in patients newly infected with pulmonary Mycobacterium tuberculosis determined using plasma tumor necrosis factor-alpha, malondialdehyde, and superoxide dismutase: an observational study

Abstract Objective: Pulmonary Mycobacterium tuberculosis infection can trigger cellular and humoral innate immune responses, which may cause death of the pathogen and or host cells/tissue. We aimed to determine the cytotoxic response of phagocytes in patients with pulmonary Mycobacterium tuberculosis infection based on plasma tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), and superoxide dismutase (SOD) levels. Methods: In this observational study, patients newly infected with pulmonary Mycobacterium tuberculosis (n = 31; age 37–62 years) and age-matched uninfected volunteers (n = 50) were recruited as test and control volunteers, respectively in Owo, Nigeria. The study protocol was reviewed and approved by the Research and Ethics Committee of the Department of Medical Laboratory Science, Achievers University, Owo, Nigeria (AUO/MLS/VII/2009/212). Anti-hepatitis C virus, human immunodeficiency virus antigen/antibody, hepatitis B virus surface antigen, and plasma TNF-α were determined by enzyme-linked immunosorbent assay, SOD, and MDA were determined by colorimetry, Plasmodium by Giemsa thick blood film staining, and acid-fast bacilli in sputum were detected by Ziehl–Neelsen staining. Results: All participants had normal blood glucose levels and tested negative for human immunodeficiency virus antigen/antibody, anti-hepatitis C virus, hepatitis B virus surface antigen, and Plasmodium spp., and had no medical history of cancer. Infected patients had significantly higher plasma MDA and TNF-α levels and significantly lower SOD levels compared with control subjects (all P &lt; 0.05). Conclusion: Mycobacterium tuberculosis infection elicited a cytotoxic response by phagocytes, evidenced by significant increases in MDA and TNF-α and a significant decrease in SOD levels.

Oxidative stress in common variable immunodeficiency

Common variable immunodeficiency (CVID) is a heterogenous group of immunologic disorders of unknown etiology. Alterations of the normal cellular balance due to an increase in reactive oxygen species and/or decrease in antioxidant defense may lead to increased oxidative stress. We aimed to evaluate the levels of oxidative stress biomarkers in patients with CVID who had different presentations. We investigated the serum catalase (CAT), erythrocyte superoxide dismutase (SOD), erythrocyte reduced glutathione as antioxidants and serum malondialdehyde levels as lipid peroxidation marker in patients with CVID in Uludag University Hospital Department of Pediatric Allergy and Immunology’s outpatient clinics. In the analysis, there were 21 patients and 27 matched healthy controls. The median levels of CAT in patients with CVID was significantly lower than in healthy controls ( p = 0.04). Among the patients with CVID, 19% had autoimmune disease, one had Sjögren’s syndrome, one had autoimmune alopecia, one had juvenile rheumatoid arthritis, and one had chronic inflammatory demyelinating polyneuropathy. Patients with autoimmune complications had significantly lower CAT levels compared to the ones without autoimmune diseases ( p = 0.03). The patients without non-infectious complications (NICs) had lower SOD levels than the patients with NICs ( p = 0.05). The analysis of oxidative stress markers in the patients with CVID suggested a series of abnormalities in the anti-oxidant system. The clinical syndrome associations may be a useful tool for future studies to set prediction markers for the prognosis of patients with CVID.

Assessment of Psychological Status and Oxidative Stress in Postmenopausal Women: A Cross-Sectional Study.

ObjectivesDuring menopause, women may experience some physical changes that can affect their psychological status. Oxidative stress also increases with menopause, as decreasing levels of estrogen reinforce the deterioration of antioxidant status. To assess total antioxidative capacity, malondialdehyde, superoxide dismutase, and glutathione peroxidase and the correlation between psychological status and oxidative stress in postmenopausal women.MethodsThis cross-sectional study was undertaken on 100 postmenopausal women (40–59 years). Blood malondialdehyde, superoxide dismutase, glutathione peroxidase, and total antioxidative capacity were analyzed, and psychological status was assessed using Rosenberg's self-esteem test, Zung's self-rating anxiety scale, and Zung's self-rating depression scale.ResultsOf the women, 38.0% had mild to moderate symptoms of anxiety (mean ± standard deviation, 50.15 ± 4.89), 21.0% showed depression, and 19.0% had low self-esteem. Twelve percent of the study population had mild to moderate symptoms of all three disorders. A statistically significant difference was found in the scores of anxiety and self-esteem (P = 0.001 and P < 0.001 in women with and without psychological disturbances, respectively). With regard to oxidative stress parameters, only superoxide dismutase levels showed a statistically significant difference (P = 0.001), with lower levels found in women with psychological disturbance.ConclusionsWomen with depression, anxiety, and low self-esteem are in an oxidative challenge, which might be associated with estrogen depletion. A lower superoxide dismutase level is associated with higher depression and anxiety scores in postmenopausal women.

Oxidative stress biomarkers in treatment-responsive and treatment-resistant schizophrenia patients.

Introduction Schizophrenia is a complex psychiatric disorder that affects approximately twenty million people worldwide. Various factors have been associated with the physiopathology of this disease such as oxidative stress, which is an imbalance between pro-oxidant and antioxidant molecules.Objective This study evaluated the association between biomarkers of oxidative stress and response to pharmacological treatment among patients with schizophrenia in the context of their clinical information, demographic data, and lifestyle.Methods A total of 89 subjects were included, 26 of whom were treatment-responsive schizophrenia patients (Group 1), 27 treatment-resistant schizophrenia patients (Group 2), and 36 healthy controls (Group 3). All of the subjects completed a questionnaire to provide clinical and demographic data, and all provided peripheral blood samples. The oxidative stress markers analyzed using spectrophotometry were catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), total glutathione (GSH-t), malondialdehyde (MDA), and Trolox-equivalent antioxidant capacity (TEAC; p < 0.05).Results When all schizophrenia patients (G1 + G2) were compared to the control group, SOD levels were found to be lower among schizophrenia patients (p < 0.0001), while MDA and CAT levels were higher (p < 0.0001 and p = 0.0191, respectively). GPx, GSH-t, and TEAC levels were similar in all three groups (p > 0.05).Conclusion Lower SOD levels and higher MDA and CAT levels indicate oxidative damage in schizophrenia patients, regardless of their response to pharmacological treatment. Smoking is associated with oxidative stress, in addition, a family history of the disease was also found to be correlated with cases of schizophrenia, which reflects the relevance of genetics in disease development.

The profibrotic effects of chronic microaspiration of bile acids on lungs of rats at different stages

This study aimed to explore the profibrotic effects of chronic microaspiration of two major bile acids, including chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA), on lungs of rats at different stages, as well as the underlying mechanisms in vivo. A rat model was induced by weekly intratracheal instillation of DCA and CDCA. Our results showed that chronic microaspiration of bile acids resulted in alveolar structure disorder, and inflammatory cells infiltration in the pulmonary interstitium at the early stage. Subsequently, numerous fibroblasts were proliferated, and collagen deposition was profoundly increased over the interstitium of the airways and vessels. Compared with control group, the expression of α-smooth muscle actin, type I collagen, hydroxyproline, transforming growth factor-β1 (TGF-β1), and matrix metalloproteinase-9 in the lung tissues were remarkably elevated at the 2nd week, reached the highest level at the 6th week, and maintained high at the 8th week in both DCA- and CDCA-treated groups (P < 0.05). Furthermore, chronic microaspiration of bile acids led to higher levels of glutathione and malondialdehyde, while lower level of superoxide dismutase in lung tissues compared with controls (P < 0.05), thereby resulting in the oxidant/antioxidant enzyme imbalance in the formation of fibrosis. In addition, we also found a consistent growth in the expression of farnesoid X receptor (FXR) in both DCA- and CDCA-treated groups. Our findings suggested that chronic microaspiration of bile acids could initiate the process of pulmonary fibrosis from the early phase and promote its progression in a time-dependent manner, which likely involved the TGF-β1, oxidative stress, and FXR-related pathways.

The Imbalance among Oxidative Biomarkers and Antioxidant Defense Systems in Thromboangiitis Obliterans (Winiwarter-Buerger Disease).

(1) Background: Thromboangiitis obliterans or Winiwarter-Buerger disease (WBD), is an inflammatory, thrombotic occlusive, peripheral vascular disease, usually occurring in young smokers. The pathophysiological mechanisms underlying the disease are not clearly understood. The aim of this study is to investigate the imbalance between oxidants and antioxidants occurring in these patients. (2) Patients and Methods: In this cross-sectional study, 22 male patients with WBD and 20 healthy male smoking habit matched control group were included. To evaluate the possible sources of oxidative stress, the antioxidant biomarkers, and the markers of lipid peroxidation and protein oxidation, serum samples were analyzed for total oxidative status (TOS), total antioxidant capacity (TAC), myeloperoxidase (MPO), coenzyme Q10 (CoQ10), superoxide dismutase (SOD), glutathione reductase (GR), malondialdehyde (MDA), and protein carbonyl (PC) activity and/or content. (3) Results: The circulating levels of TOS, TAC, and CoQ10 were significantly higher in WBD patients, with respect to healthy smokers as controls. No significant difference was found among the serum level of PC, total cholesterol, MPO, and GR activity in WBD patients and healthy smoker controls. The activity of SOD and the mean serum level of MDA were significantly lower in WBD patients, with respect to healthy smoker controls. (4) Conclusion: Considerably high levels of oxidative stress were detected in WBD patients, which were greater than the antioxidant capacity. The low level of MDA may be associated with the enzymatic degradation of lipid peroxidation products. High levels of CoQ10 and low levels of SOD may be related to a harmful oxidative cooperation, leading to the vasoconstriction of WBD, representing a promising tool to discern possible different clinical risks of this poorly understood peripheral occlusive disease.