Plasma Superoxide Dismutase Levels Research Articles

Efficacy of antioxidants in the management of psoriasis: A case control study

Introduction: Psoriasis is a chronic, immune-mediated inflammatory dermatosis. The pathophysiology of the disease is still incompletely elucidated and multiple factors are said to be involved in its initiation and perpetuation, e.g., stressors, genetic factors, environmental factors. In the last decade, a new theory is trying to explain the pathophysiology of this disease by looking at the role played by oxidative stress and chronic inflammation in the initiation of keratinocyte proliferation and differentiation. Keeping in consideration the increased oxidative stress in the patients of psoriasis, the anti-oxidant drugs can form an important part of the therapeutic ladder of psoriasis. Materials and Methods: The aim of this study was to measure the possible role of oxidative stress in psoriasis patient by measuring SOD level and comparing it with normal individuals and administer antioxidants supplements to the patients group to see the efficacy. It was a Case- Control study (1st part) and Clinical Trial without control group (2nd part). The study was carried out in Psoriasis awareness Club from June 2023 to December 2023. Purposive sampling done who fulfill the inclusion & exclusion criteria. 23 patients with psoriasis and 23 age and sex matched control subjects were recruited for this study. Clinical severity of the disease was determined by PASI score. All patients and control subjects were examined for plasma SOD level. 23 psoriatic patients were given antioxidant therapy in the form of once daily tablet for 30 days. PASI score, DLQI and SOD (Superoxide dismutase) level were measured before therapy (day 0) and after therapy (day 30) in patients group. Statistical analysis and Results: Data were expressed as mean ± standard deviation (SD) for quantitative variables and numbers. For comparison of two means (t test) and (ANOVA "F") test were used for several means. Chi-square (χ2 ) or fisher exact test were used when appropriate, (P<0.05) was considered statistically significant. The mean age of the patients and control subjects were 37.64 (±5.89) and 33.6 (11.02) years, respectively. The mean duration of the disease was 12.43 (±8) years. No significant difference was observed between SOD level of psoriatic patients & controls. No significant correlations of SOD level with severity of psoriasis and duration of disease were found. We observed no statistically significant difference in PASI and DLQI scores before and after antioxidant therapy but there was significant increase in the level of SOD after treatment. Conclusion: It is indisputable that antioxidant supplementation can reduce the overall morbidity, enhance the prognosis of psoriasis. Notably, in most cases, antioxidants alone are not able to induce significant clinical changes in the aspect and/or course of the disease, except perhaps in mild forms. They must be used in conjunction with standard pharmacological treatments to achieve measurable results.

Plasma oxidative stress marker levels related to functional brain abnormalities in first-episode drug-naive major depressive disorder

Major Depressive Disorder (MDD) is marked by abnormal brain function and elevated plasma oxidative stress markers. The specific relationship between these factors in MDD remains unclear. In this study, we conducted resting-state fMRI scans on fifty-seven first-episode, drug-naive MDD patients and sixty healthy controls. Plasma levels of oxidative stress markers (superoxide dismutase (SOD) and glutathione reductase (GSR)) were assessed using ELISA. Our results revealed a positive correlation between plasma SOD and GSR levels in MDD patients and the amplitude of low-frequency fluctuation (ALFF) values in key brain regions—thalamus, anterior cingulate gyrus, and superior frontal gyrus. Further analysis indicated positive correlations between plasma SOD and GSR levels and specific ALFF values in MDD patients without suicidal ideation, with these correlations not significant in MDD patients with suicidal ideation. Additionally, seed-based whole-brain functional connectivity analysis demonstrated a negative correlation between plasma GSR levels and connectivity between the thalamus and insula, while plasma SOD levels showed a positive correlation with connectivity between the thalamus and precuneus. These findings contribute to our understanding of MDD's pathophysiology and heterogeneity, highlighting the association between plasma oxidative stress markers and functional abnormalities in diverse brain regions.

Effects of coenzyme Q10 supplementation on oxidative stress biomarkers following reperfusion in STEMI patients undergoing primary percutaneous coronary intervention.

It is well-established that oxidative stress is deeply involved in myocardial ischemia-reperfusion injury. Considering the potent antioxidant properties of coenzyme Q10 (CoQ10), we aimed to assess whether CoQ10 supplementation could exert beneficial effects on plasma levels of oxidative stress biomarkers in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPIC). Seventy patients with the first attack of STEMI, eligible for PPCI were randomly assigned to receive either standard treatments plus CoQ10 (400 mg before PPCI and 200 mg twice daily for three days after PPCI) or standard treatments plus placebo. Plasma levels of oxidative stress biomarkers, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total antioxidant capacity (TAC), and malondialdehyde (MDA) were measured at 6, 24, and 72 hours after completion of PPCI. The changes in plasma levels of the studied biomarkers at 6 and 24 hours after PPCI were similar in the both groups (P values>0.05). This is while at 72 hours, the CoQ10- treated group exhibited significantly higher plasma levels of SOD (P value<0.001), CAT (P value=0.001), and TAC (P value<0.001), along with a lower plasma level of MDA (P value=0.002) compared to the placebo-treated group. The plasma activity of GPX showed no significant difference between the groups at all the study time points (P values>0.05). This study showed that CoQ10 has the potential to modulate the balance between antioxidant and oxidant biomarkers after reperfusion therapy. Our results suggest that CoQ10, through its antioxidant capacity, may help reduce the reperfusion injury in ischemic myocardium.

Lipid metabolism and oxidative stress in patients with Alzheimer's disease and amnestic mild cognitive impairment.

Lipid metabolism and oxidative stress are key mechanisms in Alzheimer's disease (AD). The link between plasma lipid metabolites and oxidative stress in AD patients is poorly understood. This study was to identify markers that distinguish AD and amnestic mild cognitive impairment (aMCI) from NC, and to reveal potential links between lipid metabolites and oxidative stress. We performed non-targeted lipid metabolism analysis of plasma from patients with AD, aMCI, and NC using LC-MS/MS. The plasma malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) levels were assessed. We found significant differences in lipid metabolism between patients with AD and aMCI compared to those in NC. AD severity is associated with lipid metabolites, especially TG (18:0_16:0_18:0) + NH4, TG (18:0_16:0_16:0) + NH4, LPC(16:1e)-CH3, and PE (20:0_20:4)-H. SPH (d16:0) + H, SPH (d18:1) + H, and SPH (d18:0) + H were high-performance markers to distinguish AD and aMCI from NC. The AUC of three SPHs combined to predict AD was 0.990, with specificity and sensitivity as 0.949 and 1, respectively; the AUC of three SPHs combined to predict aMCI was 0.934, with specificity and sensitivity as 0.900, 0.981, respectively. Plasma MDA concentrations were higher in the AD group than in the NC group (p = 0.003), whereas plasma SOD levels were lower in the AD (p < 0.001) and aMCI (p = 0.045) groups than in NC, and GSH-Px activity were higher in the AD group than in the aMCI group (p = 0.007). In addition, lipid metabolites and oxidative stress are widely associated. In conclusion, this study distinguished serum lipid metabolism in AD, aMCI, and NC subjects, highlighting that the three SPHs can distinguish AD and aMCI from NC. Additionally, AD patients showed elevated oxidative stress, and there are complex interactions between lipid metabolites and oxidative stress.

Superoxide dismutase activity levels in parturients on intermittent preventive treatment with sulphadoxine pyrimethamine and their controls at current confinements

Malaria prevention in pregnancy especially in endemic areas has been greatly emphasized. This is especially so during the antenatal periods. Malaria prevention is important for reducing the problems of malaria in pregnancy. Early trimester miscarriages, preterm labours, anaemia in pregnancy, small for date babies and increased admissions into special care baby units are some of the problems encountered that are traceable to malaria infection. It is also noteworthy that some favourable antioxidants have been noted to help pregnant women enjoy and cope with their pregnancies. In that same way, it has also been noted that optimal levels of superoxide dismutase is equally necessary to help pregnant women enjoy uneventful pregnancies as well as stay free from some problems associated with malaria in pregnancy. Objectives: We have comparatively and objectively assessed the plasma Levels of superoxide dismutase in Parturients on Intermittent Preventive Treatment with Sulphadoxine Pyrimethamine and their Controls at Current Confinements. Method: This comparative study was conducted at the Obstetrics and Gynaecology Department of the Federal Medical Centre (FMC) Owerri, South East Nigeria. Owerri is widely known for its heavy malaria endemicity. Prior to participant recruitment, appropriate ethical clearance was applied for and obtained from the ethics committee of FMC Owerri. This enabled the commencement of the longitudinal recruitment of participants after due counseling and adequate informed consent involving both study groups. This bench-based research and cross-sectional descriptive study involved two hundred and ninety-six (296) consented participants. The participants were made to understand clearly the study protocol as well as satisfy the inclusion criteria for either the study (case) or control groups. Upon recruitment, participants were then followed up all throughout their entire antenatal course culminating in the delivery. The follow up enabled the collection of blood samples for the estimation of Superoxide Dimutase (SOD) plasma levels at delivery. The SOD levels were estimated using the Misra and Fridovich method, 1972. The ability of superoxide dismutase to inhibit the auto oxidation of adrenaline at pH 10.2 makes this reaction a basis for the SOD assay. Superoxide anion (O2) generated by the xanthine oxidase reaction is known to cause the oxidation of adrenaline to adrenochrome. The yield of adrenochrome produced per superoxide anion introduced increased with increasing pH and also with increasing concentration of adrenaline. These led to the proposal that auto oxidation of adrenaline proceeds by at least two distinct pathways, one of which is a free radical chain reaction involving superoxide radical and hence could be inhibited by SOD. Data analysis: Data computation and analysis were done using the computer Software Package for Social Science (SPSS) version 20.0 (SPSS, Inc, 2007, Chicago). Important descriptive statistics (mean, standard deviation, range, percentages etc) were determined for continuous variables. P-value less than (&lt;0.05) at 95% confidence interval was considered statistically significant. Result: The mean serum level of superoxide dismutase (SOD) in the study group was 12.61 U/ml ± 3.105 while the minimum and maximum serum superoxide dismutase were 7 and 20 U/ml respectively. For their controls, the mean serum level of superoxide dismutase was 11.69 U/ml ± 2. 969. However, the minimum and maximum serum superoxide dismutase were 7 and 20 U/ml respectively. The difference was found to be statistically significant (p= 0.011) with odds ratio 1.12 (CI of 95% 1.024-1.193).

Online Home-Based Physical Activity Counteracts Changes of Redox-Status Biomarkers and Fitness Profiles during Treatment Programs in Postsurgery Female Breast Cancer Patients.

Breast cancer (BC) is one of the most commonly diagnosed types of cancer in women. Oxidative stress may contribute to cancer etiology through several mechanisms. A large body of evidence indicates that physical activity (PA) has positive effects on different aspects of BC evolution, including mitigation of negative effects induced by medical treatment. With the aim to verify the capacity of PA to counteract negative effects of BC treatment on systemic redox homeostasis in postsurgery female BC patients, we have examined the modulation of circulating levels of oxidative stress and inflammation markers. Moreover, we evaluated the impacts on physical fitness and mental well-being by measuring functional parameters, body mass index, body composition, health-related quality of life (QoL), and fatigue. Our investigation revealed that PA was effective in maintaining plasma levels of superoxide dismutase (SOD) activity and tGSH, as well as peripheral blood mononuclear cells' (PBMCs) mRNA levels of SOD1 and heat-shock protein 27. Moreover, we found a significant decrease in plasma interleukin-6 (≈0.57 ± 0.23-fold change, p < 0.05) and increases in both interleukin-10 (≈1.15 ± 0.35-fold change, p < 0.05) and PBMCs' mRNA level of SOD2 (≈1.87 ± 0.36-fold change, p < 0.05). Finally, PA improves functional parameters (6 min walking test, ≈+6.50%, p < 0.01; Borg, ≈-58.18%, p < 0.01; sit-and-reach, ≈+250.00%, p < 0.01; scratch right, ≈-24.12%, and left, ≈-18.81%, p < 0.01) and body composition (free fat mass, ≈+2.80%, p < 0.05; fat mass, ≈-6.93%, p < 0.05) as well as the QoL (physical function, ≈+5.78%, p < 0.05) and fatigue (cognitive fatigue, ≈-60%, p < 0.05) parameters. These results suggest that a specific PA program not only is effective in improving functional and anthropometric parameters but may also activate cellular responses through a multitude of actions in postsurgery BC patients undergoing adjuvant therapy. These may include modulation of gene expression and protein activity and impacting several signaling pathways/biological activities involved in tumor-cell growth; metastasis; and inflammation, as well as moderating distress symptoms known to negatively affect QoL.

Correlation between Superoxide Dismutase (SOD) with Malondialdehyde (MDA) level in blood plasma of seborrheic keratosis

Introduction: Seborrheic keratosis (SK) is a benign tumor of the epidermis, its development is associated with various hypotheses, but none came out as the main culprit. A few study results regarding the oxidative stress strongly associated with skin tumors have been reported. Superoxide dismutase (SOD) is a potent protective enzymatic antioxidant. Malondialdehyde (MDA) is the end product of lipid peroxidation produced by free radicals in the body. Increased levels of MDA usually accompany low levels of antioxidants. Methods: This study was an observational analytic study with a cross-sectional method involving 42 seborrheic keratosis subjects based on inclusion and exclusion criteria. We recorded the gender, age, family history, and occupation of the subjects. Diagnosis of seborrheic keratosis was made based on history taking and clinical examination—measurement of SOD level by ELISA method and MDA levels by TBARS method. The Spearman correlation test was measured and was considered significant if the p-value was &lt;0.05. Results: Seborrheic keratosis was more common in females (92.9%), with the most common age group being 40 ̶ 50 years old (57.1%), had a family history of SK (26.2%), and worked in agriculture, forestry, and fisheries (26.2%). The average blood plasma SOD level was 1.68 mmol/L, and the blood plasma MDA level was 181.19 U/L. The correlation coefficient between blood plasma SOD levels and blood plasma MDA levels was -0.393, with a significant value of p=0.01. This study showed that the lower the SOD level, the higher the MDA level in the blood plasma of seborrheic keratosis. Conclusion: There is a significant correlation between SOD and MDA levels in the blood plasma of seborrheic keratosis subjects.

Cannabinoid Receptor Agonist WIN55, 212-2 Attenuates Injury in the Hippocampus of Rats after Deep Hypothermic Circulatory Arrest

Postoperative neurological deficits remain a challenge in cardiac surgery employing deep hypothermic circulatory arrest (DHCA). This study aimed to investigate the effect of WIN55, 212-2, a cannabinoid agonist, on brain injury in a rat model of DHCA. Twenty-four male Sprague Dawley rats were randomly divided into three groups: a control group (which underwent cardiopulmonary bypass (CPB) only), a DHCA group (CPB with DHCA), and a WIN group (WIN55, 212-2 pretreatment before CPB with DHCA). Histopathological changes in the brain were evaluated by hematoxylin-eosin staining. Plasma levels of superoxide dismutase (SOD) and proinflammatory cytokines including interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-a) were determined using an enzyme-linked immunosorbent assay (ELISA). The expression of SOD in the hippocampus was detected by Western blot and immunofluorescence staining. Levels of apoptotic-related protein caspase-3 and type 1 cannabinoid receptor (CB1R) in the hippocampus were evaluated by Western blot. WIN55, 212-2 administration attenuated histopathological injury of the hippocampus in rats undergoing DHCA, associated with lowered levels of IL-1β, IL-6, and TNF-α (p < 0.05, p < 0.001, and p < 0.01, vs. DHCA, respectively) and an increased level of SOD (p < 0.05 vs. DHCA). WIN55, 212-2 treatment also increased the content of SOD in the hippocampus. The protein expression of caspase-3 was downregulated and the expression of CB1R was upregulated in the hippocampus by WIN55, 212-2. the administration of WIN55, 212-2 alleviates hippocampal injury induced by DHCA in rats by regulating intrinsic inflammatory and oxidative stress responses through a CB1R-dependent mechanism.

Prognostic value of plasma level of superoxide dismutase in HBV-related acute-on-chronic liver failure

BackgroundHepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is the most prevalent type of ACLF in China. The mortality rate of HBV-ACLF has decreased in recent years due to advances in treatment therapies; however, it is still above 50%. Many cases of HBV-ACLF are caused by HBV reactivation due to discontinuation of nucleoside analog treatment. The present study focused on plasma levels of superoxide dismutase (SOD) in HBV-ACLF patients and investigated whether the plasma level of SOD is a useful biomarker in assessing disease severity and predicting outcomes of HBV-ACLF patients, including patients treated with Entecavir (ETV) and patients who were withdrawn from ETV treatment.MethodsPlasma samples and clinical data from 200 HBV-ACLF patients and from age- and sex-matched cirrhotic and healthy controls were collected and analyzed. Plasma levels of SOD were measured using an ELISA commercial kit.ResultsAmong the HBV-ACLF patients, in the ETV withdrawal group, the mortality rate was higher than in the ETV group (69.95% vs 46.71%, P < 0.05). Moreover, HBV-DNA and SOD plasma levels were higher in the ETV withdrawal group than in the ETV group (Log10(HBV-DNA): 6.49 ± 0.24 vs 4.79 ± 0.14, P < 0.01; SOD: 463.1 ± 27.61 U/mL vs 397.2 ± 10.97 U/mL, P < 0.05). The mortality and liver transplantation rates were significantly higher in HBV-ACLF patients with plasma levels of SOD > 428 U/mL than in patients with plasma SOD levels ≤ 428 U/mL.ConclusionsReactivation of HBV and elevated oxidative stress caused by discontinuation of ETV treatment are crucial factors in the pathogenesis of HBV-ACLF. Plasma level of SOD may serve as a useful biomarker in estimating disease severity and predicting outcomes of HBV-ACLF patients who stop ETV treatment.

Association between plasma level of superoxide dismutase and survival of patients with acute-on-chronic liver failure

BackgroundFewer than 50% of patients with acute-on-chronic liver failure (ACLF) recover spontaneously, and ACLF has high mortality without liver transplantation. Oxidative stress has been shown to mediate hepatic inflammation during acute liver failure (ALF). We wanted to see if a biomarker for oxidative stress might be used to measure the severity and prognosis of ACLF patients.MethodsA retrospective cohort of 124 ACLF patients, as well as healthy individuals, liver cirrhosis and ALF patients, was studied between January 2015 and September 2018. The levels of plasma superoxide dismutase (SOD) were detected using an ELISA commercial kit, and the Kaplan–Meier method was used for survival analysis.ResultsPatients with ACLF had statistically higher plasma SOD levels than the controls did (healthy controls and liver cirrhosis patients); however, the levels did not differ from those in patients with ALF. The plasma SOD level may be an inexpensive, easily accessible, and significant independent prognostic index for mortality on multivariate analysis (HR = 1.201, 95% CI 1.001–1.403, P < 0.01) as well as the model for end-stage liver disease (MELD) score. A level of SOD > 428 U/mL was linked to a statistically significant increase in the likelihood of death or liver transplantation in ACLF patients. Combination of plasma SOD levels and MELD scores improved performance in measuring the severity and prognosis of ACLF patients.ConclusionPatients with ACLF can be classified into high-risk and low-risk groups based on their plasma SOD levels at the time of admission to the hospital. The patient outcome is more closely connected with the combination of SOD level and MELD score than either value alone. This approach might be used to predict patient prognoses and prioritize liver transplant candidates.

Exacerbation of Thrombotic Responses to Silver Nanoparticles in Hypertensive Mouse Model.

With advent of nanotechnology, silver nanoparticles, AgNPs owing majorly to their antibacterial properties, are used widely in food industry and biomedical applications implying human exposure by various routes including inhalation. Several reports have suggested AgNPs induced pathophysiological effects in a cardiovascular system. However, cardiovascular diseases such as hypertension may interfere with AgNPs-induced response, yet majority of them are understudied. The aim of this work was to evaluate the thrombotic complications in response to polyethylene glycol- (PEG-) coated AgNPs using an experimental hypertensive (HT) mouse model. Saline (control) or PEG-AgNPs (0.5 mg/kg) were intratracheally (i.t.) instilled four times, i.e., on days 7, 14, 21, and 28 post-angiotensin II-induced HT, or vehicle (saline) infusion. On day 29, various parameters were assessed including thrombosis in pial arterioles and venules, platelet aggregation in whole blood in vitro, plasma markers of coagulation, and fibrinolysis and systemic oxidative stress. Pulmonary exposure to PEG-AgNPs in HT mice induced an aggravation of in vivo thrombosis in pial arterioles and venules compared to normotensive (NT) mice exposed to PEG-AgNPs or HT mice given saline. The prothrombin time, activated partial thromboplastin time, and platelet aggregation in vitro were exacerbated after exposure to PEG-AgNPs in HT mice compared with either NT mice exposed to nanoparticles or HT mice exposed to saline. Elevated concentrations of fibrinogen, plasminogen activator inhibitor-1, and von Willebrand factor were seen after the exposure to PEG-AgNPs in HT mice compared with either PEG-AgNPs exposed NT mice or HT mice given with saline. Likewise, the plasma levels of superoxide dismutase and nitric oxide were augmented by PEG-AgNPs in HT mice compared with either NT mice exposed to nanoparticles or HT mice exposed to saline. Collectively, these results demonstrate that PEG-AgNPs can potentially exacerbate the in vivo and in vitro procoagulatory and oxidative stress effect in HT mice and suggest that population with hypertension are at higher risk of the toxicity of PEG-AgNPs.

Anticryptosporidium Efficacy of Olea europaea and Ficus carica Leaves Extract in Immunocompromised Mice Associated with Biochemical Characters and Antioxidative System.

Cryptosporidiosis is caused by an opportunistic protozoan parasite (Cryptosporidium parvum and C. hominis) known as a parasite of humans, especially children and immunocompromised patients. The current study was designed to evaluate the therapeutic efficacy of a mixture of fig and olive leaf extracts as an alternative medicinal plant. Parasitological examination for oocysts in the stool and histopathological alterations in the small intestines were examined. Additionally, biochemical analyses of liver and kidney functions in addition to antioxidant parameters such as superoxide dismutase (SOD), glutathione peroxidase (GSH) and catalase (CAT) in the plasma were evaluated. Our results showed that marked reduction in oocysts shedding and amelioration in intestinal histopathological changes and hepatic or renal functions were detected in all treated groups compared to the control infected group. Additionally, the treated groups with tested extracts at ratios 1:3 and 1:5 showed a significant decrease in the number of oocysts compared to the other treated groups. Results exhibited a significant increase in the plasma SOD, CAT and GSH levels in treated groups compared to the infected control one. This study suggested that a mixture of fig and olive leaf extracts is a convenient promising therapeutic agent for Cryptosporidiosis.

Urinary and Plasma Antioxidants in Behavioral Symptoms of Individuals With Autism Spectrum Disorder

The balance between antioxidant capacity and oxidative stress-induced free radicals may be crucial in the pathophysiological development factor of autism spectrum disorder (ASD). We measured the following urinary and plasma biomarker levels of oxidative stress and antioxidants. As urinary biomarkers, (1) hexanoyl-lysine (HEL), which is a new biomarker of oxidative stress, (2) the total antioxidant capacity (TAC), and (3) 8-hydroxy-2′-deoxyguanosine (8-OHdG), as a product of oxidative modifications to DNA; and the plasma levels of (4) the antioxidant protein superoxide dismutase (SOD), which is the crucial defense again oxygen reactive species, and (5) transferrin and (6) ceruloplasmin, which are biomarkers of iron and copper neurotransmission and oxidant-antioxidant systems. We examined the relationship between these urinary and plasma biomarkers and behavioral symptoms in 19 individuals with ASD (mean age, 10.8 ± 5.2 years) and 10 age-matched healthy controls (mean age, 14.2 ± 7.0 years). Behavioral symptoms were estimated using the Aberrant Behavior Checklist (ABC). Urinary TAC levels were significantly lower, whereas urinary HEL levels were significantly increased in the ASD group as compared with the control group. The five ABC subscale and total scores were significantly raised in the autism group than in the control group. The results of a linear regression analysis revealed that plasma SOD levels may be a more accurate predictor of differences in ABC scores between individuals with ASD and control individuals. The present study firstly revealed the important findings that the cooperation between the urinary antioxidant TAC and plasma SOD levels may contribute to the ABC subscale scores of stereotypy. Urinary TAC activity and antioxidant protein SOD may be associated with incomplete mineral body store and antioxidant-related transcription factor and browning reactions. Consequently, a critical imbalance between TAC urinary levels and plasma SOD levels may be an important contributor to autistic behavioral symptoms.

The role of anakinra in the modulation of intestinal cell apoptosis and inflammatory response during ischemia/reperfusion

Background/aim Even though interleukin-1 receptor antagonist, IL-1Ra, is used in certain inflammatory diseases, its effect on ischemia-reperfusion injury is a current research topic. We aimed to investigate the protective effects of anakinra, an IL-1Ra, on the I/R induced intestinal injury.Materials and methods The rat model of intestinal ischemia-reperfusion was induced. Rats were randomized into 4 groups: (group 1) control group, (group 2) I/R group, (group 3 and 4) treatment groups (50 mg/kg and 100 mg/kg, respectively). Gene expressions of caspase-3, TNF-α, IL-1α, IL-6, and apoptotic cells in tissue samples were evaluated by PCR and TUNEL methods, respectively. Plasma levels of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) were studied by the ELISA method and tissue samples were examined histopathologically as well.Results Anakinra inhibited the expression of IL-1α, IL-6, and TNF-α and decreased the SOD, CAT, and MDA caused by ischemia-reperfusion injury in both treatment groups. Caspase-3 expression and TUNEL-positive cell number in treatment groups were also less. Histopathologically, anakinra better preserved the villous structure of the small intestine at a dose of 100 mg/kg than 50 mg/kg. Conclusion Anakinra decreased the intestinal damage caused by ischemia-reperfusion and a dose of 100 mg/kg was found to be histopathologically more effective.

Mitigation of transportation stress in common carp, Cyprinus carpio, by dietary administration of turmeric

Stress is an inevitable and unpredictable process, which can be interceded through various aquaculture practices. Transportation is one of those aqua-husbandry practices that induces stress and immunosuppression in cultured fish. The present study intended to evaluate the ameliorative effects of dietary turmeric on common carp, Cyprinus carpio, based on antioxidant, immunological and tissue health characteristics at pre- and post-transportation. Diets containing four different levels of turmeric [0% (CTL), 0.5% (0.5 T), 1% (1 T), and 2% (2 T)] were fed to common carp (average weight: 45.2 g) for 2 weeks; then, the fish were placed in plastic bags containing 2.5 L water and 5 L pure oxygen and transported for 3 h in a van. Samples of blood and water were collected before and after the transportation. Transportation led to deterioration of the water quality parameters, as evidenced by declines in dissolved oxygen and pH levels, but elevations in alkalinity, total ammonia and unionized ammonia levels. Fish from 1 T treatment exhibited significantly highest water dissolved oxygen post transportation. Significant decrements in plasma total antioxidant capacity (TAC) and total immunoglobulin (Ig) were observed due to transportation-induced stress. Whereas, plasma cortisol, glucose, lactate, alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and lysozyme levels enhanced due to transportation-mediated stress in the fish. The transportation stress was mitigated in 0.5 T and 1 T treatments, which were reflected in terms of decrements in plasma cortisol, glucose, ALT, AST, ammonia, SOD (just in 1 T), CAT, and MDA levels, as well as increments in plasma total Ig and TAC levels in the fish. The above findings conclude that turmeric supplementation at 1% could be used as an excellent feed additive in order to ameliorate the adverse effects of transportation in common carp.

Association between glucose fluctuation during 2-hour oral glucose tolerance test, inflammation and oxidative stress markers, and β-cell function in a Chinese population with normal glucose tolerance.

BackgroundsGlucose fluctuation (GF) may have detrimental effects in individuals with diabetes; however, clinical data on the association between short-term GF, inflammation/oxidative stress markers, and islet β-cell function based on a population with normal glucose tolerance (NGT) are insufficient. Therefore, we aimed to explore these associations in a Chinese population of 209 individuals with NGT in a cross-sectional analysis.MethodsIndividuals were categorized based on GF tertiles, calculated as the maximum-minimum glucose levels among four time points (0, 30, 60, 120 min) during 2-hour oral glucose tolerance test (OGTT). Plasma inflammation markers tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and oxidative stress markers superoxide dismutase (SOD), and 8-oxo-2'-deoxyguanosine (8-oxo-dG) were measured. Islet β-cell function was estimated according to the disposition index (DI) at the early (30 min) and total (120 min) phase of the OGTT, adjusted for insulin sensitivity.ResultsIndividuals in the middle and highest tertile of GF had reduced β-cell function, and increased plasma SOD and TNF-α levels compared with those in the lowest tertile of GF (P<0.05). Multiple linear regression analysis indicated that GF was positively associated with TNF-α, 8-oxo-dG and SOD levels, but negatively associated with β-cell function, whereas IL-6, TNF-α, 8-oxo-dG and SOD levels were negatively associated with β-cell function (P<0.05).ConclusionsGF may increase inflammation and oxidative stress markers in individuals with NGT, which could contribute to reduced β-cell function. Thus, maintaining glucose stability after a meal may have beneficial effects on delaying β-cell dysfunction, suggesting that diet and exercise strategies to decrease diet related GF are warranted.

Clinical, echocardiographic parameters and markers of oxidative stress associated with atrial fibrillation in patients undergoing coronary artery bypass graft surgery

Aim. To estimate the association of clinical, echocardiographic parameters and markers of oxidative stress with postoperative atrial fibrillation (POAF) in patients with coronary artery disease (CAD) undergoing coronary artery bypass graft (CABG) surgery. Material and methods . This case-control study included 158 patients with CAD who were scheduled for CABG surgery. Patients were divided into two groups: group 1 (n=111) — patients without POAF (men — 82%, median age — 62,0 [56,0;66,0] years); group 2 (n=47) — patients with POAF (men — 84,4%, median age — 65,0 [61,0;70,0] years). The median of POAF development was 5,2 [2,0;7,0] days after CABG. We studied plasma and erythrocyte superoxide dismutase (SOD) levels, plasma nitrogen oxide and myeloperoxidase levels, erythrocyte levels of catalase, malondialdehyde, reduced glutathione, glutathione reductase and glutathione peroxidase, and advanced oxidation protein products. The determination was carried out before and on average 3-4 days after CABG. All the patients also underwent echocardiography. Results. Multivariate regression revealed following parameters associated with POAF: left atrial diameter >41 mm (odds ratio (OR) 4,1,95% confidence interval (CI) 1,7-8,9, р=0,001), postoperative plasma levels of SOD >1100,5 U/g (OR 3,0, 95% CI 1,3-9,7, р=0,04), postoperative levels of reduced glutathione 1,25 Mmol/g Hb (OR 1,9, 95% CI 1,1-7,2, р 36,4 Mmol/l (OR 1,4, 95% CI 1,03-4,8, р=0,001). Conclusion. Our study showed significant association of increased left atrial diameter, high activity of oxidative stress and low activity of antioxidant system with POAF in patients with CAD undergoing CABG surgery.

Vitamin D&lt;sub&gt;3&lt;/sub&gt; supplementation on plasma antioxidant enzymes in D&lt;sub&gt;3&lt;/sub&gt; deficient patients with COPD - a randomized controlled trial

Background: Free radical is a crucial factor for progression of COPD. Antioxidant enzymes, including superoxide dismutase (SOD) and catalase (CAT) have been well known to reduce morbidity of chronic disease. Vitamin D3 has antioxidant effect in human body.&#x0D; Objectives: To assess the effects of D3 supplementation on plasma SOD and CAT levels in D3 deficient COPD patients.&#x0D; Method: A double blinded placebo controlled randomized clinical trial was carried out on 30 vitamin D3 deficient male, smoker and stable COPD patients of age &gt;40 years. All the patients were randomly allocated to ‘Study’ (n=15) or ‘Control’ (n=15) and their baseline plasma SOD and CAT were measured. Study patients received 80,000 IU (2 oral capsules) of D3 per week for first 13 weeks. Subsequently, after checking their serum 25(OH)D or Ca2+, they received 40,000 IU (1 oral capsule) of D3 either per 1 week or per 2 weeks or per 6 weeks or no further supplementation for next 13 weeks. All the ‘Control’ patients received two oral capsules of placebo weekly for consecutive 26 weeks. Additionally, all patients of both groups were also advised to have sunlight exposure (within 11 to 14 hrs) at least for 5 to 15 minutes daily. After 26 weeks of follow up, both enzymes, serum 25(OH)D or Ca2+of all patients were measured by spectrophotometry. Data were analyzed by paired sample and independent sample ‘t’ test.&#x0D; Results: The baseline plasma SOD (14.80±3.86U/ml vs 11.95±4.03U/ml) and CAT (11.0±7.59U/ml vs14.41±4.83U/ml) in study and control was almost similar (p&gt;0.05). However, the mean SOD (18.98±2.98U/ml) and CAT (32.75±9.70U/ml) significantly increased (p&lt;0.01; p&lt;0.001) after 26 weeks of follow up only in ‘Study’ patients. In addition, both enzymes were significantly (p&lt;0.001) higher in the D3 supplemented patients than those of placebo treated patients after 26 weeks of follow up.&#x0D; Conclusion: The present study reveals that vitamin D3 supplementation increases the plasma antioxidant enzymes in D3 deficient patients with COPD.&#x0D; Trial registration: www.clinicaltrials.gov identifier NCT04011930&#x0D; J Bangladesh Soc Physiol. 2020, June; 15(1): 23-32

Long-Term Ketogenic Diet Induces Metabolic Acidosis, Anemia, and Oxidative Stress in Healthy Wistar Rats.

Background Ketogenic diet has been used as supportive therapy in a range of conditions including epilepsy, diabetes mellitus, and cancer. Objective This study aimed to investigate the effects of long-term consumption of ketogenic diet on blood gas, hematological profiles, organ functions, and superoxide dismutase level in a rat model. Materials and Methods Fifteen male Wistar rats were divided into control (n = 8) and ketogenic (n = 7) groups. Controls received standard diet contained 52.20% of carbohydrates, 7.00% fat, and 15.25% protein; meanwhile, the ketogenic group received a high-fat-low-carbohydrate diet which contained 5.66% of carbohydrate, 86.19% fat, and 8.15% protein. All rats were caged individually and received 30g of either standard or high-fat-low-carbohydrate pellets. The experiment was carried out for 60 days before the blood samples were taken and analyzed to obtain blood gas, cell counts, organ biomarkers, and plasma antioxidant superoxide dismutase (SOD) levels. Results The rats subjected to ketogenic diet experienced a marked decrease in body weight, blood sugar, and increased blood ketones (p < 0.05). The average blood pH was 7.36 ± 0.02 and base excess was −5.57 ± 2.39 mOsm/L, which were significantly lower than controls (p < 0.05). Hematological analysis showed significantly lower erythrocyte, hemoglobin, and hematocrit levels. No significant changes were found in alanine aminotransferase, aspartate aminotransferase, urea, and creatinine levels, indicating normal liver and kidney functions. Nevertheless, plasma SOD level significantly reduced with ketogenic diet. Conclusion Long-term ketogenic diet induces metabolic acidosis, anemia, and reduced antioxidant enzyme level in rats following 60 days of consuming high-fat-low-carbohydrate diet.

Hypomethylation of the cyclin D1 promoter in hepatitis B virus-associated hepatocellular carcinoma

The hypomethylation of the Cyclin D1 (CCND1) promoter induced by excess oxidative stress likely promotes the development of hepatitis B virus-associated hepatocellular carcinoma (HBV-HCC). We aimed to evaluate methylation status of the CCND1 promoter as a new plasma marker for the detection of HBV-HCC.We consecutively recruited 191 participants, including 105 patients with HBV-HCC, 54 patients with chronic hepatitis B (CHB), and 32 healthy controls (HCs). Using methylation-specific polymerase chain reaction, we identified the methylation status of the CCND1 promoter in plasma samples. We analyzed the expression levels of the CCND1 mRNA in peripheral blood mononuclear cells by using quantitative real-time PCR. We assessed the plasma levels of superoxide dismutase, 8-hydroxydeoxyguanosine and malondialdehyde by using enzyme-linked immunosorbent assays.Patients with HBV-HCC (23.81%) presented a reduced methylation frequency compared with patients with CHB (64.81%) or HCs (78.13%) (P < .001). When receiver operating characteristic curves were plotted for patients with HBV-HCC versus CHB, the methylation status of the CCND1 promoter yielded diagnostic parameter values for the area under the curve of 0.705, sensitivity of 76.19%, and specificity of 64.81%, thus outperforming serum alpha-fetoprotein (AFP), which had an area under the curve of 0.531, sensitivity of 36.19%, and specificity of 90.74%. Methylation of the CCND1 promoter represents a prospective diagnostic marker for patients with AFP-negative HBV-HCC and AFP-positive CHB. The expression levels of CCND1 mRNA was increased in patients with HBV-HCC compared with patients with CHB (Z = -4.946, P < .001) and HCs (Z = -6.819, P < .001). Both the extent of oxidative injury and antioxidant capacity indicated by the superoxide dismutase, 8-hydroxydeoxyguanosine and malondialdehyde levels were increased in patients with HBV-HCC. Clinical follow up of patients with HBV-HCC revealed a worse overall survival (P = .012, log-rank test) and a decreased progression-free survival (HR = 0.109, 95%CI: 0.031-0.384) for the unmethylated CCND1 group than methylated CCND1 group.Our study confirms that oxidative stress appears to correlate with plasma levels of CCND1 promoter methylation, and the methylation status of the CCND1 promoter represents a prospective biomarker with better diagnostic performance than serum AFP levels.