Serum Oxidative Stress Markers Research Articles

High BDNF serum levels are associated to good cognitive functioning in bipolar disorder

BackgroundNeurotrophins such as brain-derived neurotrophic factor (BDNF), inflammation and oxidative damage may contribute to the pathophysiology of bipolar disorder (BD) in terms of illness activity. To date, there is a lack of studies linking the cognitive impairment observed in BD with these neurobiological mechanisms. This study aimed to investigate the role of these neurobiological factors in clinical and cognitive outcomes in a sample of bipolar individuals. MethodsWe measured serum BDNF, cytokines and oxidative stress markers in a sample of 133 individuals: 52 euthymic bipolar patients, 32 manic patients and 49 healthy controls. They were all assessed with a comprehensive cognitive battery. Sociodemographic and clinical data were collected. Multiple linear regression models were built to study associations of neurotrophins and inflammatory and oxidative measures with cognitive functioning. ResultsBDNF levels were decreased in euthymic (p = 0.039) and manic (p < 0.001) individuals. Conversely, inflammatory (interleukin 6 (IL-6)) (p = 0.019) and oxidative stress (p = 0.003) measures were increased in bipolar individuals compared to controls. BDNF levels were associated with executive functioning (β = 0.01, p = 0.02) and verbal memory (β = 0.013, p = 0.005), together with other demographic variables. In particular, verbal memory was also associated with obesity (β=-0.04, p = 0.005). Neither inflammatory markers, oxidative stress markers nor other relevant clinical variables showed any association with cognitive outcome. ConclusionsOf all the peripheral neurobiological factors analysed, BDNF was the only one significantly associated with cognitive dysfunction in bipolar disorder individuals. This study emphasizes the role of BDNF not only across mood phases but also in cognitive functioning.

Platycodon grandiflorum Saponins attenuate scrotal heat-induced spermatogenic damage via inhibition of oxidative stress and apoptosis in mice

Abstract The aim of the present study was designed to investigate that Platycodon grandiflorum saponins (PGS) exerted protective effects against testicular injury induced by scrotal hyperthermia. PGS (15, 30 mg/kg) were administered intragastrically to mice for 14 days, then exposed to a single scrotal heat treatment at 43 °C for 18 min on the 7th day. Heat stress (HS) induced spermatogenic damage was associated with a significant loss of leydig cells and the changes of serum testosterone, oxidative stress and apoptosis markers, and activated MAPK signaling pathway. In contrast, PGS treatment normalized HS-induced histopathological changes and prevented the activation of MAPK signaling pathway, which was contributed to oxidative stress and apoptosis in the testis of treated mice. In conclusion, our findings clearly demonstrated that PGS exhibited a significant protective effect against HS-induced testicular dysfunction, largely dependent upon the inhibition of oxidative stress associated apoptosis via partly regulation of MAPK signaling pathway.

Impaired vascular function in exercising anovulatory premenopausal women is associated with low bone mineral density.

In estrogen-deficient post-menopausal women, osteoporosis shares a common link with cardiovascular disease risk, including endothelial dysfunction. The current study sought to examine associations between bone mineral density (BMD) and endothelial function in estrogen-deficient premenopausal women with exercise-associated menstrual disturbances. Recreationally trained women (24.3±0.8years; overall mean±SEM) who were estrogen deficient (amenorrheic or eumenorrheic anovulatory cycles; E2Def; n=13) or estrogen replete (eumenorrheic ovulatory cycles; E2Rep; n=14) were studied. Total body and lumbar BMD (L1-L4) were determined using dual-energy X-ray absorptiometry. Serum markers of oxidative stress (oxidized low-density lipoprotein; OxLDL), energy deficiency (triiodothyronine), and bone turnover (osteocalcin, c-telopeptide X, P1NP) were assessed. Estrogen exposure was determined by assessing daily urinary estrone-3-glucuronide (E1G) across a monitoring period. Calf blood flow (CBF), an index of endothelial function, was measured using strain-gauge plethysmography. CBF, total body and L1-L4 BMD, triiodothyronine and E1G were lower (P<0.05), and c-telopeptide crosslinks higher (P<0.05) in E2Def. Osteocalcin and OxLDL did not differ (P>0.05) between groups. L1-L4 BMD, osteocalcin, and E1G were the strongest predictors of CBF (R2 =0.615, P<0.001). CBF was the strongest predictor of L1-L4 BMD (R2 =0.478, P<0.001). L1-L4 (r=0.558, P=0.008) and CBF (r=0.534, P=0.004) were independently correlated with E1G. In young recreationally trained premenopausal women with anovulatory menstrual disturbances, low CBF predicts decreased lumbar BMD, suggesting impaired peripheral endothelial function may predict early unfavorable changes in bone metabolism. This finding may be of relevance in the early detection of cardiovascular and bone health decrements in otherwise healthy estrogen-deficient premenopausal women.

Antioxidant and Anti-Inflammatory Effects of Nano-Selenium against Cypermethrin-Induced Liver Toxicity

Cypermethrin (Cym) is a synthetic class II pyrethroid that is widely used and has a big risk to health. Cypermethrin produces oxidative stress and enhances inflammatory damage of liver. The present study was designed to investigate the ameliorating effects of NSe against Cym-induced hepatotoxicity in rats. For this purpose, twenty four male rats were divided into three groups. Group (I) was gavaged with Cym (control group), group (II) gavaged daily with Cym (1 mg/kg body weight), and group (III) gavaged with Cym + NSe (2.5 mg kg body weight/day, three times a week) for 21 days. Cypermethrin increased serum liver enzymes, oxidative stress and inflammatory markers. Administration of NSe significantly reduced the increased serum liver enzymes and inflammatory parameters and restored the antioxidant capacity in liver. Our results suggest that Nse exhibits promising hepato-protective effects against Cym-induced oxidative damage and inflammation.

Influence of the TLR4-mediated p38MAPK signaling pathway on chronic intermittent hypoxic-induced rat's oxidative stress and inflammatory cytokines in rats.

To investigate the influence of the TOLL-like receptor 4 (TLR4)-mediated p38MAPK signaling pathway on chronic intermittent hypoxic (CIH)-induced oxidative stress and inflammatory cytokines in rats. A total of 120 healthy male Sprague Dawley (SD) rats, aged between 8-10 weeks, were randomly divided into 9 groups (normoxia control group, CIH 2 weeks group, CIH 4 weeks group, CIH 6 weeks group, CIH 8 weeks group, CIH 6 weeks + p38MAPK receptor inhibit group, CIH 6 weeks + Tempol group, CIH 8 weeks + p38MAPK receptor inhibitor group and CIH 8 weeks + Tempol group). The expression of TLR4 and p38MAPK in the adipose tissue was evaluated, as well as the level of serum oxidative stress markers (SOD, TRx-1, MDA) and inflammatory cytokines (adiponectin, TNF-α, hsCRP and IL-6). RT-PCR and Western-blot were conducted to detect the expression of TLR4 and p38MAPK mRNA. With increased hypoxia, the levels of SOD and adiponectin in the serum of the CIH group decreased significantly, and the levels of TNF-α, hsCRP, IL-8 and IL-6 in serum increased significantly. After the intervention of antioxidant Tempol and p38MAPK inhibitor SB203580, SOD increased significantly but with significant MDA reduction. The levels of TNF-α, hsCRP, IL-8 and IL-6 in serum significantly decreased. The results of RT-PCR and Western-Blot indicated that the P-p38 and TLR4 proteins related to the MAPK pathway were expressed in rat adipose tissue. With the hypoxia intensity, expression of P-p38 decreased after initially increasing. The expression of TLR4 showed a continuously growing trend. After Tempol treatment, the expression of p38MAPK protein decreased, and the expression of TLR4 did not change significantly, indicating the inhibiting effect of Tempol on p38MAPK, without a significant inhibiting effect on TLR4. The TLR4-mediated p38MAPK signaling pathway was active in adipose tissue and the expression of the corresponding molecules increased as the duration of intermittent hypoxia increased. The expression of TLR4 and p38MAPK components regulated the level of oxidative stress and inflammatory cytokines; the application of p38MAPK inhibitors and antioxidant free radical scavengers improved the levels of oxidative stress and inflammatory cytokines.

Effects of Percutaneous Kyphoplasty on Bone Metabolism and Oxidative Stress in Elderly Patients with Osteoporotic Spinal Fractures.

To investigate the effects of percutaneous kyphoplasty on bone metabolism and oxidative stress in elderly patients with osteoporotic spinal fractures. An experimental study. Department of Orthopedics, ZhangYe People's Hospital Affiliated to HeXi University, from February 2016 to October 2017. A total of 100 elderly patients with osteoporotic spinal fractures were randomly divided into the observation group treated with percutaneous kyphoplasty (PKP) and the control group treated with percutaneous vertebroplasty (PVP), with 50 cases in each group. One month after surgery, the content of serum bone metabolic markers bone gla protein (BGP), carboxyl-terminal collagen I crosslinks (- &beta;), bone alkaline phosphatase (BALP) and tartrate-resistant acid phosphatase (TRACP), oxidative stress markers malondialdehyde (MDA), total antioxidant capacity (TAC) and superoxide dismutase (SOD) were compared between the two groups. Visual analogue scale (VAS) and the Oswestry Disability Index (ODI) were used to evaluate the degree of pain and functional status of the two groups, and the Cobb angles were measured in both groups. One month after surgery, the level of the serum bone metabolic marker BGP in the observation group was higher than the control group (p<0.001), and the levels of -CTX, BALP and TRACP in the observation group were lower than the control group (all p<0.001). The level of the serum oxidative stress marker MDA in the observation group was lower than the control group (p<0.001), and the levels of TAC and SOD in the observation group were higher than the control group (all p<0.001). There were no significant differences in VAS scores and ODI values between the two groups (p=0.806 and 0.913, respectively). Cobb's angle of the injured vertebrae in the observation group was smaller than the control group (p<0.001). Compared with PVP, PKP is more effective in treating elderly patients with osteoporotic spinal fractures. It can effectively optimise bone metabolism, promote fracture healing, and reduce the oxidative stress reactions after surgery, with a relatively larger application value.

Enhanced oxidative stress and the treatment by edaravone in mice model of amyotrophic lateral sclerosis.

Oxidative stress is associated with the degeneration of both motor neurons and skeletal muscles in amyotrophic lateral sclerosis (ALS). A free radical scavenger edaravone has been proven as a therapeutic drug for ALS patients, but the neuroprotective mechanism for the oxidative stress of ALS has not been fully investigated. In this study, we investigated oxidative stress in ALS model mice bearing both oxidative stress sensor nuclear erythroid 2-related factor 2 (Nrf2) and G93A-human Cu/Zn superoxide dismutase (Nrf2/G93A) treated by edaravone. In vivo Nrf2 imaging analysis showed the accelerated oxidative stress both in spinal motor neurons and lower limb muscles of Nrf2/G93A mice according to disease progression in addition to the enhancement of serum oxidative stress marker dROMS. These were significantly alleviated by edaravone treatment accompanied by clinical improvements (rotarod test). The present study suggests that in vivo optical imaging of Nrf2 is useful for detecting oxidative stress in ALS, and edaravone alleviates the degeneration of both motor neurons and muscles related to oxidative stress in ALS patients.

ANTIHYPERGLYCEMIC AND ANTIOXIDATIVE EFFECTS OF LYGODIUM MICROPHYLLUM IN ALLOXAN INDUCED DIABETIC RATS

Objective: The antihyperglycemic and antioxidative effects of L. microphyllum were evaluated by using in vivo methods in normal and alloxan induced diabetic rats.Methods: Diabetes was induced in Sprague Dawley rats by injecting alloxan through intravenous (i. v) at a dose of 100 mg/kg of body weight. Aqueous extract of L. microphyllum at different doses (400, 200 and 100 mg/kg of body weight) was administered orally (orogastric intubation) for 14 d. Blood glucose and oxidative stress markers were measured. Hematoxylin and eosin staining method were used to examine the pancreatic tissues.Results: At the 14 d interval, fasting blood glucose showed a reduction in serum glucose levels in animals pretreated with L. microphyllum compared with alloxan alone treated group. Oxidative stress was noticed in rat’s pancreatic tissue as evidenced by a significant decrease in glutathione level, glutathione reductase, glutathione-S-transferase, and catalase activities. Malondialdehyde showed a significant increase compared to the normal saline-treated control group. Serum biochemistry and oxidative stress markers were consistent with the pancreatic histopathological studies. Treatment of diabetic rats with L. microphyllum at a dose level of 100, 200 and 400 mg/kg body weight leaves extract for 14 d significantly prevented these alterations and attenuated alloxan-induced oxidative stress (P&lt;0.05).Conclusion: The results of the present study indicated that the antihyperglycemic potential of L. microphyllum might be ascribable to its antioxidant and free radical scavenging properties. Thus, it is concluded that L. microphyllum may be helpful in the prevention of diabetic complications associated with oxidative stress.

Association of serum markers of oxidative stress with myocardial infarction and stroke: pooled results from four large European cohort studies.

Oxidative stress contributes to endothelial dysfunction and is involved in the pathogenesis of myocardial infarction (MI) and stroke. However, associations of biomarkers of oxidative stress with MI and stroke have not yet been addressed in large cohort studies. A nested case-control design was applied in four population-based cohort studies from Germany, Czech Republic, Poland and Lithuania. Derivatives of reactive oxygen metabolites (d-ROMs) levels, as a proxy for the reactive oxygen species burden, and total thiol levels (TTL), as a proxy for the reductive capacity, were measured in baseline serum samples of 476 incident MI cases and 454 incident stroke cases as well as five controls per case individually matched by study center, age and sex. Statistical analyses were conducted with multi-variable adjusted conditional logistic regression models. d-ROMs levels were associated with both MI (odds ratio (OR), 1.21 [95% confidence interval (CI) 1.05-1.40] for 100 Carr units increase) and stroke (OR, 1.17 [95% CI 1.01-1.35] for 100 Carr units increase). TTL were only associated with stroke incidence (OR, 0.79 [95% CI 0.63-0.99] for quartiles 2-4 vs. quartile 1). The observed relationships were stronger with fatal than with non-fatal endpoints; association of TTL with fatal MI was statistically significant (OR, 0.69 [95% CI 0.51-0.93] for 100μmol/L-increase). This pooled analysis of four large population-based cohorts suggests an important contribution of an imbalanced redox system to the etiology of mainly fatal MI and stroke events.

Polycystic ovarian syndrome is linked to increased oxidative stress in Omani women.

PurposeLiterature emerging from Western countries has reported increased levels of serum oxidative stress markers among polycystic ovarian syndrome (PCOS) women. In the Arab region, there is limited research about the association between oxidative stress and PCOS. This study aimed to compare sociodemographic and clinical characteristics, sex hormones, and oxidative stress indices between PCOS women and non-PCOS women and to investigate the correlation between oxidative stress biomarkers and sex hormones.MethodsThis hospital-based case-control study was conducted among reproductive-aged women. The study included 51 women diagnosed with PCOS (as per Rotterdam 2003 criteria) and 45 control women who were not diagnosed with PCOS. Serum samples were collected to measure the mean levels of the following sex hormones: total testosterone, dehydroepiandrosterone sulfate, estradiol and progesterone, as well as to measure biomarkers of oxidative stress including glutathione peroxidase (GPx), glutathione reductase (GR), glutathione (GSH), and total antioxidant capacity (TAC).ResultsPCOS women exhibited clinical characteristics including irregular menses, hirsutism, and acne compared to the control group (P≤0.05). Significant differences were observed in the waist-hip ratio of PCOS women compared to controls (P=0.004). GPx and GR activity levels appeared to be higher among PCOS women compared to controls; however, no statistically significant differences were observed between the two groups (P>0.05). PCOS women had lower GSH and TAC levels compared to controls with a statistically significant difference observed for GSH levels (P=0.006). Correlation analysis showed a significant negative correlation between estradiol and TAC in the total sample (r=−0.284, P=0.005).ConclusionThis study provides supportive evidence that oxidative stress might play a role in the pathogenesis of PCOS and, hence, oxidative stress parameters could be suggested as diagnostic markers for early diagnosis of high-risk groups. Also, the study provides supportive evidence that obesity and sex hormones, particularly estradiol, in PCOS may contribute to enhanced oxidative stress.

Adalimumab mitigates ovarian ischemia-reperfusion injury in rats by regulating oxidative stress, apoptosis and resolution of inflammation.

Ovarian torsion is a rare but an important reason of acute lower abdominal pain in women and associated with serious morbidity and mortality, if not treated promptly. The aim of this study was to evaluate the effects of an antitumor necrosis factor-α antibody on ovarian torsion in a rat model of ischemia-reperfusion (I/R) injury. Forty female Wistar Albino rats were used in the present study. The rats were randomly divided into four groups: group I (sham), group II (I/R), group III (I/R + isotonic saline) and group IV (I/R + adalimumab). The I/R model was induced by torsion of both ovaries. Immunohistochemical staining for interleukin-1β (IL-1β), nuclear factor-κB (NF-κB), and inducible nitric oxide synthase was performed. Tissue and serum oxidative stress markers in conjunction with apoptotic index (AI) with the terminal deoxynucleotidyl transferase dUTP nick end labeling method were also calculated. Tissue total oxidant status, oxidative stress index and nitric oxide values were significantly decreased, and tissue total antioxidant status was found to be increased in group IV. Inflammation, vascular congestion and hemorrhagia were significantly lower in adalimumab-treated group. Serum oxidative stress markers and tissue malondialdehyde levels did not differ in study groups. The AI was significantly increased in groups 2 and 3. Adalimumab treatment significantly decreased the AI. Adalimumab therapy in rats attenuated I/R induced ovarian injury, possibly suppressing inflammation, inhibiting oxidative stress, and altering apoptotic pathways.

Serum Oxidative Stress Marker Levels in Unmedicated and Medicated Patients with Schizophrenia.

Oxidative stress has been suggested to be involved in schizophrenia, but studies have demonstrated inconsistent results on oxidative stress marker level/activity in patients with schizophrenia. In order to clarify the circulating oxidative stress marker level/activity in patients with schizophrenia, this study recruited 80 schizophrenia patients (40 first-episode, drug-free and 40 chronically medicated patients) and 80 controls to analyze serum activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC), and levels of lipid peroxidation marker malondialdehyde (MDA) in schizophrenia patients, and whether they associate with the severity of the disease. We showed that only serum GSH-Px activity was significantly reduced in unmedicated patients with schizophrenia when compared with control subjects, whereas the other three analyzed oxidative stress markers did not show significant differences between cases and controls. Moreover, our results demonstrated that chronic medication increased GSH-Px activity and MDA levels in patients with schizophrenia, but reduced SOD activity in the patients. We also found that short-term antipsychotic treatments on the patients with schizophrenia reduced the SOD activity. Correlation analyses indicated that the oxidative stress marker activity/level is not significantly associated with the severity of schizophrenia, except that SOD level correlated with PANSS positive score significantly. Taken together, the data from the present study suggested that the dysfunctions of oxidative stress markers in patients with schizophrenia were mainly caused by antipsychotics, emphasizing increased oxidative stress as a potential side effect of antipsychotics on the patients.

Associations of serum fetuin-A and oxidative stress parameters with polycystic ovary syndrome.

ObjectiveThe aim of this study was to compare serum fetuin-A levels and oxidative stress markers, as indicators of insulin resistance, in women with polycystic ovary syndrome (PCOS) and in healthy controls.MethodsThis prospective case-control study included 46 patients with PCOS and 48 age- and body mass index–matched control women. Levels of serum hormones, fetuin-A, and oxidative stress markers were measured in blood samples taken during the early follicular period from each participant.ResultsFollicle-stimulating hormone (FSH), luteinising hormone (LH), total testosterone levels, and the LH/FSH ratio were found to be significantly higher in women with PCOS than in controls. Serum total antioxidant status, total oxidant status, and oxidative stress index parameters all indicated significantly higher levels of oxidative stress in PCOS patients than in controls. Serum fetuin-A levels, which were analyzed as an indicator of insulin resistance, were higher in the PCOS group than in the control group (210.26±65.06 µg/mL and 182.68±51.20 µg/mL, respectively; p=0.024).ConclusionThe data obtained from the present study suggest that higher levels of both serum fetuin-A and oxidative stress markers might be related with PCOS.

Evaluation of neuroprotective effects of insulin on immuno-inflammatory and systemic disorders induced by kaliotoxin, a Kv1.3 channel blocker.

Kaliotoxin2 (KTX2) is a highly selective blocker of voltage-dependent potassium channels Kv1.3 containing 37 amino acid residues. It is purified from Androctonus australis scorpion venom. The binding of KTX2 to its targets is able to alter the neuronal excitability leading to neurological disorders, accompanied by an inflammatory response. In brain, activation of insulin receptor signaling pathway by insulin induces current suppression and concomitant tyrosine phosphorylation of Kv1.3 channel. The aim of this study is to evaluate the effect of insulin injected by i.c.v. route on the neuro-pathophysiological and systemic disorders induced by KTX2. Tissue damage, inflammatory response and oxidative stress biomarkers were assessed in NMRI mice at 24h after co-injection of KTX2 and insulin by intracerebroventricular route. Obtained results revealed that the central administration of insulin prevents cerebral cortex injury, brain edema and blood-brain barrier alteration induced by KTX2, these are accompanied by significant decrease of systemic disorders including serum cytokines, inflammatory and oxidative stress markers and tissue damage. These results indicate that insulin is able to reduce neuro-immunological effects and systemic disorders induced by KTX2. The neuroprotective effect of insulin may be due to its crucial role in the regulation of inflammation response and its properties to modulate the activity of Kv1.3 channels in brain.

Efficacy of Melatonin on Serum Pro-inflammatory Cytokines and Oxidative Stress Markers in Relapsing Remitting Multiple Sclerosis

Multiple sclerosis (MS) is a chronic inflammatory disease, which leads to focal plaques of demyelination and tissue injury in the central nervous system (CNS). Neuroinflammation and oxidative stress are involved in the pathogenesis of MS, promoting tissue damage and demielinization. Current research findings suggest that melatonin has antioxidant and neuroprotective effects. The aim of this study was to evaluate the efficacy of melatonin on serum pro-inflammatory cytokines and oxidative stress markers in relapsing-remitting multiple sclerosis (RRMS). 36 patients diagnose with RRMS treated with Interferon β-1b (IFNβ-1b) were enrolled in a double bind, randomized, placebo controlled trial. The experimental group received orally 25mg/d of melatonin for 6months. After melatonin administration, we observed a significant decrease in serum concentration of pro-inflammatory cytokines and oxidative stress markers; 18% for TNF-α (p <0.05), 34.8% for IL-1β (p <0.05), 34.7% for IL-6 (p <0.05), 39.9% for lipoperoxides (LPO) (p <0.05) and 24% for nitric oxide catabolites (NOC) levels (p <0.05), compared with placebo group. No significant difference in clinical efficacy outcomes were found between groups. Melatonin treatment was well tolerated and we did not observe significant differences in rates of side effects between the two groups. We concluded that melatonin administration during 6months period is effective in reducing levels of serum pro-inflammatory cytokines and oxidative stress markers in patients with RRMS. These data support future studies evaluating the safety and effectiveness of melatonin supplementation in RRMS patients.

ASSESSMENT OF SERUM PARAOXONASE-1 ENZYME ACTIVITY, MALONDIALDEHYDE AND VITAMIN-C IN ORAL PREMALIGNANCIES

Background: Oral premalignancies are a group of disease or syndromes which if left untreated can lead to cancer. It carries a great significance in Indian perspective. The actual figure of oral cancers arising from oral premalignancies is not known and to predict accurately the malignant transformations of them is still not possible. Oxidative stress is a known player behind cancerogenesis. Recently decreased Paraoxonase-1 activity and increased oxidative stress markers ware found to be associated with Oral Squamous Cell Carcinoma. So, there is a strong possibility of a similar finding in Oral Premalignancies too. Aim: This study aims to investigate the correlation between serum PON-1 activity and oxidative stress markers (MDA &amp; Vitamin C) in patients with Oral Premalignancies. Material and Methods: A total of 62 patients with clinically diagnosed oral premalignant lesions and diseased controls were chosen for the study. Venous blood samples were collected and PON-1, MDA (in serum) &amp; Vitamin c (in plasma) were analysed spectro-photometrically. Results: significant decreased serum PON-1 activity (P&lt;0.05) and concomitant significantly increased serum MDA (P &lt;0.05) and decreased Vitamin C levels (P&lt;0.05) were observed in premalignancies compared to the controls. These finding were more pronounced in Oral Leukoplakia (OL) than in Oral Submucous Fibrosis (OSMF) with a significant difference. Mean levels of the analysed parameters differed accordingly in the clinical grades of oral premalignancies. Conclusion: It can be envisaged that serum PON-1 activity and increased oxidative stress might be a contributing factor behind pathogenesis and progression of Oral Premalignant Diseases.

Effects of vitamin C on the outcome of in vitro fertilization-embryo transfer in endometriosis: A randomized controlled study.

ObjectiveThis study was performed to investigate the effect of vitamin C (VitC) supplementation on the outcomes of in vitro fertilization–embryo transfer (IVF-ET) in patients with endometriosis (EMs).MethodsA total of 280 patients with EMs underwent IVF-ET (VitC treatment group, n=160; VitC non-treatment group, n=120). An additional 150 patients who did not have EMs but underwent IVF-ET (control group) were also enrolled in this study. Superoxide dismutase (SOD), total antioxidant capacity (TAC), malondialdehyde (MDA) and reactive oxygen species (ROS) were measured to determine the role of VitC on oxidative stress markers in serum and follicular fluid (FF).ResultsIn total, 245 patients with EMs and 132 patients without EMs underwent successful IVF-ET and follow-up. The serum or FF levels of VitC, SOD, and TAC were lower in the EMs than control group; however, the MDA and ROS levels in serum or FF were higher in the EMs than control group. After 2 months of VitC treatment, the serum VitC levels in serum and FF were significantly increased, while oxidative stress markers were unaffected.ConclusionTreatment with VitC oral formulation improved the serum and FF levels of VitC but did not affect oxidative stress markers in patients with EMs.

Association of serum markers of oxidative stress with myocardial infraction and stroke: Pooled results from four large European cohort studies

Introduction Oxidative stress contributes to endothelial dysfunction and is involved in the pathogenesis of myocardial infarction (MI) and stroke. However, associations of biomarkers of oxidative stress with MI and stroke have not yet been addressed in large cohort studies. Methods A matched case-control design was applied in four population-based cohort studies from Germany, Czech Republic, Poland and Lithuania. Derivatives of reactive oxygen metabolites (d-ROM) levels, as a proxy for the reactive oxygen species (ROS) burden, and total thiol levels (TTL), as a proxy for the reductive capacity, were measured in serum samples of 476 incident MI cases and 454 incident stroke cases as well as five controls per case individually matched by study center, age and sex. Statistical analyses were conducted with multi-variable adjusted conditional logistic regression models. Results d-ROM levels were associated with both MI (odds ratio [OR]: 1.21 [95% confidence interval (CI): 1.05–1.40] for 100 Carr units increase) and stroke (OR: 1.17 [95% CI: 1.01–1.35] for 100 Carr units increase). TTL were only associated with stroke incidence (Quartiles 2–4 vs. quartile 1: OR: 0.79 [95% CI: 0.63–0.99]). The noted relationships were stronger with fatal than with non-fatal endpoints and the associations of TTL with fatal MI was statistically significant (OR: 0.69 [95% CI: 0.51–0.93] for 100 μmol/L-increase). Conclusions This pooled analysis of four large cohort studies suggests an important contribution of an imbalanced redox system to the etiology of mainly fatal MI and stroke events.

Effects of maternal serine supplementation on high-fat diet-induced oxidative stress and epigenetic changes in promoters of glutathione synthesis-related genes in offspring

To elucidate the effects of maternal serine supplementation during pregnancy on high-fat (HF) diet-induced oxidative stress in the offspring and the epigenetic mechanisms involved, a control diet, HF diet, or HF diet supplemented with different concentrations of serine dissolved in water was fed to C57BL/6J mouse dams during gestation. Eight male offspring from each dietary group were sacrificed at weaning, Consequently, the serum and hepatic oxidative stress markers and lipid levels in weanlings from dams fed the HF diet supplemented with 1% serine were lower than those of offspring from dams fed the HF diet. Maternal serine supplementation prevented promoter DNA hypermethylation of HF diet-induced glutathione synthesis-related genes, and increased the gene expression and resultant protein contents in the weanlings. Our results therefore suggest that maternal serine supplementation during pregnancy alleviates HF diet-induced oxidative stress by epigenetically regulating glutathione synthesis in the weanling.

The evaluation of protective and mitigating effects of vitamin C against side effects induced by radioiodine therapy.

The goal of this study was to evaluate the protective and mitigative effect of vitamin C on oxidative stress in differentiated thyroid cancer (DTC) patients ablated with radioiodine. 58 DTC patients selected for radioactive iodine therapy (RAIT) with 5550MBq 131Iodine were divided into four groups. Group 1 (control group) consisted of patients who underwent RAIT routinely. Other patients received 1500mg vitamin C daily 2days after (group 2), 2 days before to 2days after (group 3) and 2days before RAIT (group 4). Serum oxidative stress markers including malondialdehyde (MDA), glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) were measured immediately before and 2days after RAIT. A significant increase in MDA after RAIT was observed in all groups (p < 0.05). The concentrations of MDA were significantly higher in the control group compared to the intervention groups (p < 0.05). A significant decrease in the control group (p < 0.05) and increase in group 4 (p < 0.05) were observed in GSH level after RAIT (p < 0.05). Mean variation of GSH was significant between control group with groups 3 (p < 0.01) and 4 (p < 0.01). The results indicate that activity of SOD remained unchanged in all groups (p > 0.05). A significant increase was observed in CAT activity after RAIT in all groups (p < 0.05), which was higher in control group than intervention groups. In groups 3 (p < 0.05) and 4 (p < 0.05), this increase in CAT activity was significantly lower than the control group. RAIT causes serum oxidative stress, which can be ameliorated using vitamin C as an antioxidant. These results indicate that radioprotective effect of vitamin C is preferable to its mitigative effect.