Biological Markers Of Oxidative Stress Research Articles

The corrective effect of Au/Ag/Fe nanoparticles on oxidative stress in terms induced colon adenocarcinoma

ABSTRACT. Studying biological markers of oxidative stress is crucial and relevant, as this process can trigger the transition from an organ's "normal state" to a "malignant lesion". The use of metal nanoparticles to correct oxidative stress manifestations in oncology is one of the most popular subjects of modern science and is actively being introduced into modern medicine. Practically all possible types of nanoparticles have found their use in solving different problems in oncology. Therefore, our study aimed to investigate the possibility of Au/Ag/Fe nanoparticles use for the correction of redox balance disorders of the antioxidant system under the conditions of induced colon adenocarcinoma. Materials and methods. The study was performed on 150 white male rats. Animals were kept in standard vivarium conditions. Division of experimental rats into groups: I - control intact group (40 individuals); II - experimental group (70 individuals) with N,N-dimethylhydrazine hydrochloride administration once a week for 30 weeks; ІІІ – an experimental group (40 animals) with daily intragastric administration of Au/Ag/Fe nanoparticles. Oxidative stress was assessed in colon tissue homogenate by changes in the concentrations of 8-iso-prostaglandin F2α (8-iso-PGF2α), TBC-active products, diene and triene conjugates, Schiff bases, as well as by the activities of catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, and reduced glutathione. Results. Due to this research, we established that Au/Ag/Fe nanoparticles use leads to a decrease in the concentration of 8-iso-prostaglandin F2α (8-iso-PGF2α), TBC-active substances, diene, triene conjugates, Schiff bases. As a result of the above, we observed a reduction of manifestations of oxidative stress and restoration of enzymes of the antioxidant system and its biological mediators of a non-enzymatic nature. The activity of catalase, superoxide dismutase, glutathione peroxidase, and the concentration of reduced glutathione was restored to control indicators. Conclusions. Therefore, the use of Au/Ag/Fe nanoparticles leads to the restoration of the balance of redox equilibrium, improving the antioxidant system with induced adenocarcinoma of the large intestine.

Ameliorative effects of phlorotannin-rich fraction of Sargassum tenerrimum in high-fat diet and low dose streptozotocin-induced metabolic changes and oxidative stress in diabetic rats

Introduction: Type 2 diabetes mellitus (T2D) is a progressing polygenic disease demanding a multitargeted treatment strategy. Sargassum tenerrimum (ST) is a marine brown alga with potentially bioactive chemicals that could be used as innovative biotherapeutics for diabetes treatment. The current research examined the potential of the phlorotannin-rich fraction from S. tenerrimum (PST) to mitigate diabetes in Wistar albino rats induced with high-fat diet (HFD) and streptozotocin (STZ) administration. Methods: Diabetic rats were given PST (200 and 400 mg/kg) or metformin (250 mg/kg) orally three weeks, and followed by the measurements of insulin, glycemic factors, biological markers of oxidative stress, tumor necrosis factor-alpha (TNF-α), as well as hepatic and pancreatic histopathological changes. Results: PST treatment significantly decreased fasting blood glucose, insulin resistance, lipid profile, hepatic profile, and TNF- α levels and improved serum insulin and glucose tolerance in diabetic rats. In the skeletal muscles of diabetic rats, PST led to a significant rise in antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) reductase, and a decrease in lipid peroxidation. Furthermore, PST treatment significantly reduced pancreatic-cell damage and hepatic fatty accumulation. PST was more efficacious at 400 mg/kg exhibiting a dose-dependent effect. Conclusion: PST improves glucolipid metabolism in HFD and STZ-induced diabetic rats, probably by reducing hyperglycemia, insulin resistance, dyslipidemia, oxidative stress, inflammation, and damage to pancreatic and hepatic architectures. The findings suggest that PST has a curative impact on diabetes mellitus type 2 and represents a new subject of study for the treatment of diabetes naturally.

Performance, blood biochemistry, carcass fatty acids, antioxidant status, and HSP70 gene expressions in Japanese quails reared under high stocking density: the effects of grape seed powder and meal.

Japanese quails reared under high stocking density (SD) were evaluated for the effects of grape seed powder (GSP) and meal (GSM) supplementation on performance, blood biochemistry, thigh and breast muscle fatty acids, antioxidant status, and HSP70 gene expression. We randomly assigned 288 (15-day-old) quail chicks to six treatment groups in a factorial design (2 × 3) with four replicates, involving two density levels [160 cm2/bird (LD) and 80 cm2/bird (HD)] and three feed forms (FFs) [no supplementation, grape seed powder (3% GSP), grape seed meal (3% GSM)]. SD had a significant effect on live weight, but not on weekly feed intake, daily weight gain, and feed conversion ratio. Serum creatinine and aspartate aminotransferase levels were significantly affected by FF and SD × FF (p < 0.05). A high SD reduced the n-3/n-6 ratio of breast muscle and a significant interaction was found between FF (p < 0.001). The SD × FF interaction reduced the Σn-6 ratio in HDM's thigh muscle, whereas in LDM, the ratio increased (p < 0.01). At high SD, neither GSP nor GSM reduced biological markers of oxidative stress (p > 0.05). Compared to GSP, GSM had higher efficacy at reducing HSP70 levels related to high SD levels. Despite this, at high SD, a diet containing 3% of GSP and GSM was not effective in overcoming oxidative stress. Therefore, more studies using different doses of GSM and GSP in quail diets would be beneficial.

Parameter Estimation for Quantitative EPR Spectroscopy

Electron paramagnetic resonance (EPR) is a spectroscopy and imaging method based on detecting the spin resonance of electrons. EPR is particularly suited for detecting and quantifying free radicals and biological markers of oxidative stress, for which it is the only quantitative imaging method at the moment. Its application in clinical contexts is a major challenge because of the lack of standardized procedures for estimating the measurement quality. Previous work analyzed the Lorentzian model of single-line EPR spectra in the derivative limit. For the general case, a modified acquisition procedure called overmodulation improves the signal-to-noise ratio (SNR). This article studies single-line EPR spectra with Lorentzian line shape under overmodulation and proposes maximum likelihood estimates (MLEs) as well as formulas for the expected relative error. The results are validated with simulated spectra and in vitro experimental results. The computed relative error is shown to be a good estimate of the observed instrumental variation.

Identification of potential oxidative stress biomarkers for spinal cord injury in erythrocytes using mass spectrometry.

Oxidative stress is a hallmark of secondary injury associated with spinal cord injury. Identifying stable and specific oxidative biomarkers is of important significance for studying spinal cord injury-associated secondary injury. Mature erythrocytes do not contain nuclei and mitochondria and cannot be transcribed and translated. Therefore, mature erythrocytes are highly sensitive to oxidative stress and may become a valuable biomarker. In the present study, we revealed the proteome dynamics of protein expression in erythrocytes of beagle dogs in the acute and subacute phases of spinal cord injury using mass spectrometry-based approaches. We found 26 proteins that were differentially expressed in the acute (0-3 days) and subacute (7-21 days) phases of spinal cord injury. Bioinformatics analysis revealed that these differentially expressed proteins were involved in glutathione metabolism, lipid metabolism, and pentose phosphate and other oxidative stress pathways. Western blot assays validated the differential expression of glutathione synthetase, transaldolase, and myeloperoxidase. This result was consistent with mass spectrometry results, suggesting that erythrocytes can be used as a novel sample source of biological markers of oxidative stress in spinal cord injury. Glutathione synthetase, transaldolase, and myeloperoxidase sourced from erythrocytes are potential biomarkers of oxidative stress after spinal cord injury. This study was approved by the Experimental Animal Centre of Ningxia Medical University, China (approval No. 2017-073) on February 13, 2017.

Plasma GSH levels and Alzheimer's disease. A prospective approach.: Results from the HELIAD study

BackgroundPotential links between oxidative stress and the pathophysiology of Alzheimer's disease (AD) have been reported in the existing literature. Biological markers of oxidative stress, such as the reduced form of glutathione (GSH), may have a potential role as predictive biomarkers for AD development. The aim of the present study was to explore the longitudinal associations between plasma GSH and the risk of developing AD or cognitive decline, in a sample of community-dwelling, non-demented older adults. MethodsParticipants from the Hellenic Longitudinal Investigation of Aging and Diet (HELIAD) were included in the present prospective study. The sample used in the analyses consisted of 391 non-demented individuals over the age of 64 (mean age = 73.85 years; SD = 5.06), with available baseline GSH measurements and longitudinal follow-up. Plasma GSH was treated both as a continuous variable and as tertiles in our analyses. Cox proportional hazards models were used to evaluate the hazard ratio (HR) for AD incidence as a function of baseline plasma GSH. Generalized estimating equations (GEE) models were deployed to explore the associations between baseline plasma GSH and the rate of change of performance scores on individual cognitive domains over time. Models were adjusted for age, years of education and sex. Supplementary exploratory models were also adjusted for mild cognitive impairment (MCI) at baseline, risk for malnutrition, physical activity and adherence to the Mediterranean dietary pattern. ResultsA total of 24 incident AD cases occurred during a mean (SD) of 2.99 (0.92) years of follow-up. Individuals in the highest GSH tertile group (highest baseline plasma GSH values) had a 70.1% lower risk for development of AD, compared to those in the lowest one [HR = 0.299 (0.093–0.959); p = 0.042], and also demonstrated a slower rate of decline of their executive functioning over time (5.2% of a standard deviation less decline in the executive composite score for each additional year of follow-up; p = 0.028). The test for trend was also significant suggesting a potential dose-response relationship. ConclusionIn the present study, higher baseline plasma GSH levels were associated with a decreased risk of developing AD and with a better preservation of executive functioning longitudinally.

Biological markers of oxidative stress in exhaled air

Biological markers of oxidative stress in exhaled air

2,4-D exposure and urinary markers of oxidative DNA damage and lipid peroxidation: a longitudinal study

Objective2,4-Dichlorophenoxyacetic acid (2,4-D) is a herbicide that is commonly used commercially, agriculturally and residentially worldwide. There is concern about its potential for carcinogenicity based on studies in laboratory animals demonstrating...

Cardioprotective effect of levosimendan against homocysteine-induced mitochondrial stress and apoptotic cell death in H9C2

Levosimendan is a cardiac inotropic and vasodilator agent that has been reported to have anti-oxidative, anti-inflammatory, and smooth muscle vasodilatory properties. The purpose of this study was to examine the effect of levosimendan on homocysteine-induced cardiomyocyte injury and to explore its underlying mechanisms. H9C2 myocardial cells were incubated with levosimendan 30 min before exposure to homocysteine (Hcy) for 24 h. The effect of levosimendan on cell viability was assessed using the MTT assay. Biological markers of oxidative stress were examined by assessment of lipid peroxidation (LPO), total antioxidant power (TAP), and total thiol groups. Moreover, the expression of caspase-3, Bcl-2, and Bax proteins was determined by western blot analysis. These results showed that levosimendan increased survival of cardiomyocytes in Hcy condition. Treatment with levosimendan decreased lipid peroxidation level. It also enhanced the TAP and total thiol groups. Further, levosimendan pretreatment upregulated the expression of Bcl-2 and downregulated the expression of Bax. The experiments also demonstrated that levosimendan could decrease the expression and activity of caspase-3, which is a key factor in regulating apoptosis. Taken together, these results indicated that levosimendan protects H9C2 myocardial cells against Hcy-induced oxidative stress and apoptosis by scavenging free radicals and modulating the mitochondrial-mediated apoptotic signaling pathway.

Multiple Micronutrient Plasma Level Changes Are Related to Oxidative Stress Intensity in Critically Ill Children.

Micronutrient supplementation in critically ill adults remains controversial. In the pediatric setting, the impact of oxidative stress on the overall micronutrient status has been poorly explored, due to the limited number of studies and to confounding factors (i.e., malnutrition or extra losses). In order to better understand this phenomenon, we aim to describe micronutrient status, focusing on seven micronutrients, in well-nourished critically ill children presenting with severe oxidative stress. Prospective, transversal, observational, single-center study. PICU, and anesthesiology department, Lyon, France. Three groups of patients were clinically defined: severe oxidative stress PICU group (at least two organ dysfunctions), moderate oxidative stress PICU group (single organ dysfunction), and healthy control group (prior to elective surgery); oxidative stress intensity was controlled by measuring plasma levels of glutathione peroxidase and glutathione. Children presenting any former condition leading to micronutrient deficiency were excluded (malnutrition, external losses). Plasma levels of selenium, zinc, copper, vitamin A, vitamin E, vitamin C, and β-carotene were measured in PICU oxidative stress conditions and compared with those of healthy children. Two hundred one patients were enrolled (51, 48, and 102 in severe, moderate, and healthy control groups, respectively). Median age was 7.1 years (interquartile range, 2.1-13.8 yr). There was a significant trend (p < 0.02) toward plasma level decrease of six micronutrients (selenium, zinc, copper, vitamin E, vitamin C, and β-carotene) while oxidative stress intensity increased. Biological markers of oxidative stress (glutathione peroxidase and glutathione) were in accordance with the clinical definition of the three groups. A multiple micronutrient deficiency or redistribution occurs in critically ill children presenting with severe oxidative stress. These findings will help to better identify children who might benefit from micronutrient supplementation and to design adapted supplementation trials in this particular setting.

Evaluation of oxidative stress and brain-derived neurotrophic factor levels related to crack-use detoxification

Crack is a central nervous system stimulant extracted from the Erythroxylum coca plant. It is considered the most potent and addictive form of cocaine, and its euphoric effects are attained within a few seconds after consumption. Alteration of biological markers of oxidative stress and brain-derived neurotrophic factor (BDNF) could be related to the severity of crack withdrawal symptoms in patients undergoing rehabilitation. Thus, the objective of this study was to evaluate if the crack consumption and the drug detoxification process during 14 days in hospitalization regime was able to modify the oxidative status and BDNF levels, in male crack-abstinent patients. The crack detoxification process increased the glutathione (GSH), total thiol content (GST), nitric oxide (NO), and superoxide dismutase (SOD) levels, and reduced the mean BDNF levels. Moreover, a positive correlation was found between the number of hospital admission days and SOD values and between the GST levels and crack-use time after 14 days of detoxification. Furthermore, a negative correlation between the frequency of crack use and NO levels on the first day of hospitalization was also found. In conclusion, the results of this study indicated that crack consumption causes increased oxidative stress in drug users and that the detoxification process during 14 days was sufficient to improve oxidative parameters and antioxidant defenses of the patients, which could positively contribute to rehabilitation process. In addition, we also observed a great variability in the BDNF levels of the patients during the detoxification process, resulting in a reduction in the mean values of this neurotrophin.

Biological markers of oxidative stress and allopurinol therapy: A meta-analysis of randomized controlled trials

Aim: Oxidative stress contributes to the development of atherosclerosis via production of reactive oxygen species (ROS). Xanthine oxidase is an important enzyme that generates ROS and mediates oxidative modification of low-density lipoprotein (LDL) which is a key step in fatty streak and subsequent atheroma formation. Allopurinol is a xanthine oxidase inhibitor that has been shown to reduce the concentrations of the biological markers of oxidative stress. This meta-analysis was designed to summarize the effect of allopurinol treatment on markers of oxidative stress. Methods: Medline, PubMed, Pro Quest Health & Medical Complete, Clinical Key, Wiley Online Library, and Cochrane Central Register of Controlled Trials were searched till 29th July, 2017. Meta-analysis was planned for randomized controlled trials (RCTs) that investigated allopurinol effects on oxidative stress. A random-effect model was used to calculate the raw mean difference or the standardized mean difference (with 95% confidence intervals: CI) as an estimate of effect size. Heterogeneity was quantified by four types of information; Q-statistic, I2 statistic, T2, and T. Results: 37 eligible studies were identified; 14 were included in the final analysis and subdivided between two oxidative stress markers: there were 8 Malondialdehyde (MDA)-based studies (198 subjects) and 6 oxidized Low-density lipoprotein (Ox-LDL)-based studies (347 subjects). Allopurinol treatment was associated with a statistically significant reduction in mean MDA serum concentration, by 0.403 nmol/ml (95% CI; -0.618, -0.189) (P<0.001) and a non-significant reduction in Ox-LDL serum concentration assessed by the standardized mean difference, by 0.409 (95% CI; -1.332, 0.515) (P=0.386). Conclusion: The antioxidant potential of allopurinol has been confirmed by a significant reduction of the serum concentration of MDA in a heterogeneous group of patients and healthy adults. The non-significant reduction in Ox-LDL may reflect methodological differences. To confirm whether or not allopurinol has clinically relevant antioxidant properties, future studies require reproducible measurement techniques and clearer characterization and quantification in different patient groups.

Contribution of oxidative stress in acute intestinal mucositis induced by 5 fluorouracil (5-FU) and its pro-drug capecitabine in rats

This study was designed to examine the contribution of oxidative stress in gastrointestinal disorders after an intraperitoneal administration of 5 fluorouracil (5-FU; 100 mg/kg of body weight (b.w.)) and capecitabine oral administration (500 mg/kg b.w.). The animals were divided into three groups: Group A (NaCl,10 ml/kg of b.w.) considered as control group, group B was intoxicated by 5-FU and group C was the group of animals treated with capecitabine (CAP). To evaluate the secretory and enteropooling effects, we used magnesium sulfate (MgSO4), 1 ml/100 g of b.w. as a hypersecretion agent . The mucosal gastro-intestinal specimens were scraped and examined for biological markers of oxidative stress and intracellular mediators. These anticancer drugs caused many intestinal damages manifested by an elevation of fluid accumulation and imbalance in electrolytes secretion. The intestinal tissues from treated rats not only showed a significant increase in malondialdehyde (MDA), protein carbonylation and hydrogen peroxide (H2O2) production. but also showed a significant depletion of enzymatic and non-enzymatic antioxidant, such as, glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and sulfhydryl groups (-SH). These effects were related with histopathological damage and a perturbation of intracellular mediators. As expected, these disturbances were observed in the group of rats poisoned by the MgSO4. Data suggest the contribution of oxidative stress in chemotherapy-induced many disorders in intestinal tract.

Modulation of Oxidative Damage by Green and Black Tea: Role of Smoking and Gender in a Randomized Trial

Background: Oxidative stress has been implicated as an important modulator of human health and can play a role in both disease prevention and disease development. Objectives: The overall goal of this study was to determine the effects of high tea consumption on biological markers of oxidative stress that mediate lung cancer risk, including, 8-hydroxydeoxy-guanosine (8-OHdG) and F2-isoprostanes (8-iso-PGF2α). Design: We completed a 6-month randomized, controlled, double-blinded trial in a group of former and current smokers who were randomized to receive green or black tea preparations or a matching placebo. Results: A total of 146 participants (80 females and 66 males) completed the study. At the end of the 6-month intervention, female smokers in the green tea group showed a 35% decrease (p=0.04) in DNA damage while female former smokers in the black tea group showed a 26% decrease (p=0.015) in lipid damage. No significant changes in markers of oxidative stress were observed in men. Conclusion: This data confirm our previous findings related to the beneficial effect of green tea on oxidative DNA damage among female smokers. The significant beneficial effect of black tea on oxidative lipid damage as well as the gender difference merit further studies.

Magnetic resonance imaging biomarkers of exercise-induced improvement of oxidative stress and inflammation in the brain of old high-fat-fed ApoE-/- mice.

Vascular brain lesions and atherosclerosis are two similar conditions that are characterized by increased inflammation and oxidative stress. Non-invasive imaging in a murine model of atherosclerosis showed vascular brain damage and peripheral inflammation. In this study, exercise training reduced magnetic resonance imaging-detected abnormalities, insulin resistance and markers of oxidative stress and inflammation in old ApoE-/- mice. Our results demonstrate the protective effect of exercise on neurovascular damage in the ageing brain of ApoE-/- mice. Vascular brain lesions, present in advanced atherosclerosis, share pathological hallmarks with peripheral vascular lesions, such as increased inflammation and oxidative stress. Physical activity reduces these peripheral risk factors, but its cerebrovascular effect is less documented, especially by non-invasive imaging. Through a combination of in vivo and post-mortem techniques, we aimed to characterize vascular brain damage in old ApoE-/- mice fed a high-cholesterol (HC) diet with dietary controlled intake. We then sought to determine the beneficial effects of exercise training on oxidative stress and inflammation in the brain as a treatment option in an ageing atherosclerosis mouse model. Using in vivo magnetic resonance imaging (MRI) and biological markers of oxidative stress and inflammation, we evaluated the occurrence of vascular abnormalities in the brain of HC-diet fed ApoE-/- mice >70 weeks old, its association with local and systemic oxidative stress and inflammation, and whether both can be modulated by exercise. Exercise training significantly reduced both MRI-detected abnormalities (present in 71% of untrained vs. 14% of trained mice) and oxidative stress (lipid peroxidation, 9.1±1.4 vs. 5.2±0.9μmolmg-1 ; P<0.01) and inflammation (interleukin-1β, 226.8±27.1 vs. 182.5±21.5pgmg-1 ; P<0.05) in the brain, and the mortality rate. Exercise also decreased peripheral insulin resistance, oxidative stress and inflammation, but significant associations were seen only within brain markers. Highly localized vascular brain damage is a frequent finding in this ageing atherosclerosis model, and exercise is able to reduce this outcome and improve lifespan. In vivo MRI evaluated both the neurovascular damage and the protective effect of exercise.

Cigarette Smoking and Oxidative Stress in Patients with Coronary Artery Disease.

AIM:To determine whether cigarette smoking, as a risk factor for CAD, affects (anti)oxidant status.MATERIAL AND METHODS:The study included patients with CAD, divided according to their smoking status and the number of cigarettes smoked during a day. Biological markers of oxidative stress (concentration of oxidants and activity of antioxidant enzymes) were measured in all subjects.RESULTS:The study included 300 patients with CAD, (average age of 63 ± 11 years), predominantly males. Of the total, 34.0% were active smokers, 23.0% were former smokers, and 43.0% were non-smokers. Most of the active smokers smoked 1-20 cigarettes/day. In terms of concentration of oxidants (MDA and HP) there was not a significant difference between smokers versus non-smokers. As for the activity of antioxidant enzymes (SOD, CAT and GPX), a statistically significant difference was found in the activity of GPX among the active smokers with CAD and the non-smokers with CAD (p = 0.039).CONCLUSION:Smoking as a risk factor for CAD is closely associated with increased oxidative stress, and the number of cigarettes smoked plays an important role in increasing the level of oxidative damage and reducing antioxidant defence.

Advanced oxidation protein products and malondialdehyde - the new biological markers of oxidative stress - are elevated in postmenopausal women.

The aim of the study was to measure advanced oxidation protein products (AOPPs) as markers for oxidative stress to evaluate cardiovascular risk in pre- and postmenopausal women and to compare the results with malondialde-hyde (MDA) levels. Twenty premenopausal women and 84 naturally postmenopausal patients were enrolled in the study. AOPP and MDA plasma levels were measured. The postmenopausal group was further subdivided into two groups: postmenopausal age of 40-49 and of 50-59 years. AOPP and MDA levels were compared between premenopausal, 40-49 and 50-59 year old menopausal women. Plasma AOPP and MDA levels in postmenopausal women were increased when compared with their premeno-pausal peers (123.83 ± 55.51 μmol/L vs. 61.59 ± 16.42 μmol/L and 6.50 ± 1.05 μmol/L vs. 5.98 ± 0.77 μmol/L; respectively). Mean plasma AOPP levels in the two menopausal age groups were both significantly higher from the premenopausal group (118.64 ± 59.1 μmol/L vs. 61.59 ± 16.42 μmol/L and 132.31 ± 48.97 μmol/L vs. 61.59 ± 16.42 μmol/L; respectively). No significant difference was found in mean AOPP levels between postmenopausal subjects of 40-49 and 50-59 years age (118.64 ± 59.12 μmol/L vs. 132.31 ± 48.97 μmol/L). Mean plasma MDA levels of each of two postmenopausal age groups were both significantly higher from the premenopausal group (6.50 ± 1.04 μmol/L vs. 5.98 ± 0.77 μmol/L and 6.50 ± 1.10 μmol/L vs. 5.98 ± 0.77 μmol/L; respectively). However, no statistically significant difference between the two postmenopausal age groups (6.50 ± 1.04 μmol/L vs. 6.50 ± 1.10 μmol/L) was found. AOPP and MDA levels are elevated in postmenopausal women as compared to their premenopausal peers, suggesting they can be used as markers for cardiovascular risk in postmenopausal women.

Toxicopathological Alterations Induced by High Dose Dietary T-2 Mycotoxin and its Residue Detection in Wistar Rats

T-2 toxin is one of the most potent cytotoxic and food-borne mycotoxins. Most experimental studies on the T-2 toxin have been performed at extremely low doses (ppb level). However, several field reports of contaminated feed have shown concentration of T-2 toxin to be as high as ≥20ppm. Therefore, the impact of high dose T-2 toxin (20ppm) after subacute exposure was investigated in an experimental setup with respect to growth performance, oxidative stress, and detailed pathomorphology in young male Wistar rats. Furthermore, to see the effect of such a high dose on the accumulation of T-2 toxin, its residues in various organs were quantified by high-performance thin-layer chromatography (HPTLC). Apart from obvious clinical toxicosis, rats in the toxin-fed group showed significant hemato-biochemical alterations and increased levels of biological markers of oxidative stress with concomitant decrease in levels of serum and tissue catalase and superoxide dismutase. These alterations were strongly supported by histopathological changes, such as hyperkeratosis and hyperplasia of the squamous gastric mucosa, oxidative damage to hepatocytes, atrophy of the thymus and spleen, and overall decrease in the spermatogenic activity of testes. An economical, simple, reliable, and quick method for the detection and quantification of T-2 toxin residues by HPTLC is also reported here. No residual T-2 toxin was detected in any of the organs tested, suggesting that T-2 toxin does not accumulate in tissues even at such a high exposure level.

Tai Chi exercise increases SOD activity and total antioxidant status in saliva and is linked to an improvement of periodontal disease in the elderly.

The aim of this study was to determine the effect of Tai Chi on biological markers of oxidative stress in saliva and its relationship with periodontal disease (PD) in older adults. We carried out a quasi-experimental study with a sample of 71 sedentary volunteers with PD who were divided into a control group of 34 subjects and an experimental group of 37 subjects who performed Tai Chi 5 days a week for a period of 6 months. PD status was characterized using the Periodontal Disease Index (PDI). Superoxide dismutase (SOD), total antioxidant status (TAS), and TBARS levels of both groups were measured by spectrophotometric methods. In addition, inflammation markers (TNF-α, IL-1β, IL-6, IL-8, and IL-10) were measured by flow cytometry. We found a statistically significant increase in SOD activity (P < 0.001) and TAS concentration (P < 0.05), whereas levels of IL-1β were significantly lower (P < 0.01). Likewise, a statistically significant decrease in the PDI (P < 0.05) was observed in subjects who performed Tai Chi during a period of 6 months. Our findings suggest that the practice of Tai Chi has both antioxidant and anti-inflammatory effects that are linked to the improvement of PD in older adults.

Ascorbylperoxide from parenteral nutrition induces an increase of redox potential of glutathione and loss of alveoli in newborn guinea pig lungs

BackgroundBronchopulmonary dysplasia is one of the main complications associated with extreme prematurity. Oxidative stress is suspected to be a trigger event of this lung disease, which is characterized by impaired alveolar development. Peroxides, mainly ascorbylperoxide and H2O2, are known contaminant of parenteral nutrition. We hypothesize that these oxidant molecules induce bronchopulmonary dysplasia development. The aim was to determine if the infusion of ascorbylperoxide, whether in presence or absence of H2O2, is associated with oxidative stress, apoptosis and loss of alveoli in the lungs of newborn guinea pigs. MethodThree-day-old guinea pigs received parenteral solutions containing 0, 20, 60 or 180 µM ascorbylperoxide in the presence or not of 350 µM H2O2 (concentrations similar to those measured in parenteral nutrition). After 4 days, the lungs were collected for determination of glutathione's redox potential, caspase-3 activation (an apoptosis marker), alveolarization index (by histology), activation of Nrf2 and NFκB (biological markers of oxidative stress), and IL-6 and PGJ2 levels (markers of NFκB activation). Groups were compared by ANOVA, p < 0.05. ResultsLoss of alveoli was associated with ascorbylperoxide in a dose-dependent manner, without an influence of H2O2. The dose-dependent activation of caspase-3 by ascorbylperoxide was lower in the presence of H2O2. Ascorbylperoxide induced an increase of redox potential in a dose-dependent manner, which reached a plateau in presence of H2O2. Nrf2 and NFκB were activated by H2O2 but not by ascorbylperoxide. ConclusionResults suggest that ascorbylperoxide, generated in parenteral nutrition, is involved in the development of bronchopulmonary dysplasia, independently of the increase of the redox potential. This study underlines the importance of developing a safer formulation of parenteral nutrition.