Indicator Of Oxidative Damage Research Articles

Exosomes-Mediated LncRNA ZEB1-AS1 Facilitates Cell Injuries by miR-590-5p/ETS1 Axis Through the TGF-β/Smad Pathway in Oxidized Low-density Lipoprotein-induced Human Umbilical Vein Endothelial Cells.

Atherosclerosis is a chronic lipid-induced inflammation of the vessel wall. Oxidized low-density lipoprotein was confirmed to drive the onset of atherogenesis. Zinc finger e-box-binding homeobox 1 antisense 1 (ZEB1-AS1) is a long noncoding RNA that is involved in human diseases, including atherosclerosis. In this study, the role of exosomes-mediated ZEB1-AS1 and its underlying mechanisms in atherosclerosis were explored in oxidized low-density lipoprotein (ox-LDL)-treated human umbilical vein endothelial cells (HUVECs). Exosomes were extracted from HUVECs. Quantitative real-time polymerase chain reaction was conducted to measure the expression of ZEB1-AS1, microRNA-590-5p (miR-590-5p), or erythroblastosis virus E26 oncogene homolog 1 (ETS1) in cells or exosomes. Cell proliferation and apoptosis were assessed by MTT assay and flow cytometry analysis, respectively. Western blot was performed to detect apoptosis-related factors, ETS1, and TGF-β/Smad pathway protein levels. The secretion of inflammatory factors in supernatant was detected by ELISA assay. Oxidative stress damage indicators were used to assess cellular damage. Relationship between miR-590-5p and ZEB1-AS1 or ETS1 was analyzed. Our data indicated that ox-LDL-induced exosomes-mediated ZEB1-AS1 in HUVECs. Ox-LDL treatment resulted in limited proliferation, proapoptosis, inflammation, and oxidative stress damage, whereas knockdown of ZEB1-AS1 could reverse these effects. Mechanically, ZEB1-AS1 sponged miR-590-5p to regulate ETS1 expression. MiR-590-5p knockdown inverted effects above of si-ZEB1-AS1 on HUVECs under ox-LDL exposure. Moreover, ETS1 reversed miR-590-5p-induced effects and activated the TGF-β/Smad pathway in ox-LDL-treated HUVECs. Taken together, our findings demonstrated that exosomes-mediated ZEB1-AS1 enhanced cell injuries by miR-590-5p/ETS1 axis through the TGF-β/Smad pathway in ox-LDL-induced HUVECs, suggesting that inhibiting ZEB1-AS1 might be an effective way for atherosclerosis treatment.

Analysis of Global Oxidative Status Using Multimarker Scores Reveals a Specific Association Between Renal Dysfunction and Diuretic Therapy in Older Adults

Abstract Aging and chronic kidney disease (CKD) are important interrelated cardiovascular risk (CVR) factors linked to oxidative stress, but this relationship has not been well studied in older adults. We assessed the global oxidative status in an older population with normal to severely impaired renal function. We determined the oxidative status of 93 older adults (mean age 85 years) using multimarker scores. OxyScore was computed as index of systemic oxidative damage by analyzing carbonyl groups, oxidized low-density lipoprotein, 8-hydroxy-2′-deoxyguanosine, and xanthine oxidase activity. AntioxyScore was computed as index of antioxidant defense by analyzing catalase and superoxide dismutase (SOD) activity and total antioxidant capacity. OxyScore and AntioxyScore were higher in subjects with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 than in peers with eGFR >60 mL/min/1.73 m2, with protein carbonyls, catalase, and SOD activity as major drivers. Older adults with a recent cardiovascular event had similar OxyScore and AntioxyScore as peers with eGFR >60 mL/min/1.73 m2. Multivariate linear regression analysis revealed that both indices were associated with decreased eGFR independently of traditional CVR factors. Interestingly, AntioxyScore was also associated with diuretic treatment, and a more pronounced increase was seen in subjects receiving combination therapy. The associations of AntioxyScore with diuretic treatment and eGFR were mutually independent. In conclusion, eGFR is the major contributor to the imbalance in oxidative stress in this older population. Given the association between oxidative stress, CKD, and CVR, the inclusion of renal function parameters in CVR estimators for older populations, such as the SCORE-OP, might improve their modest performance.

Systemic RNA oxidation can be used as a biomarker of infection in challenged with Vibrio parahaemolyticus

More and more evidence support the concept that RNA oxidation plays a substantial role in the progress of multiple diseases; however, only a few studies have reported RNA oxidation caused by microbial pathogens. Urinary 8-oxo-7,8-dihydroguanosine (8-oxo-Gsn) and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxo-dGsn), which are broadly used as indicators of oxidative damage of RNA and DNA, were analyzed in this study to determine which can be used as a biomarker of infection in challenged with Vibrio parahaemolyticus (V. parahaemolyticus). In this work, 24 specific-pathogen-free (SPF) male SD rats were randomly divided into two groups: an infection group and a phosphate-buffered saline (PBS) control group. Our results proved that 8-oxo-Gsn rather than 8-oxo-dGsn was significantly increased after challenged with V. parahaemolyticus in urine and tissue samples of SD rats compared with the PBS control group. Simultaneously, white blood cells (WBCs) counts, intestinal inflammation and inflammatory factors (including CRP, IL-6, IL-1β, TNF-α, IL-10, and IL-17A) were also increased sharply. Which has more clinical value is that the trend of urinary 8-oxo-Gsn was consistent with WBCs, intestinal inflammation and all kinds of inflammatory factors. More importantly is that urinary 8-oxo-Gsn of infection group was positively correlated with WBCs and various inflammatory cytokines. In a word, our results demonstrated that as a systemic RNA oxidation biomarker, we hope 8-oxo-Gsn can be used as a biomarker of the severity of microbial pathogens infection, rather than a specific biomarker of microbial pathogens infection.

The Effects of Curcumin Supplementation on Muscle Damage, Oxidative Stress, and Inflammatory Markers in Healthy Females with Moderate Physical Activity: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial.

Background:Exercise-induced oxidative stress, muscle damage, and inflammation represent major contributors to why athletes use ergogenic aids. Turmeric is used as a spice because of its polyphenol ingredient named curcumin. We assessed the effects of curcumin supplementation on inflammatory, oxidative stress markers, muscle damage, and anthropometric indices in women with moderate physical activity.Methods:This double-blind, placebo-controlled clinical trial was conducted on 80 women with moderate physical activity levels (defined as walking or swimming for at least 1 h per day) for 8 weeks. Mean ± SD of age (years) all participants was 21 ± 2. Participants were randomly assigned into two groups: curcumin (500 mg/day) and placebo (500 mg/day cornstarch). Serum C-reactive protein (CRP), total antioxidant capacity (TAC), malondialdehyde (MDA), lactate dehydrogenase (LDH) levels, body composition, and maximum oxygen uptake (VO2 max) were evaluated before and after an intervention.Results:Sixty-five subjects completed the 8-week intervention. Within analysis indicated a significant decrease in CRP, LDH, MDA levels, and a significant increase in VO2 max in the curcumin group after an intervention (P < 0.05). There were significant decreases in CRP (P = 0.002), LDH (P = 0.041), and MDA (P = 0.005), no significant increase in TAC, and significant increase in VO2 max (P = 0.0001) levels in the curcumin group compared with placebo group. There were no significant changes in weight, body mass index, body fat, and lean body mass between two groups.Conclusions:Our findings indicated that 8-week curcumin administration could significantly improve CRP, LDH, MDA, and VO2 max. Curcumin supplementation did not elicit significant changes in anthropometric indices in this study.

Improved salinity tolerance of Medicago sativa and soil enzyme activities by PGPR

Abstract Abiotic stresses such as salinity are common adverse conditions that significantly affect agricultural productivity worldwide. This study aimed to select halotolerant plant-growth-promoting rhizobacteria (PGPR) capable to promote plant growth and to improve soil functioning under salinity stress conditions. Thirty-two bacterial isolates were studied for their PGP traits and NaCl resistance. Four selected potential PGPR were identified by using 16S rDNA sequencing and tested for their PGP traits in the presence of 2–6% NaCl. Their effect on growth, chlorophyll content, oxidative stress and root arbuscular mycorrhizal (AM) colonization of Medicago sativa, was studied under salt stress in pots experiment. The bacteria were also tested for their effect on soil enzyme activities. Overall results showed that the isolates displayed various PGP properties and variable levels of NaCl resistance. The four selected potential PGPR strains were identified as Pseudomonas putida, Alcaligenes sp., Klebsiella sp., and Pseudomonas cedrina. The bacteria retained most of the PGP traits in the presence of the tested concentrations of NaCl. The inoculation of M. sativa plants by the four strains allowed overcoming the negative effects of stress due to NaCl and increased plant growth, roots AM colonization and the leaves chlorophyll content, compared to the non-inoculated control. It also lowered the levels of the indicators of oxidative damage, malondialdehyde, hydrogen peroxide, and proline. Besides, the strains had a positive effect on soil phosphatase, β-galactosidase, and arylamidase activities. This study showed that the selected isolates have an interesting potential to be used as bio-inoculants for plants growing under salt stress.

Oxidative stress markers in patients suffering from opioid and psychostimulant dependence syndrome

Background. The available data from clinical studies suggest the essential role of free radical processes in the pathogenesis of drug dependence syndrome. At the same time, there is a limited understanding of using markers of oxidative stress in laboratory monitoring and prediction of drug pathology.Objective. To characterize changes in promising indicators of oxidative stress in patients with psychostimulant and opioid dependence syndrome.Material and Methods. The total study population was divided into three groups of men aged 23–35: healthy controls (n = 20), patients with the opioid (n = 20) and psychostimulant (n = 20) dependence syndrome. Patients were analyzed for the oxidative stress markers while being in therapy for addiction syndrome aimed at treating mental disorders and detoxification.Results. The study of antioxidant activity and blood plasma thiol groups did not reveal any significant differences between patients suffering from opioid and psychostimulant addiction. The values of the parameters mentioned above were maintained by 20–30% lower than the control indices throughout the entire study. The nature of changes in erythrocyte suspension parameters was not so unambiguous. Thus, patients with opioid dependence syndrome were characterized by a 91% increase in thiobarbituric acid (TBA)-reactive materials in the setting of a slightly altered state of the glutathione system parameters. Psychostimulant dependent patients revealed relatively low level of the products of biomolecule oxidative modifications in the erythrocytes that is 52% higher compared to the control values. It decreased during the therapy, but glutathione concentration reduction by 33% and an imbalance of glutathione metabolism were determined.Conclusion. The course of the opioid dependence syndrome is characterized by a pronounced intensification of free radical processes while the common trait for psychostimulant abusers is significant changes in the antioxidant defense system. Therefore, in the first case, it is most justified to conduct a laboratory assessment of indicators of oxidative damage, and in the second one, it is also advisable to determine the markers of the state of individual links of the antioxidant system.

Ramipril blunts glycerol-induced acute renal failure in rats through its antiapoptosis, anti-inflammatory, antioxidant, and renin-inhibiting properties.

Acute kidney injury (AKI) is a malady with a sudden onset resulting in buildup of waste matters in the body, but a specific cure hasn't been found as a lasting solution to AKI. In this study, ramipril was evaluated for its potential therapy in glycerol-induced AKI in rats. Twenty animals were divided into four groups of five animals each. Group I was the control while group II was given glycerol on day 8 only, groups III and IV were administered with pioglitazone (reference drug) and ramipril for seven days respectively and on day 8 received glycerol. On the ninth day, blood and tissue samples were taken to assayfor serum indicators of oxidative damage, enzymatic and nonenzymatic antioxidants, and creatinine and blood ureanitrogen. Animals were sacrificed thereafter; kidney washarvested for histological and immunohistochemical analysis. Expressions of caspase 3, renin receptor, NK-KB, and KIM-1 were carried out. Ramipril significantly inhibited indicators of oxidative damage while also significantly increasing levels of enzymatic and nonenzymatic antioxidant markers. These drugs also significantly lowered the levels of creatinine and blood urea nitrogen. Histology also indicated that while there were massive infiltration of leucocytes and congestion of the kidney in toxicant group, the ramipril-treated group showed a milder condition. In immunohistochemistry, the two drugs significantly inhibited the expressions of the four proteins, which were highly expressed in the toxicant group. The study showed that ramipril and pioglitazone have nephroprotective effect and thus have the ability to blunt AKI through their anti-inflammatory, antiapoptosis, antirenin, and antioxidant properties.

The Protective Effects of Lupine (Lupinus albus) Fruit Extract Against to Destructive Effects of Hyperglycemia in Type I Diabetic Rats.

Lupinus albus is a member of the Fabaceae family. As a natural or cultivated plant, Lupinus albus is distributed in Europe, the Balkans and Turkey, especially in Marmara and Aegean regions. The lupine is a nutritious and protective plant against diabetes. In the present study, the effects of Lupinus albus fruits on malondialdehyde (MDA), reduced glutathione (GSH), total protein, ADEK vitamins, and cholesterol values, which are the indicators of oxidative damage and antioxidant defense. In this regard, muscle, liver, renal, and brain tissues of STZ-induced type I diabetes rats were studied. The analyzes of ADEK vitamins and cholesterol levels in tissues were performed via Shimadzu HPLC device. The lipid peroxidation levels were measured at 532 nm in spectrophotometer. Determination of GSH was read at 412 nm against blank, and for the total protein levels Lowry method was applied. According to the results obtained, it was determined that among the rats with induced type I diabetes, the group applied lupine fruit extract was found to have increased GSH level and decreased MDA levels in all the tissues. The protein values were increased in liver tissues but decreased in the other tissues. The level of vitamins was significantly increased in almost all the tissues in the diabetic group. In the present study, it was shown that the lupine reduced the devastating effects of type I diabetes by decreasing the fasting blood glucose and lipid peroxidation values and increasing the glutathione level in comparison to the diabetic group.

18F-Fluorodeoxyglucose Positron Emission Tomography Tracks the Heterogeneous Brain Susceptibility to the Hyperglycemia-Related Redox Stress.

In cognitively normal patients, mild hyperglycemia selectively decreases 18F-Fluorodeoxyglucose (FDG) uptake in the posterior brain, reproducing Alzheimer disease pattern, hampering the diagnostic accuracy of this widely used tool. This phenomenon might involve either a heterogeneous response of glucose metabolism or a different sensitivity to hyperglycemia-related redox stress. Indeed, previous studies reported a close link between FDG uptake and activation of a specific pentose phosphate pathway (PPP), triggered by hexose-6P-dehydrogenase (H6PD) and contributing to fuel NADPH-dependent antioxidant responses in the endoplasmic reticulum (ER). To clarify this issue, dynamic positron emission tomography was performed in 40 BALB/c mice four weeks after administration of saline (n = 17) or 150 mg/kg streptozotocin (n = 23, STZ). Imaging data were compared with biochemical and histological indexes of glucose metabolism and redox balance. Cortical FDG uptake was homogeneous in controls, while it was selectively decreased in the posterior brain of STZ mice. This difference was independent of the activity of enzymes regulating glycolysis and cytosolic PPP, while it was paralleled by a decreased H6PD catalytic function and enhanced indexes of oxidative damage. Thus, the relative decrease in FDG uptake of the posterior brain reflects a lower activation of ER-PPP in response to hyperglycemia-related redox stress in these areas.

Electrochemical screening of genoprotective and antioxidative effectiveness of Origanum vulgare L. and its functionality in the prevention of neurodegenerative disorders

A new way of electrochemical DNA sensor using as a screening tool for the determination of phytochemicals with high genoprotective functionality is proposed. The biosensor's detection layer was prepared with double stranded deoxyribonucleic acid (ds DNA) that were subjected to oxidative stress induced by •OH radicals generated by Fenton reaction. The oxidized guanine derivative, 8-oxo-7,8-dihydro-2′-deoxyguanosine, was treated as an indicator of DNA oxidative damage. This derivative may cause mutation through its ability to pair with adenine. The abnormalities of DNA structure and DNA repair system are known to be directly related to progressive neurodegeneration. The present study showed that during oxidative stress, the 2.5% oregano extract protected guanine from undergoing oxidation to 8-oxoguanine. The results revealed that this genoprotective effectiveness can make oregano a very efficient protective barrier against oxidative stress. Due to these unique properties of oregano we propose the recipe of a functional bread with its addition. It was found that the functionality of the prepared bread was not limited to antioxidative activity but also is expressed in the inhibition of cholinesterases. These findings indicate that oregano can act as an important component in the therapeutic diet recommended in neurodegenerative disorders.

Associations of ozone exposure with urinary metabolites of arachidonic acid

BackgroundOzone (O3) exposure has been associated with biomarkers of platelet activation and oxidative stress. The metabolism of arachidonic acid (AA) plays an important role in platelet activation and oxidative stress. However, AA metabolic pathways have not been examined in relation to O3 and other air pollutants. MethodsEarly morning urine and fasting blood were longitudinally collected up to four times from 89 healthy adults (22–52 years old, 25 women) in Changsha City, China. We measured three urinary AA metabolites, namely 11-dehydro-Thromboxane B2 (11-dhTXB2) produced from the arachidonic cyclooxygenase pathway, 20-hydroxyeicosatetraenoic acid (20-HETE) from the CYPs pathway, and 8-isoprostane from the non-enzymatic pathway. Urinary malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were measured as indicators of oxidative damage to lipids and DNA, respectively. We measured soluble P-selectin (sCD62p) concentrations in plasma as an indicator of platelet activation. Indoor and outdoor air pollutants were measured and combined with participants’ time-activity pattern to calculate personal exposure to O3, PM2.5, NO2, and SO2 averaged over 12-hour, 24-hour, 1-week, and 2-week periods prior to biospecimen collection, respectively. Linear mixed-effects models were used to examine the relationships of AA metabolites with air pollutant exposures, plasma sCD62p, and urinary MDA & 8-OHdG. ResultsWe found that a 10% increase in 12 h and 24 h O3 exposure were associated with increases in urinary11-dhTXB2 by 1.4% (95%, 0.1% to 2.6%) and 1.3% (0.05% to 2.5%), respectively. These associations remained robust after adjusting for co-pollutant exposures. No significant associations were observed between 11-dhTXB2 and other pollutants or between O3 exposures and other AA metabolites. All the three AA metabolites were significantly and positively associated with urinary MDA and 8-OHdG, whereas only urinary 11-dhTXB2 was significantly and positively associated with plasma sCD62p. ConclusionsA metabolite of AA from the cyclooxygenase pathway was positively associated with short-term O3 exposure, and with a plasma marker of platelet activation and two urinary markers of oxidative stress. The results suggest that O3 exposure may contribute to increased platelet activation and oxidative damages via altering the metabolism of AA.

Physiological and biochemical responses of Damask rose (Rosa damascena Miller) to potassium silicate application under water deficit stress

In this field experiment, the effect of potassium silicate (PS) on the physiological and biochemical responses of Damask rose was investigated under the water deficit stress. The treatments were four levels of irrigation water application including 100, 75, 50 and 25% plant water requirement (PWR) and potassium silicate at three rates (0, i.e., just pure water, 0.2 and 0.4%), once (in spring or summer) or twice (once in spring and once in summer) during the plant growth. The results showed that with irrigation of 75% of plant water requirement significantly reduced the concentration of chlorophyll a (Chl a, 170%), chlorophyll b (Chl b, 163%) and carotenoids (91%), the leaf relative water content (RWC, 14.8%) and the total flower yield (20%) as compared to control. The elevated malondialdehyde (MDA) content and ion leakage, as two indicators of oxidative damage, were observed in the plants subjected to the water deficit stress. In response to oxidative stress induced by water deficit stress, the leaf catalase (CAT, 59.5%) activity and concentration of proline (64.8%) as compared to control increased. The foliar-applied Si at two rates of 0.2 and 0.4% in spring and summer resulted in a higher concentration of Chl a (57.3% and 61.7%), Chl b (31% and 24.6%) and carotenoid content as compared to control, respectively. The increased concentration of proline and higher activity of CAT in the plants supplied with Si led to the higher leaf RWC and less intensity of oxidative damage, namely ion leakage and MDA content. According to the results, with the potassium silicate spraying in 0.2 or 0.4% both in spring and summer at the irrigation level equal to 50% of the PWR, the optimum flower yield was achieved.

Survival Training Effects on Oxidative Stress and Muscle Damage Biomarkers of Naval Cadets.

INTRODUCTION: It is important for military commanders to know the extent of fatigue experienced by soldiers undergoing a long-term military training. This knowledge can enable them to determine the level of physical capabilities of soldiers. The present study aimed to evaluate changes in the level of chosen biochemical parameters in blood during the survival training of Polish Naval Academy cadets.METHODS: Participating voluntarily in the research study were 14 cadets. All subjects were men, ages 23.1 2.0 yr. During the 36-h survival training, the subjects were deprived of sleep. The following biochemical parameters were assessed in venous blood collected from the cadets: creatine kinase (CK) activity, concentration of lipid hydroperoxides (LOOHs), superoxide dismutase activity (SOD), and glutathione peroxidase activity (GPx).RESULTS: After 36 h of training a significant increase was observed in CK (from 183.1 up to 530.2 U L1), LOOHs (from 1.72 up to 3.74 mol L1), and GPx (from 27.4 up to 36.4 U gHb1). After 12 h of rest, the level of LOOHs returned to the initial level, GPx activity did not change significantly, and CK activity was significantly higher than those at baseline (422.3 U L1).DISCUSSION: The 36-h survival training increased oxidative stress, which contributed to the damage to muscle cells in the group of cadets of the Polish Naval Academy. The intensity of postexercise changes in the level of oxidative damage indicators is dependent on the initial level of enzymatic antioxidant defense. The 12-h recovery proved to be too short to regenerate the damaged muscle tissue.Tomczak A, Jwko E, Raski P. Survival training effects on oxidative stress and muscle damage biomarkers of naval cadets. Aerosp Med Hum Perform. 2020; 91(9):720724.

Neurotoxicity in pre-eclampsia involves oxidative injury, exacerbated cholinergic activity and impaired proteolytic and purinergic activities in cortex and cerebellum.

Women with a history of pre-eclampsia (PE) tend to have a higher risk of developing cardiovascular and neurological diseases later in life. Imbalance in oxidative markers and purinergic enzymes have been implicated in the pathogenesis of neurological disease. This study investigated the effect of PE on oxidative imbalance, purinergic enzyme inhibitory activity, acetylcholinesterase and chymotrypsin activities in the brain of PE rat model at post-partum/post-natal day (PP/PND) 60. Pregnant rats divided into early-onset and late-onset groups were administered with Nω-nitro-l-arginine methyl through drinking water at gestational days 8-17. Rats were allowed free access to water throughout the pregnancy and allowed to deliver on their own. The mother and the pups were euthanized at PP and PND 60, respectively, the cortex and the cerebellum excised, homogenized and stored for analyses of the enzymes. Results showed an increase in nitric oxide and malondialdehyde with a concomitant decrease in reduced glutathione and superoxide dismutase, an indication of oxidative damage. Also, there was an increase in acetylcholinesterase activity with a decrease in chymotrypsin, adenylpyrophosphatase and ecto-nucleoside triphosphate diphosphohydrolase activities in both the cortex and the cerebellum of the mother and the pups at PND 60. These results indicate the involvement of oxidative stress, increased cholinergic activity and depleted proteolytic and purinergic activities in PE-induced neurotoxicity.

Differential modulation of oxidative stress, antioxidant defense, histomorphology, ion-regulation and growth marker gene expression in goldfish (Carassius auratus) following exposure to different dose of virgin microplastics

Goldfish (Carassius auratus) juveniles were exposed to virgin polyvinyl chloride microplastics (PVC-MPs) in triplicate at 0, 0.1 or 0.5 mg/L for four days. Afterwards, the histopathology of the gills, liver and intestines were examined, along with various antioxidant enzymes and indicators of oxidative damage (malondialdehyde (MDA) and hydrogen peroxide (H2O2)), in the brain, liver and gills. In addition, we also studied the expression of hepatic insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein 1 (IGFBP-1) and growth hormone (GH) receptor, while cortisol receptor (CR) and cytochrome P450 1A (CYP1A) gene expression were assayed in both the liver and gills. Histological analysis revealed PVC-MPs in the intestines at 0.1 and 0.5 mg/L, along with substantially shorter villi. The gills appeared undamaged by PVC-MPs exposure and had limited or no effect to antioxidant activity, Na+/K+-ATPase and H+-ATPase activity or plasma ion levels, but there was a prominent upsurge of the detoxification enzymes glutatione S-transferase (GST) activity and CYP1A expression. Livers showed inflammation and some occurrences of hemorrhaging and necrosis at 0.5 mg/L. While the brain showed some evidence of oxidative damage, the liver was the most susceptible to oxidative damage, based on increased MDA, H2O2 and various antioxidant enzymes. Hepatic expression of IGFBP-1 and GH receptor were significantly downregulated at 0.5 mg/L while CR was upregulated. Results indicate that exposure to environmentally relevant PVC-MP can cause oxidative damage in the brain and liver, adverse histomorphological changes to the intestine and liver and alter the gene expression in goldfish.

Co-exposure to polycyclic aromatic hydrocarbons, benzene and toluene may impair lung function by increasing oxidative damage and airway inflammation in asthmatic children

As previous studies found that the direct associations between urinary polycyclic aromatic hydrocarbon (PAH), benzene and toluene (BT) metabolites and the decreased lung function were not conclusive, we further investigated relationship of oxidative damage and airway inflammation induced by PAHs and BTs exposure with lung function. A total of 262 children diagnosed with asthma and 72 heathy children were recruited. Results showed that asthmatic children had higher levels of PAHs and BTs exposure, as well as Malonaldehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) compared with healthy children. Furthermore, binary logistic regression showed that each unit increases in level of urinary 2-&3-hydroxyfluorene (2-&3-OHF), 2-hydroxyphenanthrene (2-OHPhe), 1-hydroxyphenanthrene (1-OHP) and S-phenylmercapturic acid (S-PMA) were significantly associated with an elevated risk of asthma in children with odds ratios of 1.5, 2.3, 1.7 and 1.4, respectively, suggesting that PAHs and BTs exposure could increase the risk of asthma for children. Neither PAH nor BT metabolite could comprehensively indicate the decreased lung function as only 2-&3-OHF and 1-OHP were significantly and negatively correlated with forced vital capacity (FVC). Moreover, levels of most individual PAH and BT metabolite were significantly correlated to MDA and 8-OHdG. Further hierarchical regression analysis indicated that MDA and 8-OHdG levels did not show significant effects on the decreased lung function, suggesting that they are not the suitable biomarkers to indirectly indicate the altered lung function induced by PAHs and BTs. Urinary 2-OHPhe and 1-&9-hydroxyphenanthrene (1-&9-OHPhe) were significantly correlated with fractional exhaled nitric oxide (FeNO). Moreover, FeNO significantly contributed to decreased lung function and explained 7.7% of variance in ratio of forced expiratory volume in 1 s (FEV1) and FVC (FEV1/FVC%). Hence, FeNO, rather than oxidative damage indicators or any urinary PAH and BT metabolite, is more sensitive to indirectly reflect the decreased lung function induced by PAHs and BTs exposure for asthmatic children.

Circulating markers of oxidative stress are associated with a muscle injury in patients with muscular dystrophy Duchenne

BackgroundA small number of studies have confirmed the presence of oxidative damage in patients with Duchenne muscular dystrophy (DMD). Nevertheless, it is unknown if there a relationship of circulating markers of oxidative stress with a muscle injury. ObjectiveWe evaluated if oxidative damage and anti-oxidant markers are associated with muscle damage in DMD. MethodsThis cross-sectional study included 24 patients with DMD classified in ambulatory and non-ambulatory. Markers of muscle damage (creatine kinase [CK]), oxidative damage (malondialdehyde [MDA], and 8-isoprostane), anti-oxidant function (Thiol and mRNA of NRF2 and NF-κB) and nitric oxide (NO) were quantified in circulation. ResultsTotal NO, MDA, and 8-isoprostane concentrations were significantly (p < 0.05) higher, and thiol concentration was lower in non-ambulatory than ambulatory patients. A significant correlation (p < 0.05) between muscle injury (evaluated by Vignos scale) with CK (r = −0.382), NO (r = 0.444), MDA (r = 0.503), 8-isoprostanes (r = 0.435) and thiol (r = −0.430) was observed. Conclusion: These findings suggest that non-ambulatory have high oxidative damage and low anti-oxidant function than ambulatory patients with DMD. Total nitric oxide and oxidative damage plasma markers increase, but the anti-oxidant marker thiol decreases with a muscle injury in boys with DMD. The findings of this study suggest that these markers could be considered as goods indicators of oxidative damage in longitudinal studies to evaluate the muscle injury during DMD progression. Additionally, these findings add new information about the pathophysiology of DMD.

Protective effect of lutein on oxidative stress damage caused by acute PM2.5 exposure in rats

Particulate matter (PM) is the sum of organic and inorganic substances suspended in air. Particles with a diameter equal to or smaller than 2.5 μm (PM2.5) can induce extensive oxidative stress damage in lung tissues. Lutein can prevent oxidative stress and the production of pro-inflammatory cytokines. However, its role in lung injury induced by PM2.5 is still unclear. This study used lutein to intervene in lung injury induced by PM2.5 in rats to confirm the protective function of lutein in PM2.5- induced lung injury. A total of 80 rats were divided into five groups according to body weight (bw). Rats in the blank control group and the PM2.5 exposure group were treated with normal saline. The low-, medium-, and high-dose lutein groups were treated with 12.5, 25.0, and 50.0 mg/kg·bw lutein continuously for 28 days. In addition, on days 22-28, 10 mg/kg PM2.5 was introduced by intratracheal instillation into the PM2.5 exposure group and all lutein dose groups continuously for 7 days to establish PM2.5 injury models. Lung tissues were collected and subjected to hematoxylin-eosin (HE) staining to observe histomorphological changes. Bronchoalveolar lavage fluid (BALF) was collected to detect the expression of cell damage indicators including lactate dehydrogenase (LDH), acidic phosphatase (ACP), alkaline phosphatase (AKP), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α). In addition, the levels of serum oxidative stress indicators in rats, including methane dicarboxylic aldehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), nitric oxide synthase (NOS), and 8-hydroxy-2'-deoxyguanosine (8-OHdG), as well as cytokines, including IL-6, IL-8, and TNF-α, were analyzed. Lung tissues of rats after PM2.5 exposure exhibited different degrees of pathological changes. In serum, oxidative damage indicators MDA, NOS, and 8-OHdG and inflammatory cytokines IL-6, IL-8, and TNF-α significantly increased whereas GSH levels significantly decreased (P<0.05). In BALF, cell damage indicators ACP and AKP and inflammatory cytokines IL-6, IL-8, and TNF-α all increased (P<0.05). After lutein intervention, oxidative damage and cellular inflammatory cytokines in serum and BALF all significantly decreased (P<0.05) whereas serum GSH levels increased (P<0.05). PM2.5 caused significant oxidative damage and inflammatory injury in rat lungs. Lutein alleviated these effects, playing a protective role in lung tissues.

Effect of oligoribonucleotides with D-mannitol complexes on oxidative stress indicators against thioacetamide-induced liver fibrosis

The aim of the study. To determine the effect of oligoribonucleotides-D-mannitol complexes (ORN-D-M) on the indicators of oxidative destruction of biomolecules and the antioxidant system of cells in thioacetamide (TAA)-induced liver fibrosis.Materials and methods. Liver fibrosis was induced for 8 weeks by intraperitoneal administration of TAA (150 mg/kg body weight). ORN-D-M (200 mg/kg per os) was administered orally during intoxication. At the end of the experiment, the liver was excised and examined for the content of oxidative stress products and the activity of antioxidant enzymes. Data were analyzed using the ANOVA test followed by Tukey post hoc testing.Results. It is shown that the monotherapeutic treatment of ORN-D-M in TAA-induced liver fibrosis has a pronounced protective effect, which is manifested in the reduction of oxidative stress. ORN-D-M led to the attenuation of free radical damage of biopolymers, which was manifested in a decrease in the levels of peroxidation products of lipids and proteins with a simultaneous increase in the level of protein thiol groups and reduced glutathione. In addition, treatment with complexes increased the activity of the antioxidant defence system of cells.Conclusions. The obtained results indicate that ORN-D-M complexes have a potential hepatoprotective effect in TAA-induced liver fibrosis. The complexes are able to effectively reduce the indicators of oxidative damage of biomolecules with a simultaneous increase in the activity of enzymes of the antioxidant system in TAA-induced fibrosis

Oxidative Stress Investigation in Anemia

Introduction: Increased membrane rigidity, decreased deformability and hemolysis in erythrocytes are the result of oxidative damage. Our study included patients diagnosed with anemia and a control group of healthy individuals and in these groups, it was aimed to measure the level of Nitric Oxide (NO), which is an indicator of oxidative damage, and to determine the superoxide dismutase enzyme (SOD) activity, which are the most important components of the antioxidant system. Material and Method: Ethics Committee approval was obtained for the study and patients who were diagnosed with iron deficiency anemia, B12 deficiency anemia, Talassemia minor at the hematology polyclinic of the Manisa Celal Bayar University Medical Faculty Hafsa Sultan Hospital were included in the study. Nitrite / nitrate levels were measured spectrophotometrically, SOD enzyme activity was measured by ELISA method. Results: The difference between the study groups in terms of SOD values was not statistically significant. When nitric oxide results are compared; Thalassemia minor group values were significantly higher than control group (p &lt;0.05). Conclusions: Increased levels of NO, especially in the thalassemia patient group, it is thought to be the cause of hemolytic anemia as a result of oxidative stress and lipid peroxidation in this patient group. Supporting Institutions: Manisa Celal Bayar University Scientific Researches Unit (2015-092). Keywords: Anemia, Antioxidant System, Nitric Oxide, Superoxide Dismutase. DOI: 10.7176/JHMN/75-03