The consequences of increased oxidative stress, measured as the level of malondialdehyde (MDA) during ischemia/reperfusion, were studied in 48 patients in the acute phase of myocardial infarction (AMI) and a control group (21 blood donors). The serum levels of a-tocopherol and b-carotene were followed. Immediately after the treatment onset the level of a-tocopherol started to decrease, reaching a plateau after 24 h. The consumption of b-carotene was delayed by 90 min. Steady decline was detected during the whole time interval studied (48 h). Glutathione peroxidase (GPx) activity, as a representative of antioxidant enzymes, was estimated in whole blood. The influx of oxygenated blood was accompanied by a stimulation of GPx activity, which reached its maximum at the time of completed reperfusion. When comparing the AMI patients with the control group, the levels of MDA were found significantly increased, which indicates that oxidative stress is already increased during ischemia. Lower antioxidant levels found in the patients might either already be the result of vitamin consumption during ischemia or be a manifestation of their susceptibility to AMI. Monitored consumption of a-tocopherol and b-carotene during reperfusion indicated that in the case of patients, whose level of antioxidant vitamins is below the threshold limit, a further substantial decrease of antioxidant vitamins during reperfusion could enhance the oxidative damage of the myocardium., V. Mužáková, R. Kanďár, P. Vojtíšek, J. Skalický, R. Vaňková, A. Čegan, Z. Červinková., and Obsahuje bibliografii
Present study aimed to explore the levels and correlation of oxidative stress biomarkers with anthropometry in a population of young Saudi females. One hundred six normotensives, non-diabetic Saudi females, with minimally active lifestyle, based on their body mass index (BMI) were divided as; normal-weight (NW; n=52), overweight (OW; n=24) and obese (OB; n=30). Anthropometric measurements [BMI, Waist Circumference (WC), Waist-Hip Ratio (WHR), Body Density (BD), Body Adiposity Index (BAI), % Body fat] and oxidative stress biomarkers; Thiobarbituric acid reactive substances (TBARS), 8-hydroxy-2- deoxyguanosine (8-OH-2dG: indicative of DNA/RNA damage), Superoxide dismutase, Serum total antioxidant capacity) were recorded. There was statistically significant higher 8-OH-2dG (pg/ml) in OB compared to NW (800.63±6.19 vs. 780.22±3.34; p=0.007), as determined by one-way ANOVA and Tukey post hoc test. 8-OH-2dG was significantly and positively associated with BMI (r=0.286, p=0.004), WC (r=0.280, p=0.005), BAI (r=0.26, p=0.008), and % body fat (r=0.27, p=0.006). There may be significantly increased DNA damage in normoglycemic, normotensive obese adolescent females. This can be linked to the amount of adipose tissue in the body as depicted by strong positive association between DNA damage and BMI, WC, BAI, and % body fat., R. Latif, N. Rafique., and Obsahuje bibliografii
Pneumatic tourniquets are widely used in pediatric extremity surgery to provide a bloodless field and facilitate dissection. This prospective study was carried out to examine possible effect of different anesthesia techniques on oxidative stress and endothelial dysfunction connected with ischemia-reperfusion injury during extremity operations at children's age. Patients were randomized into three groups of 15 patients each: general inhalational anesthesia with sevoflurane (group S), total intravenous anesthesia with propofol (group T) and regional anesthesia (group R). Venous blood samples for determination of the malondialdehyde in plasma and erythrocytes, protein carbonyl groups concentration as well as plasma nitrites and nitrates level and xanthine oxidase activity were obtained at four time points: be fore peripheral nerve block and induction of general anesthesia (baseline), 1 min before tourniquet release, 5 and 20 min after tourniquet release. This study demonstrates that total intravenous anesthesia with propofol and regional anesthesia techniques provide better antioxidant defense and reduce endothelial dysfunct ion than general inhalational anesthesia with sevoflurane during tourniquet application in pediatric extremity surgery., I. Budic ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Oxidative stress may be caused by an increased rate of ATP resynthesis during physical exercise. The aim of this study was to compare changes in the prooxidant-antioxidant state of blood plasma between men and women after maximal-intensity exercise, and to assess the relationship between these changes and the value of the maximal oxygen uptake (VO2max) as well as between these changes and the value of post-exercise disruptions in acid-base balance. Study participants comprised 10 women (20.7±0.5 years) and 10 men (22.3±0.5 years) who were physically active but did no t engage in competitive sports training. VO2max was determined via treadmill incremental test (VO2max relative to body mass: 44.48±1.21 ml/kg/min and 59.16±1.55 ml/kg/min for women and men, respectively). The level of acid-base balance indicators (ABB), lactate concentration (La-), the level of total oxidative status (TOS), the level of total antioxidative capacity (TAC), an d uric acid (UA) concentration were measured before and after the test. An oxidative stress indicator (OSI) was also calculated. Men showed a significant post-exercise increase in the level of TOS and OSI, while women showed a significant post-exercise increase in the level of TAC. Post-exercise changes in UA concentration were insignificant. Post-exercise changes in TOC in men depended on the absolute values of VO2max , on VO2max/LBM, and on post-exercise changes in La- concentration., M. Wiecek, M. Maciejczyk, J. Szymura, Z. Szygula., and Obsahuje bibliografii
Free radicals and proinflammatory cytokines from phagocytes have been implicated in the pathogenesis of endotoxic shock, a disease with high mortality caused by Gram-negative bacterial endotoxin. In the present study, male BALB/c and Swiss mice received intraperitoneally lipopolysaccharide (LPS) at 100 mg/kg and 150 mg/kg, respectively, that led to a lethal endotoxic shock (100 % of mortality before 30 h). Swiss mice injected with 100 mg/kg, that did not show lethal endotoxic shock, were also studied. Peritoneal macrophages were obtained from animals at 2, 4, 12 or 24 h after injection of LPS or saline (control) solutions. Superoxide anion and tumor necrosis factor (TNFα) production were determined in these cells as well as other functions such as adherence capacity, chemotaxis and phagocytosis. The increase in superoxide anion production after endotoxin injection was higher in cells from mice with lethal shock than in those with non-lethal shock. However, the enhancement of TNFα production was similar in all cases, although in Swiss mice the highest levels of TNFα were observed at 1.5 h after endotoxin injection, while in BALB/c mice they occurred at 2 h after LPS injection. This oxidative stress was also revealed by the other functions analyzed, since adherence to substrate and phagocytosis were stimulated and chemotaxis was decreased after endotoxin injection as compared to controls, the differences being even more significant in animals with lethal shock. These data suggest that these changes, mainly the increased production of free radicals even more than the TNFα release, could be involved in mouse mortality caused by LPS., V. M. Víctor, M. de la Fuente., and Obsahuje bibliografii
Mitochondrial dysfunction and oxidative stress participate in the development of diabetic complications, however, the mechanisms of their origin are not entirely clear. Coenzyme Q has an important function in mitochondrial bioenergetics and is also a powerful antioxidant. Coenzyme Q (CoQ) regenerates alpha-tocopherol to its active form and prevents atherogenesis by protecting low-density lipoproteins against oxidation. The aim of this study was to ascertain whether the experimentally induced diabetes mellitus is associated with changes in the content of endogenous antioxidants (alpha-tocopherol, coenzymes Q9 and Q10) and in the intensity of lipoperoxidation. These biochemical parameters were investigated in the blood and in the isolated heart and liver mitochondria. Diabetes was induced in male Wistar rats by a single intravenous injection of streptozotocin (45 mg.kg-1), insulin was administered once a day for 8 weeks (6 U.kg-1). The concentrations of glucose, cholesterol, alpha-tocopherol and CoQ homologues in the blood of the diabetic rats were increased. The CoQ9/cholesterol ratio was reduced. In heart and liver mitochondria of the diabetic rats we found an increased concentration of alpha-tocopherol, however, the concentrations of CoQ9 and CoQ10 were decreased. The formation of malondialdehyde was enhanced in the plasma and heart mitochondria. The results have demonstrated that experimental diabetes is associated with increased lipoperoxidation, in spite of the increased blood concentrations of antioxidants alpha-tocopherol and CoQ. These changes may be associated with disturbances of lipid metabolism in diabetic rats. An important finding is that heart and liver mitochondria from the diabetic rats contain less CoQ9 and CoQ10 in comparison with the controls. We suppose that the deficit of coenzyme Q can participate in disturbances of mitochondrial energy metabolism of diabetic animals., J. Kucharská, Z. Braunová, O. Uličná, L. Zlatoš, A. Gvozdjáková., and Obsahuje bibliografii
Increased oxidative stress is indisputably an important mechanism of doxorubicin side effects, especially its cardiotoxicity. To prevent impairment of non-tumorous tissue and to improve the specificity in targeting the tumor tissue, new drug nanotransporters are developed. In many cases preclinical therapeutic advantage has been shown when compared with the administration of conventional drug solution. Three forms of doxorubicin - conventional (DOX), encapsulated in liposomes (lipoDOX) and in apoferritin (apoDOX) were applied to Wistar rats. After 24 h exposition, the plasma level of 4-hydroxy-2- nonenal (4-HNE) as a marker of lipoperoxidation and tissue gene expression of thioredoxin reductase 2 (TXNRD2) and aldehyde dehydrogenase 3A1 (ALDH3A1) as an important part of antioxidative system were determined. Only conventional DOX significantly increases the level of 4-HNE; encapsulated forms on the other hand show significant decrease in plasma levels of 4-HNE in comparison with DOX. They also cause significant decrease in gene expression of ALDH3A1 and TXNRD2 in liver as a main detoxification organ, and a mild influence on the expression of these enzymes in left heart ventricle as a potential target of toxicity. Thus, 4-HNE seems to be a good potential biomarker of oxidative stress induced by various forms of doxorubicin., M. Hlaváčová, J. Gumulec, T. Stračina, M. Fojtů, M. Raudenská, M. Masařík, M. Nováková, H. Paulová., and Obsahuje bibliografii
Despite the demonstrated exercise -induced increase in reactive oxygen species (ROS) production, growing epidemiological evidence indicates that habitual, moderate physical activity reduces the incidence of several oxidative stress-based diseases. This apparent paradox can be explained taking into account that ROS produced during repeated ex ercise bouts may act as mild stressors able to trigger physiological and biomolecular hormetic responses through a number of redox-sensitive transcription pathways. Unfortunately, much more limited information is available from general population-based research, which could better reflect the condition of common people interested in achieving and maintaining good fitness levels. The present work aimed at investigatin g whether and how exercise-related habits in non-professional regular runners (n=33) can affect the systemic anti-oxidative capacity, and the resting serum levels of typical lipid peroxidation-related by-products and oxidatively- damaged proteins, in comparison with untrained sedentary individuals (n=25). We also anal yzed in both groups the redox response elicited by a modified Bruce-based maximal exercise test on the same parameters. Our findings indicated that long- term regular and moderate practice of aerobic physical activity can increase antioxidant defense systems, lower the resting protein oxidation processes and reduce the immediate up- regulation of lipid-targeting oxidative stress in response to an acute bout of exercise., S. Falone, A. Mirabilio, A. Pennelli, M. Cacchio, A. Di Baldassarre, S. Gallina, A. Passerini, F. Amicarelli., and Obsahuje bibliografii
Oxidative stress and apoptosis are proposed mechanisms of cellular injury in studies of xenobiotic hepatotoxicity. This study is focused on addressing the mutual relationship and early signals of these mechanisms in the D-galactosamine and lipopolysaccharide (D-GalN/LPS) hepatotoxicity model, with the help of standard liver function and biochemistry tests, histology, and measurement of gene expression by RT-PCR. Intraperitoneal injection of 400 mg/kg D-GalN and 50 μg/kg LPS was able to induce hepatotoxicity in rats, as evidenced by significant increases in liver enzymes (ALT, AST) and raised bilirubin levels in plasma. Heme oxygenase-1 and nitric oxide synthase-2 gene expressions were significantly increa sed, along with levels of their products, bilirubin and nitrite. Th e gene expression of glutathione peroxidase 1 remained unchanged, whereas a decrease in superoxide dismutase 1 gene expression was noted. Furthermore, the significant increase in the gene expression of apoptotic genes Bid, Bax and caspase-3 indicate early activation of apoptotic pathways, which was confirmed by histological evaluation. In contrast, the measured caspase-3 activity remained unchanged. Overall, the results have revealed differential oxidative stress and apoptotic responses, which deserves further investigations in this hepatotoxicity model., N. Lekić ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy