thiobarbituric-acid and Inflammation

Biomedical research has recently incorporated bioceramics applications into new health care approaches.. This study evaluated the effect of far infrared-emitting bioceramics wraps in the treatment of intermittent claudication.. This is a randomized double-blind placebo-controlled pilot study. Thirty-five patients met the criteria and were randomized into either control (placebo wraps) or bioceramics group (far infrared emitting-ceramics wraps) and assessed over a 90-day period for the following outcomes: six-minute walk test (6MWT), ankle-brachial index (ABI), Flow-mediated arterial dilation (FMD), quality of life and claudication. Oxidative stress and inflammatory biomarkers were measured in plasma of patients.. Intervention induced a decrease in oxidative stress, with significant lower levels of reactive substances to thiobarbituric acid (TBARS), as well as increase in superoxide dismutase and catalase enzyme activities. There was an increase in the environment subscale of the quality of life questionnaire. No statistically significant differences were found in the inflammatory cytokines, 6MWT, ABI and FMV evaluations.. In Sum, FIR treatment improved oxidative stress profile and quality-of-life of patients with intermittent claudication. The study was registered into the ensaiosclinicos.gov.br (Registro Brasileiro de Ensaios Clínicos [ReBEC]) (RBR-7nr6sy register number).

Topics: Ankle Brachial Index; Antioxidants; Biomarkers; Double-Blind Method; Humans; Inflammation; Infrared Rays; Intermittent Claudication; Oxidative Stress; Pilot Projects; Quality of Life; Superoxide Dismutase; Thiobarbiturates; Treatment Outcome; Walking

The aim of this study was to investigate the effect of plant superoxide dismutase extract (GliSODin) supplementation on the balance of oxidants and antioxidants in the serum and erythrocytes of competitive rowers. The double-blinded study included 19 members of the Polish rowing team who were participating in a preparatory camp. Subjects were randomly assigned to the supplemented group (n = 10), who received 2 capsules (500 mg) of GliSODin extract once daily for 6 weeks, or the placebo group (n = 9). At the beginning and end of the study, subjects performed a 2,000-m maximum-effort test on a rowing ergometer. Blood samples were taken from the antecubital vein before each exercise test, 1 min after completing the test, and after a 24-hr restitution period. The following redox parameters were assessed in erythrocytes: superoxide dismutase (SOD) activity, glutathione peroxidase activity, and concentrations of thiobarbituric-acid-reactive substances. In addition, creatine kinase activity and total antioxidant capacity were measured in plasma samples, lactate levels were determined in capillary blood samples, and C-reactive protein and lactate dehydrogenase concentrations were measured in serum. After supplementation, SOD activity was significantly higher (p = .0037) in the supplemented group than the placebo group, and C-reactive protein was significantly (p = .00001) lower in athletes receiving GliSODin than those in the placebo group. In conclusion, supplementation with an extract rich in SOD activity promoted antioxidant status and protected against increased inflammation in the serum of professional rowers but had no effect on oxidative damage induced by exhaustive exercise.

Topics: Administration, Oral; Antioxidants; Biomarkers; C-Reactive Protein; Creatine Kinase; Exercise; Glutathione Peroxidase; Humans; Inflammation; Lactic Acid; Male; Oxidation-Reduction; Plant Extracts; Superoxide Dismutase; Thiobarbiturates; Young Adult

Cyclooxygenase (COX)-inhibiting nitric oxide (NO) donors (CINODs) are designed to inhibit COX-1 and COX-2 while releasing NO. COX inhibition is responsible for anti-inflammatory and pain-relieving effects, whereas NO donation can improve microcirculation and exert anti-inflammatory and antioxidant actions. In an in vivo mouse model of bleomycin-induced lung fibrosis, we evaluated whether a prototype CINOD compound, (S)-(5S)-5,6-bis(nitrooxy)hexyl)2-(6-methoxynaphthalen-2-yl)propanoate (NCX 466), may show an advantage over naproxen, its congener drug not releasing NO. Bleomycin (0.05 IU) was instilled intratracheally to C57BL/6 mice, which were then treated orally with vehicle, NCX 466 (1.9 or 19 mg/kg), or an equimolar dose of naproxen (1 or 10 mg/kg) once daily for 14 days. Afterward, airway resistance, assumed as lung stiffness index, was assayed, and lung specimens were collected for analysis of lung inflammation and fibrosis. NCX 466 and naproxen dose-dependently prevented bleomycin-induced airway stiffness and collagen accumulation. NCX 466, at the highest dose, was significantly more effective than naproxen in reducing the levels of the profibrotic cytokine transforming growth factor-β and the oxidative stress markers thiobarbituric acid reactive substance and 8-hydroxy-2'-deoxyguanosine. NCX 466 also decreased myeloperoxidase activity, a leukocyte recruitment index, to a greater extent than naproxen. A similar inhibition of prostaglandin E₂ was achieved by both compounds. In conclusion, NCX 466 has shown a significantly higher efficacy than naproxen in reducing lung inflammation and preventing collagen accumulation. These findings suggest that COX inhibition along with NO donation may possess a therapeutic potential in lung inflammatory diseases with fibrotic outcome.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Anti-Inflammatory Agents; Antibiotics, Antineoplastic; Bleomycin; Collagen; Cyclooxygenase Inhibitors; Deoxyguanosine; Dinoprostone; Inflammation; Lung; Male; Mice; Mice, Inbred C57BL; Naproxen; Nitrates; Nitric Oxide; Nitric Oxide Donors; Oxidative Stress; Peroxidase; Propionates; Prostaglandin-Endoperoxide Synthases; Pulmonary Fibrosis; Thiobarbiturates; Transforming Growth Factor beta

Reactive oxygen metabolites (ROM) may play a role in the pathophysiology of inflammatory bowel disease (IBD) and ischemia-reperfusion-induced intestinal injury. Although there are many reports of intestinal mucosal injury associated with neutrophil-derived ROM, free radicals themselves have not been reported to induce intestinal mucosal injury. We administered intrarectally 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) to rats, an azo compound that generates free radicals in vitro. Acute mucosal injury was assessed histologically by light microscopy and biochemically by myeloperoxidase (MPO) activity. Intrarectal administration of AAPH (60, 90, 150 mg/kg) caused erythema, edema, and histologically verifiable mucosal inflammation. MPO activity was increased 9- to 18-fold above the control level. The levels of thiobarbituric acid (TBA) reactants and sulfhydryls (SH) were significantly (P less than 0.01) increased and decreased, respectively, by 90 mg/kg AAPH. Sulfasalazine, 5-aminosalicylic acid, the LTB4 receptor antagonist SC-41930, and the antioxidant glutathione prevented the inflammation. This model of mucosal inflammation may be useful in evaluating new therapeutic agents for the treatment of IBD.

Topics: Amidines; Aminosalicylic Acids; Animals; Benzopyrans; Colitis; Inflammation; Intestinal Mucosa; Lipid Peroxidation; Male; Mesalamine; Oxidation-Reduction; Peroxidase; Rats; Rats, Inbred Strains; Sulfasalazine; Sulfhydryl Compounds; Thiobarbiturates

In order to investigate the influence of antioxidative/anti-inflammatory combination therapy (AACT) with dimethyl sulfoxide (DMSO), chlorpromazine (CPZ) and vitamin E upon the activity of the inflammation, plasma lipid peroxide was measured as thiobarbituric acid reactive substance (TBARS) 12 hrs postoperatively in the modified cecal ligation sepsis model in the mouse. Significantly higher TBARS levels were found in the male control group (13.7 +/- 0.7 nmol MDA/ml) than in the female control group (11.6 +/- 0.6 nmol MDA/ml). The operated male group had significantly higher TBARS levels (16.2 +/- 0.6 nmol MDA/ml) than the unoperated male control group (13.7 +/- 0.7 nmol MDA/ml). No increase of TBARS levels was observed in the operated female group. Both male and female operated group, when postoperatively treated with AACT had the same TBARS level as the not operated male or female control group. Survival curves of operated male and female group did not demonstrate any significant difference. The survival was better in an operated male and an operated female group, when postoperatively treated with AACT. It was concluded that the applied TBARS test is too insensitive to follow the activity of the inflammation and has no predictive value for the outcome of sepsis in this model.

Topics: Animals; Bacterial Infections; Cecal Diseases; Chlorpromazine; Dimethyl Sulfoxide; Drug Therapy, Combination; Female; Inflammation; Lipid Peroxides; Male; Mice; Sex Characteristics; Thiobarbiturates; Vitamin E

Gold (Au) thioglucose, which has been used in the treatment of rheumatoid arthritis, inhibits selenium (Se)-glutathione peroxidase. Since Au and Se play roles in inflammation, the effects of dietary Se (0, 0.2, and 2.0 ppm for 10 weeks) and injected gold thioglucose (5 mg Au/day/kg body weight for 28 days) in adjuvant-treated rats were investigated. Au toxicity was evidenced by lower body weights and higher tissue weight/body weight ratios for kidneys and spleens of Au-treated rats. Adjuvant-induced inflammation, measured by paw thickness, was not influenced by dietary Se, although Au decreased inflammation in Se-deficient rats. Liver glutathione peroxidase activity was depressed by Se deficiency and by Au. Sulfhydryl levels in liver soluble fraction and plasma were highest for Se-deficient rats. Among liver, kidney, spleen, and plasma, thiobarbituric acid reactants were highest in kidneys of Au-treated rats and lowest in plasma of rats fed 2 ppm Se. gamma-Glutamyltranspeptidase activity in plasma indicated liver damage in Se-deficient rats. Kidney PGE2 output in 24-hour urine samples was unaffected by Au, Se, or adjuvant. Au-Se interactions in vivo are complex, but decreased glutathione peroxidase activity in Au-injected rats suggests that Se nutrition of Au-treated rheumatoid arthritis patients may be a practical concern.

Topics: Animals; Aurothioglucose; Body Weight; Diet; Dinoprostone; Freund's Adjuvant; gamma-Glutamyltransferase; Glutathione Peroxidase; Gold; Inflammation; Kidney; Liver; Male; Organ Size; Prostaglandins E; Rats; Rats, Inbred Strains; Selenium; Thiobarbiturates