scholarly journals The protective effect of vildagliptin in chronic experimental cyclosporine A-induced hepatotoxicity

2016 ◽  
Vol 94 (3) ◽  
pp. 251-256 ◽  
Author(s):  
Nagla A. El-Sherbeeny ◽  
Manar A. Nader
Keyword(s):  
Oxidative Stress ◽  
Nuclear Factor Kappa B ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Nuclear Extract ◽  
Thiobarbituric Acid Reactive Substance ◽  
Histopathological Changes ◽  
Dipeptidyl Peptidase 4 ◽  
Stress Markers ◽  
Apoptosis And Inflammation

The study examined the effect of dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin, in cyclosporine (CsA)-induced hepatotoxicity. Rats were divided into 4 groups treated for 28 days: control (vehicle), vildagliptin (10 mg/kg, orally), CsA (20 mg/kg, s.c.), and CsA-vildagliptin group. Liver function was assessed by measuring serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyltransferase (γGT), lactate dehydrogenase (LDH), and albumin, and histopathological changes of liver were examined. Oxidative stress markers were evaluated. Assessment of nuclear factor-kappa B (NF-κB) activity in hepatic nuclear extract, serum DPP-4, and expression of Bax and Bcl2 were also done. CsA-induced hepatotoxicity was evidenced by increase in serum levels of AST, ALT, and γGT; a decrease in serum albumin; and a significant alteration in hepatic architecture. Also, significant increase in thiobarbituric acid reactive substance (TBARS) and decrease in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH) levels, increased expression Bax proteins with deceased expression of Bcl2, and increased hepatic activity of NF-κB and serum DPP-4 level were observed upon CsA treatment. Vildagliptin significantly improved all altered parameters induced by CsA administration. Vildagliptin has the potential to protect the liver against CsA-induced hepatotoxicity by reducing oxidative stress, DPP-4 activity, apoptosis, and inflammation.

Degradation of oxidative stress-induced denatured albumin in rat liver endothelial cells

2005 ◽  
Vol 289 (3) ◽  
pp. C531-C542 ◽  
Author(s):  
Ryuji Bito ◽  
Sayaka Hino ◽  
Atsushi Baba ◽  
Miharu Tanaka ◽  
Haruka Watabe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Rat Liver ◽  
Laser Scanning ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Endocytic Pathway ◽  
Thiobarbituric Acid Reactive Substance ◽  
Liver Endothelial Cells

We previously identified conformationally denatured albumin (D2 and D3 albumin) in rats with endotoxicosis (Bito R, Shikano T, and Kawabata H. Biochim Biophys Acta 1646: 100–111, 2003). In the present study, we attempted first to confirm whether the denatured albumins generally increase in conditions of oxidative stress and second to characterize the degradative process of the denatured albumin using primary cultured rat liver endothelial cells. We used five models of oxidative stress, including endotoxicosis, ischemic heart disease, diabetes, acute inflammation, and aging, and found that serum concentrations of D3 albumin correlate with the serum levels of thiobarbituric acid-reactive substance ( R = 0.87), whereas the concentrations of D2 albumin are 0.52. Ligand blot analysis showed that the D3 albumin binds to gp18 and gp30, which are known endothelial scavenger receptors for chemically denatured albumin. Primary cultured rat liver endothelial cells degraded the FITC-D3 albumin, and the degradation rate decreased to ∼60% of control levels in response to anti-gp18 and anti-gp30 antibodies, respectively. An equimolar mixture of these antibodies produced an additive inhibitory effect on both uptake and degradation, resulting in levels ∼20% those of the control. Furthermore, filipin and digitonin, inhibitors of the caveolae-related endocytic pathway, reduced the FITC-D3 albumin uptake and degradation to <20%. Laser-scanning confocal microscopic observation supported these data regarding the uptake and degradation of D3 albumin. These results indicate that conformationally denatured D3 albumin occurs generally under oxidative stress and is degraded primarily via gp18- and gp30-mediated and caveolae-related endocytosis in liver endothelial cells.

Rosa rugosa Attenuates Diabetic Oxidative Stress in Rats with Streptozotocin-Induced Diabetes

2004 ◽  
Vol 32 (04) ◽  
pp. 487-496 ◽  
Author(s):  
Eun Ju Cho ◽  
Takako Yokozawa ◽  
Hyun Young Kim ◽  
Naotoshi Shibahara ◽  
Jong Cheol Park
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Body Weight Gain ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Radical Scavenger ◽  
Thiobarbituric Acid Reactive Substance ◽  
Rosa Rugosa

The effects of Rosa rugosa on diabetic oxidative stress were investigated using rats with streptozotocin (STZ)-induced diabetes. The diabetic rats showed less body weight gain and heavier kidney and liver weights than normal rats, while the oral administration of Rosa rugosa at a dose of 100 or 200 mg/kg body weight/day for 20 days attenuated the physiological changes induced by diabetes. In addition, administrating Rosa rugosa to diabetic rats resulted in significant and dose-dependent decreases in the serum glucose and glycosylated protein levels, implying that Rosa rugosa improves the abnormal glucose metabolism that leads to oxidative stress. Diabetic rats had higher serum levels of superoxide and nitrite/nitrate. However, the administration of Rosa rugosa dose-dependently reduced the over-production of radicals associated with diabetes, suggesting Rosa rugosa is a radical scavenger that would play a crucial role in protecting against diabetic oxidative stress. Rosa rugosa significantly and dose-dependently reduced thiobarbituric acid-reactive substance levels in serum, hepatic and renal mitochondria, implying that Rosa rugosa would alleviate the oxidative stress associated with diabetes by inhibiting lipid peroxidation. This study provides evidence that Rosa rugosa has potential as a treatment for diabetes through attenuating oxidative stress induced by the diabetic condition

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

Oxidative Stress Markers and Metal Ions are Correlated With Cognitive Function in Alzheimer’s Disease

2017 ◽  
Vol 32 (6) ◽  
pp. 353-359 ◽  
Author(s):  
Zhengping Pu ◽  
Wenjie Xu ◽  
Yong Lin ◽  
Jincai He ◽  
Manli Huang
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Metal Ions ◽  
Serum Levels ◽  
Zinc Level ◽  
Copper Level ◽  
Iron Level ◽  
Oxidative Stress Markers ◽  
Stress Markers

We investigated oxidative stress markers and metal ions in patients with Alzheimer’s disease (AD). The serum levels of ceruloplasmin (CER), C-reactive protein (CRP), uric acid (UA), homocysteine (Hcy), copper, iron, and zinc were determined in 125 patients with AD (mild, n = 2 8; moderate, n = 42; and severe, n = 55) and 40 healthy control (HC) participants. Compared to HC, CER and UA levels were significantly lower in moderate and severe AD groups, whereas CRP and Hcy levels were significantly higher in the severe AD group. Copper level was significantly higher in moderate and severe AD groups than the other groups. Compared to HC, iron level was significantly higher in patients with AD, whereas zinc level was significantly lower in patients with AD. In patients with AD, the severity of cognitive impairment was positively correlated with CER, UA, and zinc levels, whereas it was negatively correlated with copper level. Taken together, our findings provide a novel approach to assess AD progression.

scholarly journals PSI-36 Effect of short-chain fructooligosaccharides on Trolox equivalent antioxidant capacity and thiobarbituric acid reactive substances in mature and senior stock-type horses

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 254-255
Author(s):  
Emili McClure ◽  
Courtney P Heaton ◽  
Dishnu Sajeev ◽  
Thu Dinh
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Random Effect ◽  
Thiobarbituric Acid ◽  
Short Chain ◽  
Trolox Equivalent Antioxidant Capacity ◽  
Thiobarbituric Acid Reactive Substances ◽  
Stress Markers ◽  
Trolox Equivalent ◽  
Stock Type

Abstract Oxidative stress (OS) causes health complications through the destruction of cellular components as individuals age. Reactive oxygen species are used to measure OS through Trolox equivalent antioxidant capacity (TEAC) and thiobarbituric acid reactive substances (TBARS). Other prebiotics have been used to reduce OS markers in numerous species; however, the effect of short-chain fructooligosaccharides (scFOS) on OS has not been studied in the horse. Ten healthy stock-type horses were blocked by age into 2 groups: mature (MA; n = 5; 7.0 ± 0.87 yr) and senior (SR; n = 5; 22.6 ± 1.1 yr) to analyze effects of scFOS on TEAC and TBARS. Horses were randomly assigned to 1 of 3 diets for 25 d before transition to another diet. Diets were bermudagrass hay offered at 1.5% BW/d hay as-fed, hay with a ration balancer (CON), or hay with a ration balancer and scFOS added at a rate of 2.5 g/kg (PRE). Prior to a total fecal collection for an alternate study, horses were fasted overnight for 8 h with blood samples taken immediately prior to feeding (0), 30, and 60 min postprandial. Oxidative stress markers were analyzed for the 2 ration balancer diets. Statistical analysis was performed with SAS using the MIXED procedure with horse within diet as a random effect with significance of P ≤ 0.05. Trolox equivalent antioxidant capacity was unaffected by diet (P = 0.827) or age (P = 0.347). Time (P = 0.006) was significant for TBARS which increased postprandial regardless of treatment or age. Consistent with other species, higher levels of OS was found in SR compared to MA regardless of time or diet (P = 0.037; 4.491 µM vs. 3.412 µM TBARS, respectively). These results indicate that scFOS do not seem to be effective in reducing OS in SR and MA horses.

scholarly journals Effect of percutaneous transthoracic lung biopsy on oxidative metabolism in sheep

2012 ◽  
Vol 83 (1) ◽  
Author(s):  
Andreza A. Silva ◽  
Danilo O.L. Ferreira ◽  
Bianca P. Santarosa ◽  
Adriano Dias ◽  
Débora C. Damasceno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Metabolism ◽  
Lung Biopsy ◽  
Thiobarbituric Acid ◽  
Oxidative Stress Markers ◽  
Thiobarbituric Acid Reactive Substances ◽  
Total Glutathione ◽  
Blood Samples ◽  
Stress Markers ◽  
Healthy Sheep

This study aimed to assess the effect of percutaneous transthoracic lung biopsy on the oxidative metabolism of sheep by measuring the oxidative stress markers of superoxide dismutase (SOD), total glutathione (GSH-t), peroxidase (GSH-Px) and thiobarbituric acid reactive substances (TBARS) in the red cells of these animals. Blood samples were collected from 20 clinically healthy sheep prior to, and 30 min after, percutaneous transthoracic lung biopsy. After biopsy, there was a significant decrease (p < 0.05) in SOD and GSH-Px activity, with no significant change (p ≥ 0.05) in GSH-t and TBARS concentrations. These results showed that percutaneous transthoracic lung biopsy did not significantly affect the oxidative metabolism of sheep 30 min after the procedure, which may be used widely in this species without causing serious tissue damage.  

Chronic hypoxia and glutathione-dependent detoxication in rat small intestine

1996 ◽  
Vol 270 (4) ◽  
pp. G725-G729 ◽  
Author(s):  
T. S. LeGrand ◽  
T. Y. Aw
Keyword(s):  
Oxidative Stress ◽  
Chronic Hypoxia ◽  
Thiobarbituric Acid ◽  
Redox System ◽  
Thiobarbituric Acid Reactive Substance ◽  
Sprague Dawley ◽  
Distal Intestine ◽  
Key Enzyme ◽  
Cysteine Synthetase ◽  
Glucose 6 Phosphate Dehydrogenase

It has previously been found that chronic O2 deficiency decreases activity of the enzymes of the glutathione (GSH) redox system in the liver. To study the effects of O2 deficiency on intestinal detoxication capacity, pair-fed (16 g food/day) Sprague-Dawley rats were exposed to air (20.9% O2; n = 4) or 10% O2 (n = 4) for 10 days. Animals were killed, and intestinal mucosal homogenate (20% wt/vol) was obtained and assayed for activities of glucose-6-phosphate dehydrogenase (G6PD), GSH peroxidase (GSHPx), GSH disulfide reductase (GSSGRd), and gamma-glutamyl cysteine synthetase (gamma-GCS). Hypoxia decreases activities of GSHPx, GSSGRd, and gamma-GCS by approximately 50%, which suggests compromised detoxication. A proximal-to-distal reduction in enzymatic capacity indicates impairment of detoxication may be more pronounced in the distal intestine. G6PD, a key enzyme in NADPH production, remains unchanged. Urinary malondialdehyde was also monitored. Hypoxic rats exhibited a threefold increase in thiobarbituric acid-reactive substance, consistent with a generalized oxidative stress in these animals. Taken together, the results indicate that chronic hypoxia promotes tissue oxidative stress and impairs the ability of the enterocyte to metabolize ingested oxidants.

scholarly journals Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Julie Chao ◽  
Youming Guo ◽  
Pengfei Li ◽  
Lee Chao
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Animal Models ◽  
Hypoxia Inducible Factor ◽  
Thiobarbituric Acid ◽  
Organ Injury ◽  
Thiobarbituric Acid Reactive Substance ◽  
Bacterial Killing ◽  
Antioxidant Genes ◽  
Pkc Activation

Oxidative stress has both detrimental and beneficial effects. Kallistatin, a key component of circulation, protects against vascular and organ injury. Serum kallistatin levels are reduced in patients and animal models with hypertension, diabetes, obesity, and cancer. Reduction of kallistatin levels is inversely associated with elevated thiobarbituric acid-reactive substance. Kallistatin therapy attenuates oxidative stress and increases endothelial nitric oxide synthase (eNOS) and NO levels in animal models. However, kallistatin administration increases reactive oxygen species formation in immune cells and bacterial killing activity in septic mice. High oxygen inhibits kallistatin expression via activating the JNK-FOXO1 pathway in endothelial cells. Conversely, mild oxygen/hyperoxia stimulates kallistatin, eNOS, and hypoxia-inducible factor-1 (HIF-1) expression in endothelial cells and in the kidney of normal mice. Likewise, kallistatin stimulates eNOS and HIF-1, and kallistatin antisense RNA abolishes oxygen-induced eNOS and HIF-1 expression, indicating a role of kallistatin in mediating mild oxygen’s stimulation on antioxidant genes. Protein kinase C (PKC) activation mediates HIF-1-induced eNOS synthesis in response to hyperoxia/exercise; thus, mild oxygen through PKC activation stimulates kallistatin-mediated HIF-1 and eNOS synthesis. In summary, oxidative stress induces down- or upregulation of kallistatin expression, depending on oxygen concentration, and kallistatin plays a novel role in mediating oxygen/exercise-induced HIF-1-eNOS-NO pathway.

scholarly journals Serum Levels of Oxidative Stress Markers in Patients with Type 2 Diabetes Mellitus and Non-alcoholic Steatohepatitis

2016 ◽  
Vol 54 (4) ◽  
pp. 228-236 ◽  
Author(s):  
F. Casoinic ◽  
D. Sampelean ◽  
Anca D. Buzoianu ◽  
N. Hancu ◽  
Dorina Baston
Keyword(s):  
Oxidative Stress ◽  
Fatty Liver Disease ◽  
Serum Levels ◽  
Protein Carbonyls ◽  
Oxidative Stress Markers ◽  
Multivariate Logistic Regression ◽  
Alcoholic Fatty Liver ◽  
Stress Markers ◽  
Alcoholic Fatty Liver Disease

Abstract Introduction. Oxidative stress is one of the key mechanisms responsible for disease progression in non-alcoholic fatty liver disease. The aim of this study was to evaluate the serum levels of oxidative stress markers in patients with type 2 diabetes mellitus (DMT2) and non-alcoholic steatohepatitis (NASH) and test their relationships with clinical and biochemical patient characteristics, compared to patients with DMT2 without non-alcoholic fatty liver disease (NAFLD), and controls. Materials and methods. In all, 60 consecutive patients with DMT2 and NASH, 55 with DMT2 without NAFLD, and 50 age-and-gender-matched healthy subjects participated in the study. The serum levels of protein carbonyls and 8-isoprostane were determined by ELISA methods, while the serum levels of malondialdehyde (MDA) were detected by means of the spectrophotometric method. Clinical, demographic, and laboratory parameters were examined for all the subjects included in the study. Multivariate logistic regression was used to test the independent predictive factors in the relationships investigated here. Results. Patients with DMT2 and NASH displayed significantly higher serum levels of protein carbonyls (1.112 ± 0.42 nmol/dL), MDA (6.181 ± 1.81 ng/mL), and 8-isoprostane (338.6 ± 98.5 pg/mL) compared to patients with DMT2 without NAFLD, and controls. Results of multivariate logistic regression analyses indicate that in patients with DMT2 and NASH, the serum levels of oxidative stress markers were independently and positively associated with: HbA1c, duration of diabetes, the UKPDS cardiovascular risk score (for protein carbonyls); age, LDL-cholesterol (for 8-isoprostane); and triglycerides serum levels (for MDA). Conclusions. Our findings indicate that the process of oxidative stress tends to increase in patients with DMT2 and NASH, compared to patients with DMT2 without NAFLD, and controls. This evidence suggests that an antioxidant therapy might prove useful in the treatment of patients with DMT2 and NASH.

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