The protective effect of epicatchin against oxidative stress and nephrotoxicity in rats induced by cyclosporine

2010 ◽  
Vol 30 (2) ◽  
pp. 145-151 ◽  
Author(s):  
Abdulrahman L Al-Malki ◽  
Said S Moselhy
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Protective Effect ◽  
Cell Damage ◽  
Solid Organ Transplantation ◽  
Thiobarbituric Acid ◽  
Solid Organ ◽  
Thiobarbituric Acid Reactive Substances ◽  
First Line ◽  
Human Diet

Cyclosporine A (CyA) is the first-line immunosuppressant used for the management of solid organ transplantation and autoimmune diseases. Reactive oxygen species (ROS) can attack all types of macromolecules including DNA and damage it. Epicatechin (EC) is one of the most potent antioxidants present in the human diet. Particularly high levels of this compound are found in tea, apples, and chocolate. The goal of this study was to evaluate the protective effect of EC against CyA toxicity and its antioxidant activity in transplanted patients to avoid its side effects. Results obtained showed that, CyA exert its toxic effect by increasing the free radicals and ROS that causes lipid peroxidation and cell damage, this is detected by elevation of hydroperoxides and thiobarbituric acid reactive substances, while the activities of antioxidant enzymes include (superoxide dismutase [SOD], catalase [CAT] and glutathione peroxidase [GPx]) were significantly decreased as compared with control rats. The deleterious toxic effects of CyA are, at least in part, due to increased production of free radicals and ROS. Treatment of rats with epicatchin ameliorates the toxicity of CyA by decreasing the lipid peroxidation and enhanced the antioxidants enzyme activities.

scholarly journals Biochemical Studies on Phenylhydrazine Induced Experimental Anemic Albino Rats

2015 ◽  
Vol 3 (1) ◽  
pp. 41-47
Author(s):  
Nirjala Laxmi Madhikarmi ◽  
Kora Rudraiah Siddalinga Murthy
Keyword(s):  
Lipid Peroxidation ◽  
Lipid Hydroperoxide ◽  
Thiobarbituric Acid ◽  
Albino Rats ◽  
Enzymatic Antioxidants ◽  
Medical Sciences ◽  
Thiobarbituric Acid Reactive Substances ◽  
Biochemical Studies ◽  
Healthy Control ◽  
Wistar Albino Rats

INTRODUCTION: The present study evaluated the modulatory effects of diphenylhydrazine induced experimental wistar albino rats and also to assess various biochemical parameters in whole blood and red blood cell lysate.MATERIALAND METHODS: Twenty male albino rats weighing 180-200 gm were selected for the study and divided in two groups; ten phenylhydrazine dihydrochloride (PHZ) induced anemia and ten healthy control. Thiobarbituric acid reactive substances and lipid hydroperoxide were measured as lipid peroxidation parameter. The antioxidant vitamins A, C and E and enzymatic antioxidants; catalase, glutathione peroxidase and superoxide dismutase were also assessed.RESULTS: Phenylhydrazine induced anemic rats showed a significant increase in the lipid peroxidation and decrease in the antioxidants as compared to healthy rats.CONCLUSION: The study concludes that phenylhydrazine induced experimental anemic albino rats showed increased oxidative stress than compared with healthy albino rats.Journal of Universal College of Medical Sciences Vol. 3, No. 1, 2015: 41-47 

scholarly journals The Cytoprotective and Cell Recovery Properties of Apple Extracts on H2O2 induced-NIH3T3 Cells: An Anti Aging Candidate

2018 ◽  
Vol 9 (2) ◽  
pp. 78 ◽  
Author(s):  
Nunuk Aries Nurulita ◽  
Anjar Mahardian Kusuma ◽  
Darsini Darsini ◽  
Weny Delvia ◽  
Veby Tri Yulianti
Keyword(s):  
Free Radicals ◽  
Vitamin C ◽  
Protective Effect ◽  
Cell Damage ◽  
Cell Aging ◽  
Fibroblast Cells ◽  
Cell Recovery ◽  
High Concentration ◽  
High Potency ◽  
Nih3t3 Cells

Apple contains high concentration of phenolic compounds that protect cells from oxidative stress. The prolong exposure of free radicals may induce cell damage and premature cell aging. Both local and imported apple contain flavonoid, saponin, tannin, steroid, and terpenoid. The extract of local and imported apples showed low toxicity on NIH3T3 fibroblast cells, with IC50 value of 529 and 463 µg/mL, respectively. Both apple extracts (50 – 250 µg /mL) protected three-day-H2O2 induced-cell damage and cell death. Protective effect was observed as the viability increase of treated cells compared to untreated ones. The protective effect of both extracts were higher than the effect of vitamin C as standard antioxidant at this study. Both apple extracts could reverse cell damage caused by three-hour-high concentration H2O2 exposure, similar with vitamin C. Low concentration of both extracts (50 µg /mL) induced the increase of fibroblast cells’ proliferation kinetics. The extract of imported apple showed higher properties of protective, cell recovery and proliferation of fibroblast cells tha local apple, but not statistically significance. This study concludes that the extract of local and imported apples have high potency in cytoprotective effect and cell recovery of damaged cells caused by free radicals induction. Both apple extracts have high potency to be developed the candidate of antiaging and cells’ regeneration agent.Key words: antiaging, cell recovery, cytoprotective, NIH3T3 cells

scholarly journals Plasma Lipid Peroxidation as a Marker for Seminal Oxidative Stress in Stallion

2019 ◽  
Vol 11 (6) ◽  
pp. 401
Author(s):  
Patricia Wolkmer ◽  
Andressa M. G. Stumm ◽  
Luiz F. K. Borges ◽  
Eduarda P. T. Ferreira ◽  
Bruna Favaretto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Seminal Plasma ◽  
Plasma Lipid ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Semen Collection ◽  
Semen Storage ◽  
Plasma Lipid Peroxidation ◽  
Antioxidant Enzyme Catalase

This experiment aims to evaluate the correlation between lipid peroxidation levels in serum and seminal plasma in equines. Also, it investigates the lipid peroxidation in extended semen samples and its effects and sperm motility during a 72 hr refrigeration period. Blood and semen were collected from fertile Crioulo stallions. Serum and seminal plasma lipid peroxidation levels were analyzed by thiobarbituric acid reactive substances (TBARS) immediately after semen collection. After addition of extender (hour = 0), diluted semen was refrigerated and stored at 5 °C. Semen analyses, TBARS and catalase activity were performed in extended semen at 0, 24, 48, and 72 hours. We noted that levels of plasma lipid peroxidation can be used as an indicative of seminal oxidative stress. Also, lipid peroxidation does not increase substantially during semen storage. Lipid peroxidation and the antioxidant enzyme catalase do not seem to be the major cause of loss and motility and consequently reduction in fertility in stallion semen during storage for 72 h at 5 °C.

scholarly journals Beneficial effects of mycophenolate mofetil on cardiotoxicity induced by tacrolimus in wistar rats

2016 ◽  
Vol 242 (4) ◽  
pp. 448-455 ◽  
Author(s):  
Hanen Ferjani ◽  
Rim Timoumi ◽  
Ines Amara ◽  
Salwa Abid ◽  
Abedellatif Achour ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mycophenolate Mofetil ◽  
Oral Administration ◽  
Protective Effect ◽  
Cardiac Toxicity ◽  
De Novo ◽  
Antioxidant Activities ◽  
Solid Organ Transplantation ◽  
Protein Carbonyl ◽  
Solid Organ

The immunosuppressive drug tacrolimus (TAC) is used clinically to reduce the rejection rate in transplant patients. TAC has contributed to an increased prevalence of cardiovascular disease in patients receiving solid organ transplantation. Mycophenolate mofetil (MMF), a potent inhibitor of de novo purine synthesis, is known to prevent ongoing rejection in combination with TAC. In the present study, we investigated the antioxidant and antigenotoxic effect of MMF on TAC-induced cardiotoxicity in rats. Oral administration of TAC at 2.4, 24, and 60 mg/kg b.w. corresponding, respectively, to 1, 10, and 25% of LD50 for 24 h caused cardiac toxicity in a dose-dependant manner. TAC increased significantly DNA damage level in hearts of treated rats. Furthermore, it increased malondialdehyde (MDA) and protein carbonyl (PC) levels and decreased catalase (CAT) and superoxide dismutase (SOD) activities. The oral administration of MMF at 50 mg/kg b.w. simultaneously with TAC at 60 mg/kg b.w. proved a significant cardiac protection by decreasing DNA damage, MDA, and PC levels, and by increasing the antioxidant activities of CAT and SOD. Thus, our study showed, for the first time, the protective effect of MMF against cardiac toxicity induced by TAC. This protective effect was mediated via an antioxidant process.

Oxypurinol administration fails to prevent free radical-mediated lipid peroxidation during loaded breathing

1999 ◽  
Vol 87 (3) ◽  
pp. 1123-1131 ◽  
Author(s):  
G. Supinski ◽  
D. Nethery ◽  
D. Stofan ◽  
L. Szweda ◽  
A. DiMarco
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Xanthine Oxidase ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Xanthine Oxidase Inhibitor ◽  
Air Breathing ◽  
Fatigue Development ◽  
Loaded Breathing

The purpose of the present study was to determine whether it is possible to alter the development of fatigue and ablate free radical-mediated lipid peroxidation of the diaphragm during loaded breathing by administering oxypurinol, a xanthine oxidase inhibitor. We studied 1) room-air-breathing decerebrate, unanesthetized rats given either saline or oxypurinol (50 mg/kg) and loaded with a large inspiratory resistance until airway pressure had fallen by 50% and 2) unloaded saline- and oxypurinol-treated room-air-breathing control animals. Additional sets of studies were performed with animals breathing 100% oxygen. Animals were killed at the conclusion of loading, and diaphragmatic samples were obtained for determination of thiobarbituric acid-reactive substances and assessment of in vitro force generation. We found that loading of saline-treated animals resulted in significant diaphragmatic fatigue and thiobarbituric acid-reactive substances formation ( P < 0.01). Oxypurinol administration, however, failed to increase load trial time, reduce fatigue development, or prevent lipid peroxidation in either room-air-breathing or oxygen-breathing animals. These data suggest that xanthine oxidase-dependent pathways do not generate physiologically significant levels of free radicals during the type of inspiratory resistive loading examined in this study.

scholarly journals Gene expression in human small intestinal mucosa in vivo is mediated by iron-induced oxidative stress

2006 ◽  
Vol 25 (2) ◽  
pp. 242-249 ◽  
Author(s):  
Freddy J. Troost ◽  
Robert-Jan M. Brummer ◽  
Guido R. M. M. Haenen ◽  
Aalt Bast ◽  
Rachel I. van Haaften ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Lipid Peroxidation ◽  
Small Intestine ◽  
Antioxidant Capacity ◽  
Intestinal Mucosa ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Oxidative Challenge ◽  
Gene Reporters

Iron-induced oxidative stress in the small intestine may alter gene expression in the intestinal mucosa. The present study aimed to determine which genes are mediated by an iron-induced oxidative challenge in the human small intestine. Eight healthy volunteers [22 yr(SD2)] were tested on two separate occasions in a randomized crossover design. After duodenal tissue sampling by gastroduodenoscopy, a perfusion catheter was inserted orogastrically to perfuse a 40-cm segment of the proximal small intestine with saline and, subsequently, with either 80 or 400 mg of iron as ferrous gluconate. After the intestinal perfusion, a second duodenal tissue sample was obtained. Thiobarbituric acid-reactive substances, an indicator of lipid peroxidation, in intestinal fluid samples increased significantly and dose dependently at 30 min after the start of perfusion with 80 or 400 mg of iron, respectively ( P < 0.001). During the perfusion with 400 mg of iron, the increase in thiobarbituric acid-reactive substances was accompanied by a significant, momentary rise in trolox equivalent antioxidant capacity, an indicator of total antioxidant capacity ( P < 0.05). The expression of 89 gene reporters was significantly altered by both iron interventions. Functional mapping showed that both iron dosages mediated six distinct processes. Three of those processes involved G-protein receptor coupled pathways. The other processes were associated with cell cycle, complement activation, and calcium channels. Iron administration in the small intestine induced dose-dependent lipid peroxidation and a momentary antioxidant response in the lumen, mediated the expression of at least 89 individual gene reporters, and affected at least six biological processes.

scholarly journals Decreased Erythrocyte NA+,K+-ATPase Activity and Increased Plasma TBARS in Prehypertensive Patients

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Carlos Ricardo Maneck Malfatti ◽  
Leandro Tibiriçá Burgos ◽  
Alexandre Rieger ◽  
Cássio Luiz Rüdger ◽  
Janaína Angela Túrmina ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atpase Activity ◽  
Cell Damage ◽  
Venous Blood ◽  
Thiobarbituric Acid ◽  
Normal Blood Pressure ◽  
Thiobarbituric Acid Reactive Substances ◽  
Normotensive Subjects ◽  
The Relationship ◽  
Membrane Cell

The essential hypertension has been associated with membrane cell damage. The aim of the present study is investigate the relationship between erythrocyte Na+,K+-ATPase and lipoperoxidation in prehypertensive patients compared to normotensive status. The present study involved the prehypertensive patients (systolic:136±7 mmHg; diastolic:86.8±6.3 mmHg;n=8) and healthy men with normal blood pressure (systolic:110±6.4 mmHg; diastolic:76.1±4.2 mmHg;n=8) who were matched for age (35±4years old). The venous blood samples of antecubital vein (5 mL) were collected into a tube containing sodium heparin as anticoagulant (1000 UI), and erythrocyte ghosts were prepared for quantifying Na+,K+-ATPase activity. The extent of the thiobarbituric acid reactive substances (TBARS) was determined in plasma. The statistical analysis was carried out by Student’st-test and Pearson’s correlation coefficient. AP<0.05was considered significant. The Na+,K+-ATPase activity was lower in prehypertensive patients compared with normotensive subjects (4.9 versus 8.0 nmol Pi/mg protein/min;P<0.05). The Na+,K+-ATPase activity correlated negatively with TBARS content (r=-0.6;P<0.05) and diastolic blood pressure (r=-0.84;P<0.05). The present study suggests that Na+,K+-ATPase activity reduction and elevation of the TBARS content may underlie the pathophysiological aspects linked to the prehypertensive status.

Depression of heart sarcolemmal Ca2+-pump activity by oxygen free radicals

1989 ◽  
Vol 256 (2) ◽  
pp. H368-H374 ◽  
Author(s):  
M. Kaneko ◽  
R. E. Beamish ◽  
N. S. Dhalla
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Protective Effect ◽  
Oxygen Free Radicals ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Exact Nature ◽  
Dependent Manner ◽  
Membrane Phospholipids ◽  
Generating System

Although oxygen free radicals have been implicated as mediators of cellular injury in myocardial ischemia-reperfusion, the exact nature of defects produced by these radicals is not clear. Because sarcolemmal Ca2+-pump is involved in the efflux of Ca2+ from the cell, this study was undertaken to examine the effects of oxygen free radicals on sarcolemmal ATP-dependent Ca2+ accumulation and Ca2+-stimulated Mg2+-dependent adenosinetriphosphatase (ATPase) activities as well as lipid peroxidation of membrane phospholipids. Isolated rat heart sarcolemmal membranes were incubated with xanthine + xanthine oxidase [a superoxide anion radical (O2-)-generating system], H2O2, or H2O2 + Fe2+ [a hydroxyl radical (HO.)-generating system] and assayed for Ca2+-pump activities. O2- inhibited the Ca2+-pump activities in a time-dependent manner; a significant inhibition of Ca2+-stimulated ATPase activity was seen after 1 min of incubation. Superoxide dismutase showed a protective effect on depression in Ca2+-pump activities caused by O2-.H2O2 inhibited Ca2+-pump activities in a dose-dependent manner; this inhibition was protected by the addition of catalase. HO. depressed the Ca2+-pump activities to a greater extent in comparison with H2O2. Mannitol showed a protective effect on HO.-induced inhibition of Ca2+-pump activities. The promotion of lipid peroxidation by free radicals was evident from increased formation of malondialdehyde. These results indicate that the sarcolemmal membrane is altered on exposure to oxygen free radicals, and this may result in depressing the Ca2+-pump mechanism for Ca2+ efflux from the myocardial cell.

Lipid Peroxidation and Cherniluminescence during Naproxen Metabolism in Rat Liver Microsomes

1994 ◽  
Vol 13 (12) ◽  
pp. 831-838 ◽  
Author(s):  
Hiroyuki Yokoyama ◽  
Toshiharu Horie ◽  
Shoji Awazu
Keyword(s):  
Lipid Peroxidation ◽  
Singlet Oxygen ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Thiobarbituric Acid ◽  
Rat Liver Microsomes ◽  
Oxygen Species ◽  
Thiobarbituric Acid Reactive Substances ◽  
Microsomal Suspension ◽  
Weight Protein

1 Rat liver microsomal suspension containing NADPH and MgCl2 was incubated at 37°C with naproxen, a non-steroidal anti-inflammatory drug. Thiobarbituric acid reactive substances (TBA-RS), high molecular weight protein aggregates and fluorescent substances were formed in the microsomal suspension. 2 Chemiluminescence was produced from the microsomal suspension. This chemiluminescence production was well correlated to the TBA-RS formation, indicating that the chemiluminescence production was closely associated with the lipid peroxidation. 3 The addition of SKF-525A to the microsomal suspension inhibited the production of TBA-RS, chemiluminescence and 6-demethylnaproxen (6-DMN), the oxidative product of naproxen. Further, the antioxidant, α-tocopherol and singlet oxygen quenchers like histidine, dimethylfuran and 1,4-diazabicyclo[2,2,2]octane strikingly inhibited the productions of chemiluminescence and TBA-RS. 4 Neither naproxen nor 6-DMN caused lipid peroxidation in the absence of NADPH. Thus, lipid peroxidation and chemiluminescence during the oxidation of naproxen in liver microsomes was suggested to be provoked by reactive oxygen species and an origin of chemiluminescence was shown to be singlet oxygen.

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