Ameliorating oxidative stress and inflammation by Hesperidin and vitamin E in doxorubicin induced cardiomyopathy

2018 ◽  
Vol 44 (2) ◽  
pp. 207-217
Author(s):  
Thoria Donia ◽  
Samar Eldaly ◽  
Ehab M.M. Ali
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Reduced Glutathione ◽  
Human Cancer ◽  
Serum Lactate ◽  
Serum Lactate Dehydrogenase ◽  
Clinical Use ◽  
Chemotherapeutic Drug ◽  
Cardiac Histopathology

Abstract Background Doxorubicin (DOX) is a common chemotherapeutic drug. However, it causes cardiomyopathy which reduces its clinical use in human cancer therapy. Objective The purpose of our study was to assess the cardioprotective effect of hesperidin (HSP) and vitamin E (VIT.E) against DOX-induced cardiomyopathy. Material and methods Seventy rats were allocated into seven groups: control, HSP (50 mg/kg, orally), VIT.E (100 mg/kg orally), DOX [4 mg/kg, intraperitoneally (i.p.)], DOX+HSP, DOX+VIT.E and DOX+HSP+VIT.E. Results Our findings showed that serum lactate dehydrogenase (LDH), creatine kinase (CK), myeloperoxidase (MPO), cardiac catalase and caspase activities as well as cardiac malondialdehyde (MDA) and serum nitric oxide (NO) concentrations were reduced DOX+HSP or DOX+VIT.E or DOX+VIT.E+HSP groups compared to DOX group. Whereas, cardiac reduced glutathione (GSH) level, serum arylesterase, and paraoxonase activities were higher in rats injected with DOX and administrated with HSP and VIT.E than that of rats injected with DOX only. Cardiac histopathology of DOX group showed some changes that were improved during administration with HSP and VIT.E. Conclusion HSP and VIT.E possess a protective effect against DOX-induced cardiomyopathy via inhibiting oxidative stress, inflammation, and apoptosis.

Astaxanthin, the Natural Antioxidant, Reduces Reserpine Induced Depression in Mice

2020 ◽  
Vol 16 (9) ◽  
pp. 1319-1327
Author(s):  
Ferdous Khan ◽  
Syed A. Kuddus ◽  
Md. H. Shohag ◽  
Hasan M. Reza ◽  
Murad Hossain
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reduced Glutathione ◽  
Forced Swim Test ◽  
Tail Suspension Test ◽  
Glutathione Depletion ◽  
Swim Test ◽  
Stress Markers ◽  
Immobility Time ◽  
Biochemical Level

Background: An imbalance between pro-oxidants and antioxidants determines the level of oxidative stress which is implicated in the etiopathogenesis of various neuropsychiatric disorders including depression. Therefore, treatment with antioxidants could potentially improve the balance between pro-oxidants and antioxidants. Objective: The objective of this study was to evaluate the ability of astaxanthin, a potential antioxidant, to reduce reserpine-induced depression in BALB/c mice (Mus musculus). Methods: On the behavioral level, antidepressant property of astaxanthin (50 mg/kg, orally) on reserpine (2 mg/kg, subcutaneously) induced depressed mice was evaluated by Forced Swim Test (FST) and Tail Suspension Test (TST). In the biochemical level, the ability of astaxanthin to mitigate reserpine-induced oxidative stress was evaluated by the measurement of Malondialdehyde (MDA) and nitric oxide (NO) in brain, liver and plasma samples. On the other hand, the efficiency of astaxanthin to replenish glutathione depletion and antioxidant enzyme activity augmentation in the same samples were also investigated. Results: Astaxanthin was able to lower reserpine induced immobility time significantly (p<0.05) in FST and TST. Mice treated with astaxanthin showed significantly (p<0.05) low level of oxidative stress markers such as Malondialdehyde (MDA), Nitric Oxide (NO). Consistently, the level of reduced Glutathione (GSH), and the activity of Superoxide Dismutase (SOD) and catalase were augmented due to the oral administration of astaxanthin. Conclusion: This study suggests that astaxanthin reduces reserpine-induced oxidative stress and therefore might be effective in treating oxidative stress associated depression.

scholarly journals Associations between vitamin E, oxidative stress markers, total homocysteine levels, and physical activity or cognitive capacity in older adults

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ahmad H. Alghadir ◽  
Sami A. Gabr ◽  
Shahnawaz Anwer ◽  
Heng Li
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Nitric Oxide ◽  
Older Adults ◽  
Vitamin E ◽  
Cognitive Capacity ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Total Homocysteine

AbstractThis study examined the associations between vitamin E, oxidative stress markers, total homocysteine levels, and physical activity or cognitive capacity in older adults. One hundred and six older adults (62 men, 44 women) within the age range of 56–81 years participated. The Global Physical Activity Questionnaire and the Loewenstein Occupational Therapy Cognitive Assessment were used to assess physical activity and cognitive function, respectively. Vitamin E (e.g., α-tocopherol and γ-tocopherol), oxidative stress markers (e.g., total antioxidant capacity and nitric oxide), and total homocysteine were estimated. There were significant associations between physical activity (high versus moderate versus poor) and all biomarkers (all p = 0.000, and p = 0.010 for γ-tocopherol). While total homocysteine and total antioxidant capacity were significantly associated with cognitive capacity (p = 0.000), vitamin E levels (e.g., α-tocopherol and γ-tocopherol) and nitric oxide (p = 0.354, 0.103 and 0.060, respectively) were not related to cognitive capacity in older adults. This study concludes that physical activity was associated with Vitamin E, oxidative stress markers, total homocysteine, and cognitive capacity in older adults. Although cognitive capacity was associated with total homocysteine and total antioxidant capacity, it was unrelated to vitamin E levels and nitric oxide in older adults.

scholarly journals To Evaluate the Effect of Vitamin E Therapy on the Oxidative Stress Markers (Nitric Oxide, SOD, Glutathione Peroxidase) & Vitamin E Levels in Pulmonary Tuberculosis Patients

2020 ◽  
Vol 9 (40) ◽  
pp. 2970-2975
Author(s):  
Rohit John Chaudhary ◽  
Bharti Kwatra Uppal
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Pulmonary Tuberculosis ◽  
Older Age ◽  
Control Group ◽  
Ros Production ◽  
Age Group ◽  
Sod Activity

BACKGROUND Severe oxidative stress has been reported in TB patients because of infection associated with malnutrition and poor immunity. Mycobacteria can induce reactive oxygen species (ROS) production by activating phagocytes, and enhanced ROS production may promote tissue injury and inflammation. We wanted to compare the effect of antioxidant administration in the outcome of ATT treatment between the test and the control group. METHODS This perspective study was conducted in the Departments of Biochemistry and Chest Medicine, CMC & Hospital. Hundred patients (fifty controls and fifty tests) who were diagnosed as pulmonary tuberculosis and started on DOT therapy under RNTCP during this period were included in the study. Each participant in the study was subjected to the following test at the first visit, 2nd month and 6th month follow up (biochemical markers Nitric oxide, SOD, Glutathione Peroxidase and Vitamin E levels). Statistical analysis was done using SPSS version. RESULTS The results were based on four categories (male / female, alcoholic / non-alcoholic, smoker / non-smoker, and younger / older age group). Females had responded better with greater fall in percentage of nitric oxide values (69 %) than males (64.1 %). The mean of SOD activity (277.5 + / - 31.5) was more in smokers than non-smokers (261.3 + / - 36.0) & percentage fall of nitric oxide in smokers (65 %) & non-smokers (67 %). In alcoholics the percentage fall of nitric oxide (68.3 %) was higher with more SOD activity (Mean 278.7 + / - 27.6) than non-alcoholics (Mean 256 + / - 38.0) indicating a positive correlation of smoking & alcoholism with tuberculosis. Younger age group responded better with more fall in the percentage of nitric oxide (67 %) & mean SOD activity (265.8 + / - 30.1) than older age group. CONCLUSIONS Antioxidant supplementation reduces oxidative stress, improves the effectiveness of ATT therapy, and thus helps in improving the outcome in pulmonary tuberculosis. KEY WORDS Pulmonary TB, ATT (Anti-Tubercular Treatment), Antioxidants & Free Radicals

Vitamin E reduces glomerulosclerosis, restores renal neuronal NOS, and suppresses oxidative stress in the 5/6 nephrectomized rat

2007 ◽  
Vol 292 (5) ◽  
pp. F1404-F1410 ◽  
Author(s):  
You-Lin Tain ◽  
Gary Freshour ◽  
Anna Dikalova ◽  
Kathy Griendling ◽  
Chris Baylis
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Kidney Cortex ◽  
Antioxidant Vitamin ◽  
No Production ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Endothelial Nitric Oxide

Chronic kidney disease is accompanied by nitric oxide (NO) deficiency and oxidative stress, which contribute to progression. We investigated whether the antioxidant vitamin E could preserve renal function and NO bioavailability and reduce oxidative stress in the 5/6th nephrectomy (NX) rat model. We studied the following three groups of male Sprague-Dawley rats: sham ( n = 6), 5/6 NX control ( n = 6), and 5/6 NX treated with vitamin E (5,000 IU/kg chow; n = 5). The 5/6 NX group showed increased severity of glomerulosclerosis vs. sham, and this was ameliorated by vitamin E therapy. Both 5/6 NX groups showed similar elevations in plasma creatinine and proteinuria and decreased 24-h creatinine clearance compared with sham. There was increased NADPH-dependent superoxide production in 5/6 NX rats vs. sham that was prevented by vitamin E. Total NO production was similarly reduced in both 5/6 NX groups. There was unchanged abundance of endothelial nitric oxide synthesis (NOS) in renal cortex and medulla and neuronal (n) NOS in medulla. However, in kidney cortex, 5/6 NX rats had lower nNOS abundance than sham, which was restored by vitamin E. An increased plasma asymmetric dimethylarginine occurred with 5/6 NX associated with decreased renal dimethylarginine dimethylaminohydrolase activity and increased type 1 protein arginine methyltransferase expression.

scholarly journals Gebe Ratlara uygulanan Akrilamid ve E Vitaminin Plasenta Dokusu Üzerine Olası Etkilerinin Araştırılması

2017 ◽  
Vol 5 (4) ◽  
pp. 349
Author(s):  
Mehmet Erman Erdemli ◽  
Eyüp Altınöz ◽  
Zeynep Aksungur ◽  
Zümrüt Doğan ◽  
Harika Gözükara Bağ ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Total Antioxidant Capacity ◽  
Corn Oil ◽  
Reduced Glutathione ◽  
Control Group ◽  
Vaginal Smear ◽  
Protective Agent ◽  
Pregnant Rats ◽  
Total Antioxidant

Investigate the changes that occur in the placenta tissues of pregnant rats that were administered acrylamide (AA) and vitamin E as a protective agent during pregnancy. Thirty rats that were proven positive for pregnancy with vaginal smear test were randomly distributed into control, corn oil, vitamin E, acrylamide and vitamin E + acrylamide groups. Pregnant rats were decapitated on the 20th day of the experiment. Malondialdehyde (MDA), reduced glutathione (GSH), total antioxidant capacity (TAS), total oxidant capacity (TOS) and Xanthine oxidase (XO) levels were measured in placenta tissues. It was determined that acrylamide application during pregnancy statistically significantly increased MDA, TOS and XO levels and reduced GSH and TAS levels in the placenta tissue of pregnant rats when compared to all other groups, and GAS and TAS levels statistically significantly increased in vitamin E administered group when compared to all other groups and TOS and XO levels were decreased to control group levels. It was observed that orally administered AA changed the antioxidant / oxidant equilibrium favoring the oxidants by increasing MDA, XO and TOS levels in pregnant rats and caused oxidative stress, while vitamin E administration returned the antioxidant / oxidant equilibrium back to normal levels, preventing oxidative stress induced toxicity.

scholarly journals Effects of Safranal on Tissue Oxidative Stress in Sub-Chronic Thinner-Addicted Rats

2020 ◽  
Vol 71 (1) ◽  
pp. 1997
Author(s):  
M. DÜZ ◽  
A. F. FIDAN
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protective Effect ◽  
Total Antioxidant Capacity ◽  
Reduced Glutathione ◽  
Control Group ◽  
Albino Rats ◽  
Total Antioxidant ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

The present study was carried out to determine the effects of sub-chronic thinner addiction on the oxidant-antioxidant balance and oxidative stress on certain tissues and the possible protective effect of safranal against thinner toxication in rats. Adult male Wistar albino rats were randomly divided into four groups of 10 animals each as follows: control (C), safranal (S), thinner (T) and thinner+safranal (T+S). The control group received 1cc saline by gastric gavage. Safranal was administered to S and T+S groups by using gastric gavage at a dose of 100 mg/kg/day and volume of 0.1 mL/kg/day. Thinner inhalation was applied to T and T+S groups in a container with NaOH tablets twice a day. Levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NOx) metabolites, total antioxidant capacity (TAS) and total oxidant capacity (TOS) were determined in liver, lung, brain, kidney and testis tissues of the rats. In the T+S group, it was observed that the MDA levels significantly decreased in all tissues, except the kidney, in comparison to the thinner inhalation group (p = 0.000). When the NOx levels of the T+S group were compared with the levels of the T group, it was concluded that there existed a statistically significant decrease in the NOx levels in alltissues (p = 0.000). In T+S group, it was observed that safranal either eliminated or mitigated oxidative stress that developed in tissues through decreasing MDA and TOS levels and increasing GSH and TAS levels and caused significant decreases in NOX levels in all tissues. As a result, it was determined that safranal, although not uniform for all tissue types, had a protective potential against the damaging effects of oxidative stress caused by sub-chronic thinner inhalation.

Gender comparisons of exercise-induced oxidative stress: influence of antioxidant supplementation

2007 ◽  
Vol 32 (6) ◽  
pp. 1124-1131 ◽  
Author(s):  
Allan H. Goldfarb ◽  
Michael J. McKenzie ◽  
Richard J. Bloomer
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Reduced Glutathione ◽  
Protein Carbonyls ◽  
Plasma Vitamin ◽  
Oxidized Glutathione ◽  
Antioxidant Supplementation ◽  
Plasma Vitamin E ◽  
Exercise Induced ◽  
Response To Exercise

The purpose of this study was to determine the influence of gender and antioxidant supplementation on exercise-induced oxidative stress. Twenty-five men and 23 women ran for 30 min at 80% VO2 max, once before and once after 2 weeks of supplementation, and again after a 1-week wash-out period. Subjects were randomly assigned to either placebo (P), antioxidant (A: 400 IU vitamin E + 1 g vitamin C), or a fruit and vegetable powder (FV) treatment. Blood was obtained at rest and immediately after exercise. Before supplementation, women had higher resting reduced glutathione, total glutathione, and plasma vitamin E compared with men. With both A and FV supplementations, plasma vitamin E gender differences disappeared. Protein carbonyls, oxidized glutathione, and malondialdehyde all increased similarly for both genders in response to exercise. Both A and FV attenuated the reduced glutathione decrease and the oxidized glutathione and protein carbonyls increase compared with P, with no gender differences. 8-Hydroxydeoxyguanosine was lower with treatment A compared with FV and P only for men. Plasma vitamin C increased 39% (A) and 21% (FV) compared with P. These data indicate that women have higher resting antioxidant levels than men. Markers of oxidative stress increased similarly in both genders in response to exercise of similar intensity and duration. Two weeks of antioxidant supplementation can attenuate exercise-induced oxidative stress equally in both genders.

Wie altern Gefäße? Mechanismen und klinische Implikationen

VASA ◽  
2004 ◽  
Vol 33 (1) ◽  
pp. 3-11 ◽  
Author(s):  
van der Loo ◽  
Koppensteiner ◽  
Lüscher
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Nitric Oxide Synthase ◽  
Vitamin C ◽  
Oxide Synthase ◽  
Klinische Implikationen

Altern ist ein wichtiger kardialer und vaskulärer Risikofaktor. Für das Gefäßaltern sind genetische, mechanische und hämodynamische Faktoren ausschlaggebend. So sind altersabhängige Veränderungen in Gefäßen, welche weniger Pulsatilität und Blutdruck ausgesetzt sind, wie Kapillaren und Venen, geringer oder abwesend. Vor allem in den großen Widerstandsgefäßen kommt es im Laufe des Alterns morphologisch zu einer Intima- und Mediaverdickung, verknüpft mit einer vermehrten Einlagerung von Matrixsubstanzen, und letztlich resultierend in verminderter Compliance der Gefäße. Es lassen sich Funktionsstörungen des Endothels nachweisen. Hier kommt es zu einer deutlichen Heraufregulierung der endothelialen Nitric Oxide Synthase (eNOS), welche für die Produktion des endogenen Vasodilatators Nitric Oxide (NO) verantwortlich ist. Paradoxerweise sind trotzdem die Vasorelaxationen im Alter vermindert, da es gleichzeitig zu einer erhöhten Produktion freier Radikale, im Besonderen Superoxid (O2-) kommt. O2- und NO bilden in einer schnell ablaufenden chemischen Reaktion Peroxinitrit (ONOO-), welches Proteine nitriert. Durch diese Nitrierung kommt es zur funktionellen Beeinträchtigung dieser Proteine, so dass verschiedene Signalübertragungswege, z.B. Tyrosilierung von Enzymen, blockiert werden. Primärer Ort der Bildung freier Sauerstoffradikale sind die endothelialen Mitochondrien. Bislang ungeklärt ist, ob der oxidative Stress als ein zentrales Ereignis des Gefäßalterns pharmakologisch beeinflussbar ist. Hier standen vor allem antioxidativ wirkende Vitamine im Mittelpunkt des Interesses. Überraschenderweise wird jedoch Vitamin E im Tiermodell vermehrt mit steigendem Alter in der aortalen Wand eingelagert, was im Rahmen eines altersassoziierten gegenregulatorischen Mechanismus zur Abwendung des vermehrten oxidativen Stresses erfolgt. Umgekehrt ist Vitamin C signifikant vermindert. Es bleibt abzuwarten, ob das Gefäßaltern durch Vitamin C oder andere Antioxidantien günstig beeinflusst werden kann. Für Statine und ACE-Hemmer wurden schon Wirkungen beschrieben, die mit Schlüsselmechanismen des Gefäßalterungsprozesses interferieren. Die Entwicklung therapeutischer Interventionen zur Verlangsamung des Gefäßalterns wird für das Auftreten von Herz- und Gefäßerkrankungen im Alter in Zukunft große Bedeutung haben.

Oxidative stress in the brain of nicotine-induced toxicity: protective role of Andrographis paniculata Nees and vitamin E

2009 ◽  
Vol 34 (2) ◽  
pp. 124-135 ◽  
Author(s):  
Subhasis Das ◽  
N. Gautam ◽  
Sankar Kumar Dey ◽  
Tarasankar Maiti ◽  
Somenath Roy
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Body Mass ◽  
Brain Mitochondria ◽  
Brain Regions ◽  
Protective Role ◽  
Andrographis Paniculata ◽  
Protective Effects ◽  
The Brain

Mitochondria are the crossroads of several crucial cellular activities; they produce considerable quantities of superoxide radical and hydrogen peroxide, which can damage important macromolecules. Nicotine affects a variety of cellular processes, from induction of gene expression to modulation of enzymatic activities. The aim of this study was to elucidate the protective effects of andrographolide (ANDRO) aqueous extract (AE-Ap) of Andrographis paniculata, and vitamin E on nicotine-induced brain mitochondria. In this investigation, nicotine (1 mg·kg body mass–1·day–1) was treated, for the period of 7 days, simultaneously with 2 A. paniculata products, ANDRO and AE-Ap (250 mg·kg body mass–1·day–1); and vitamin E (50 mg·kg body mass–1·day–1) was supplemented in different group of male Wistar rats. The activities of mitochondrial electron transport chain (Mito–ETC) complexes (I, II, III), nitric oxide production, superoxide anion, catalase, glutathione reductase, glutathione peroxidase, glutathione-S-transferase, and concentrations of reduced glutathione and oxidized glutathione were measured in discrete regions of brain (the cerebral hemisphere, cerebellum, diencephalons, and brain stem). The study revealed that nicotine inhibits the Mito–ETC complexes and produces nitric oxide, which suppressed the mitochondrial oxidative stress scavenger system in different brain regions. In these circumstances, lipid peroxidation and protein oxidation were noted in different discrete regions of brain mitochondria. ANDRO, AE-Ap, and vitamin E showed the protective potentiality against nicotine toxicity. The analysis of such alterations is important in determining the basis of normal dysfunction in the brain associated with nicotine toxicity, which could be ameliorated by A. paniculata and vitamin E, and may help to develop therapeutic means against nicotine-induced disorders.

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