Protective effect of vitamin E and epicatechin against nicotine-induced oxidative stress in rats

2012 ◽  
Vol 29 (2) ◽  
pp. 202-208 ◽  
Author(s):  
Abdulrahman L Al-Malki ◽  
Said S Moselhy
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Combined Treatment ◽  
Antioxidant Properties ◽  
Free Radical Scavenger ◽  
Individual Treatment ◽  
Antioxidant Vitamin ◽  
Radical Scavenger ◽  
Pharmacologically Active ◽  
Chemopreventive Activity

Nicotine is a major pharmacologically active and addictive component of tobacco smoke, which is regarded to be a primary risk factor in the development of cardiovascular and pulmonary diseases. Epicatechin 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. It has been reported that tea extracts and/or its constituents have antibacterial, antiviral, antioxidative, antitumor and antimutagenic activities. Vitamin E is a major lipid-soluble antioxidant vitamin and free radical scavenger, presents as an integral component of cellular membranes and has important biological functions. The primary mechanism by which vitamin E is proposed to prevent cancer is through their antioxidant properties. The goal of this study is to evaluate the effect of epicatechin alone or combined with vitamin E in inhibiting the oxidative stress induced by nicotine in rats. Results obtained indicated that there was a significant elevation in the levels of malondialdhyde (MDA) in nicotine injected rats. The combined treatment (epicatechin + Vit E) group showed a potential reduction of these parameters more than individual treatment. The activities of superoxide dismutase, catalase and glutathione peroxidase were found significantly higher in combined treated than untreated rats. In nicotine group, a negative significant correlation between reduced glutathione and MDA ( r = −0.92) was observed. In conclusion, these results suggested that the supplementation of diet with epicatechin and vitamin E provided antioxidant defense with strong chemopreventive activity against nicotine-induced carcinogenesis.

Vitamin E Does Not Reduce Cardiomyopathy In Doxorubicin treated Rats

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4944-4944
Author(s):  
Jhon A Guerra ◽  
Maribel Torres-Serrant ◽  
Pedro J Santiago
Keyword(s):  
Vitamin E ◽  
Conflicts Of Interest ◽  
Cardiac Injury ◽  
Free Radical Scavenger ◽  
Alpha Tocopherol ◽  
Control Group ◽  
Antioxidant Vitamin ◽  
Radical Scavenger ◽  
Doxorubicin Treatment ◽  
Doxorubicin Group

Abstract Abstract 4944 Introduction: The clinical efficacy of doxorubicin is severely limited by its cardiotoxicity. Antioxidants represent the largest class of chemicals examined as potential protective agents and for which there is continuing interest. Dexrazoxane is the current agent used for the control of doxorubicin related cardiotoxicity. However, in large trials the incidence was reduced only by 50% (1). Vitamin E, a known antioxidant and free radical scavenger agent, has been evaluated in the past as a cardio protective drug in animal models receiving doxorubicin but contradictory conclusions regarding this effect have been reported (2, 3). We hypothesized whether Vitamin E has an effect in cardioprotection in rats receiving doxorubicin. Design and Methods: Three groups of 6 Rats each were used for the experiment. Group 1 received doxorubicin 1.5mg/kg intraperitoneally (IP) weekly for 9 weeks for a total cumulative dose of 13.5mg/kg. Group 2 received Vitamin E 100 IU/kg/weekly by IP injection, 48 hours prior to the doxorubicin. Group 3 received 0.5 cc of saline solution 0.9% IP weekly for 9 weeks as control group. Functional parameters including plasmatic nitric oxide (NO) levels and cardiac ejection fraction (EF) were determined on each group at the end of the experiment. Results: Doxorubicin treatment significantly increased plasmatic NO concentration when compared with controls (35.30 ± 5.63 mM vs. 14.72 ± 2.66 mM, n=6, P=0.016); however, in the group of rats receiving Vitamin E prior to doxorubicin, NO did not have a significant decrease (from 35.30 ± 5.63 mM to 31.77± 8.91 mM n=6, P=0.75). Regarding EF, doxorubicin treatment decreased EF significantly when compared with saline controls rats (59 ± 5.61% vs. 77 ± 3.89 %, n=6, P<0.05); however, in the group of rats receiving Vitamin E prior to doxorubicin, EF did not have a significant improvement (from 59 ± 5.61% to 69.17 ± 4.4, n=6, P=0.24). Conclusion: These results suggest that Vitamin E does not prevent or reduce cardiac injury in rats treated with doxorubicin. Different alternatives including other antioxidants could be explored in an attempt to decrease cardiotoxicity produced by doxorubicin and to improve the effect of the standard cardioprotective agent used Dexrazoxane. Further studies are necessary. References: 1. Swain SM. Adult multicenter trials using dexrazoxane to protect against cardiac toxicity. Semin Onco 1998; 25 (4 Suppl 10):43-7 2. Breed JG, Zimmerman AN, Dormans JA, Pinedo HM. Failure of the antioxidant vitamin E to protect against adriamycin-induced cardiotoxicity in the rabbit. Cancer Res 1980; 40:2033-8 3. Myers CE, McGuire W, Young R. Adriamycin: amelioration of toxicity by alpha-tocopherol. Cancer Treat Rep 1976; 60:961-2 Disclosures: No relevant conflicts of interest to declare.

Pleiotropic roles of melatonin against oxidative stress mediated tissue injury in the gastrointestinal tract: An overview

2019 ◽  
Vol 2 (2) ◽  
pp. 158-184 ◽  
Author(s):  
Palash K Pal ◽  
Bharati Bhattacharjee ◽  
Aindrila Chattopadhyay ◽  
Debasish Bandyopadhyay
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Clinical Symptoms ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Gi Tract ◽  
Pathological Conditions

The excessive production of free radicals and/or reactive oxygen species (ROS) in gastrointestinal (GI) tract leads to oxidative damages in GI tissues with development of varied pathological conditions and clinical symptoms. Many endogenous as well as exogenous factors are involved in such pathogenesis, herein, focus was given to the factors of metal toxicity, non-steroidal anti-inflammatory drugs (NSAIDs), ischemia-reperfusion, consumption of high fat diet and alcohol, and different pathological conditions and diseases. Since ROS is more or less involved in the GI damages caused by these factors, therefore attempts have been made to develop appropriate therapeutic agents that possess antioxidant properties. Being a potent antioxidant and free radical scavenger, melatonin was suggested as a potent therapeutic answer to these GI damages. The discovery of different binding sites and receptors of melatonin in the GI tissues further proves its local actions to protect these tissues from oxidative stress.  In the review, we attempt to try our best to summarize the current developments regarding the GI injuries caused by oxidative stress and the potential beneficial effects of melatonin on these injuries. The important molecular mechanisms associated with these changes were also highlighted in the discussion. We hope that this review will provide valuable information to consider melatonin as a suitable molecule used for GI tract protection.

scholarly journals S-allyl Cysteine, a Garlic Compound, Produces an Antidepressant-Like Effect and Exhibits Antioxidant Properties in Mice

2020 ◽  
Vol 10 (9) ◽  
pp. 592
Author(s):  
Elizabeth Ruiz-Sánchez ◽  
José Pedraza-Chaverri ◽  
Omar N. Medina-Campos ◽  
Perla D. Maldonado ◽  
Patricia Rojas
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Forced Swim Test ◽  
Antioxidant Properties ◽  
Free Radical Scavenger ◽  
Antidepressant Effect ◽  
Radical Scavenger ◽  
Oxidative Stress Markers ◽  
Sod Activity ◽  
Stress Markers

Depression is a psychiatric disorder, and oxidative stress is a significant mechanism of damage in this mood disorder. It is characterized by an enhancement of oxidative stress markers and low concentrations of endogenous antioxidants, or antioxidants enzymes. This suggests that antioxidants could have an antidepressant effect. S-allyl cysteine (SAC) is a compound with antioxidant action or free radical scavenger capacity. The purpose of the current research was to evaluate the antidepressant-like effect as well as the antioxidant role of SAC on a preclinical test, using the Porsolt forced swim test (FST). SAC (30, 70, 120, or 250 mg/kg, ip) was administered to male BALB/c mice daily for 17 days, followed by the FST at day 18. Oxidative stress markers (reactive oxygen species, superoxide production, lipid peroxidation, and antioxidant enzymes activities) were analyzed in the midbrain, prefrontal cortex, and hippocampus. SAC (120 mg/kg) attenuated the immobility scores (44%) in the FST, and protection was unrelated to changes in locomotor activity. This antidepressant-like effect was related to decreased oxidative stress, as indicated by lipid peroxidation and manganese-superoxide dismutase (Mn-SOD) activity in the hippocampus. SAC exerts an antidepressant-like effect that correlated, in part, with preventing oxidative damage in hippocampus.

Investigation of Antioxidant Activity of Pomegranate Juices by Means of Electron Paramagnetic Resonance and UV-Vis Spectroscopy

2015 ◽  
Vol 98 (4) ◽  
pp. 866-870 ◽  
Author(s):  
Violetta Kozik ◽  
Krystyna Jarzembek ◽  
Agnieszka Jędrzejowska ◽  
Andrzej Bąk ◽  
Justyna Polak ◽  
...  
Keyword(s):  
Electron Paramagnetic Resonance ◽  
Free Radical ◽  
Epr Spectroscopy ◽  
Antioxidant Properties ◽  
Free Radical Scavenger ◽  
Pomegranate Juice ◽  
Radical Scavenger ◽  
Paramagnetic Resonance ◽  
Vis Spectroscopy ◽  
Electron Paramagnetic

Abstract Pomegranate fruit (Punica granatum L.) is a source of numerous phenolic compounds, and it contains flavonoids such as anthocyanins, anthocyanidins, cyanidins, catechins and other complexes of flavonoids, ellagitannins, and hydrolyzed tannins. Pomegranate juice shows antioxidant, antiproliferative, and anti-atherosclerotic properties. The antioxidant capacity (TEAC) of the pomegranate juices was measured using electron paramagnetic resonance (EPR) spectroscopy and 1,1-diphenyl-2-picrylhydrazyl (DPPH•) as a source of free radicals, and the total phenolic (TP) content was measured using UV-Vis spectroscopy. All the examined pomegranate juices exhibited relatively high antioxidant properties. The TEAC values determined by means of EPR spectroscopy using Trolox (TE) as a free radical scavenger were in the range of 463.12 to 1911.91 μmol TE/100 mL juice. The TP content measured by the Folin-Ciocalteu method, using gallic acid (GA) as a free radical scavenger, widely varied in the investigated pomegranate juice samples and ranged from 1673.62 to 5263.87 mg GA/1 L juice. The strongest antioxidant properties were observed with the fresh pomegranate juices obtained from the fruits originating from Israel, Lebanon, and Azerbaijan. Correlation analysis of numerical data obtained by means of EPR spectroscopy (TEAC) and UV-Vis spectroscopy (TP) gave correlation coefficient (r) = 0.90 and determination coefficient (r2) = 0.81 (P &lt;0.05).

scholarly journals Synergistic Activity of Carfilzomib and Panobinostat in Multiple Myeloma Cells via Modulation of ROS Generation and ERK1/2

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Lu Gao ◽  
Minjie Gao ◽  
Guang Yang ◽  
Yi Tao ◽  
Yuanyuan Kong ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Combined Treatment ◽  
Free Radical Scavenger ◽  
Ros Generation ◽  
Radical Scavenger ◽  
Synergistic Activity ◽  
Inhibition Of Proliferation ◽  
Synergistic Inhibition ◽  
Deacetylase Inhibitor ◽  
Pretreated Patients

Relapse of disease and subsequent resistance to established therapies remain as major challenges in the treatment of multiple myeloma (MM). New therapeutic options are needed for these extensively pretreated patients. To explore an optimized combinational therapy, interactions between the irreversible proteasome inhibitor carfilzomib exhibiting a well-tolerated side-effect profile and histone deacetylase inhibitor (HDACi) panobinostat (LBH589) were examined in MM cells. Coadministration of carfilzomib and LBH589 led to a synergistic inhibition of proliferation in MM cells. Further studies showed that the combined treatment synergistically increased mitochondrial injury, caspase activation, and apoptosis in MM cells. Lethality of the carfilzomib/LBH589 combination was associated with the reactive oxygen species (ROS) generation and ERK1/2 inactivation. In addition, the free radical scavenger N-acetylcysteine (NAC) could block carfilzomib and LBH589-induced oxidative stress and the subsequent apoptosis. Together, these findings argue that the strategy of combining carfilzomib and LBH589 warrants attention in MM.

scholarly journals Traumatic Brain Injury: Oxidative Stress and Novel Anti-Oxidants Such as Mitoquinone and Edaravone

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 943 ◽  
Author(s):  
Helene Ismail ◽  
Zaynab Shakkour ◽  
Maha Tabet ◽  
Samar Abdelhady ◽  
Abir Kobaisi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuroprotective Effect ◽  
Treatment Options ◽  
Free Radical Scavenger ◽  
Health Concern ◽  
Radical Scavenger ◽  
History Of ◽  
Ionic Imbalance

Traumatic brain injury (TBI) is a major health concern worldwide and is classified based on severity into mild, moderate, and severe. The mechanical injury in TBI leads to a metabolic and ionic imbalance, which eventually leads to excessive production of reactive oxygen species (ROS) and a state of oxidative stress. To date, no drug has been approved by the food and drug administration (FDA) for the treatment of TBI. Nevertheless, it is thought that targeting the pathology mechanisms would alleviate the consequences of TBI. For that purpose, antioxidants have been considered as treatment options in TBI and were shown to have a neuroprotective effect. In this review, we will discuss oxidative stress in TBI, the history of antioxidant utilization in the treatment of TBI, and we will focus on two novel antioxidants, mitoquinone (MitoQ) and edaravone. MitoQ can cross the blood brain barrier and cellular membranes to accumulate in the mitochondria and is thought to activate the Nrf2/ARE pathway leading to an increase in the expression of antioxidant enzymes. Edaravone is a free radical scavenger that leads to the mitigation of damage resulting from oxidative stress with a possible association to the activation of the Nrf2/ARE pathway as well.

Cellular Cysteine Network and Neurodegeneration

2020 ◽  
pp. 303-325
Author(s):  
Shubhangi H. Pawar ◽  
Vishal S. Gulecha ◽  
Manoj S. Mahajan ◽  
Aman B Upaganiawar ◽  
Chandrashekhar D. Upasani
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanism ◽  
Free Radical Scavenger ◽  
Cellular Damage ◽  
Radical Scavenger ◽  
Post Translational Modifications ◽  
Cellular Defense ◽  
Brain Antioxidants ◽  
The Brain ◽  
Oxidative Species

Oxidative stress is strongly linked to neurodegeneration and oxidative species can modify many amino acids and proteins in the brain. Cysteine amino acid is most susceptible to oxidative post-translational modifications (PTMs). Reversible or irreversible cysteine PTMs can cause dyshomeostasis, which further continued to cellular damage. Many cysteine dependent proteins and many non-proteins using cysteine as their structural components are affected by oxidative stress. Several cysteine dependent enzymes are acting as antioxidants. Cysteine is a major contributor to glutathione (GSH) and superoxide dismutase (SOD) synthesis. Cysteine precursor N-acetylcysteine (NAC) supplementation is proven as a potent free radical scavenger and increase brain antioxidants and subsequently potentiates the natural antioxidant cellular defense mechanism. Thus, in this chapter, the authors explore the linkage of cellular cysteine networks and neurodegenerative disorders.

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 Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Kazuyuki Miyamoto ◽  
Hirokazu Ohtaki ◽  
Kenji Dohi ◽  
Tomomi Tsumuraya ◽  
Dandan Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Death ◽  
Time Window ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Therapeutic Time Window

Traumatic brain injury (TBI) is a major cause of death and disability in young people. No effective therapy is available to ameliorate its damaging effects. Our aim was to investigate the optimal therapeutic time window of edaravone, a free radical scavenger which is currently used in Japan. We also determined the temporal profile of reactive oxygen species (ROS) production, oxidative stress, and neuronal death. Male C57Bl/6 mice were subjected to a controlled cortical impact (CCI). Edaravone (3.0 mg/kg), or vehicle, was administered intravenously at 0, 3, or 6 hours following CCI. The production of superoxide radicals (O2∙-) as a marker of ROS, of nitrotyrosine (NT) as an indicator of oxidative stress, and neuronal death were measured for 24 hours following CCI. Superoxide radical production was clearly evident 3 hours after CCI, with oxidative stress and neuronal cell death becoming apparent after 6 hours. Edaravone administration after CCI resulted in a significant reduction in the injury volume and oxidative stress, particularly at the 3-hour time point. Moreover, the greatest decrease inO2∙-levels was observed when edaravone was administered 3 hours following CCI. These findings suggest that edaravone could prove clinically useful to ameliorate the devastating effects of TBI.

Sign in / Sign up

Export Citation Format

Share Document