Activation of endogenous lipid peroxidation in the brain during oxidative stress induced by iron and its prevention by vitamin E

1990 ◽  
Vol 109 (1) ◽  
pp. 43-45
Author(s):  
G. M. Kainova ◽  
D. Markovska ◽  
D. Staneva ◽  
V. E. Kagan
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Vitamin E ◽  
Endogenous Lipid ◽  
The Brain

Sodium Valproate Affect Brain Antioxidant/Oxidant Status in Mice: Ameliorative Effect of Vitamin E and Chrysanthemum fontanesii Extract

2020 ◽  
Vol 16 (5) ◽  
pp. 576-580
Author(s):  
Amel Amrani ◽  
Nassima Boubekri ◽  
Ouahiba Benaissa ◽  
Fadila Benayache ◽  
Samir Benayache ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Vitamin E ◽  
Sodium Valproate ◽  
Protective Effects ◽  
Butanol Extract ◽  
Aerial Parts ◽  
Ameliorative Effect ◽  
Oxidant Status ◽  
The Brain

Background: This study was aimed to evaluate the protective effects of n-butanol extract of Chrysanthemum fontanesii against oxidative stress induced by sodium Valproate (VPA) in the brain of female mice in comparison to Vitamin E (Vit E). Methods: Mice were divided into 5 groups and treated daily for 12 days. They received VPA (300 mg/kg i.p. injection), C. fontanesii butanolic extract (100 mg/kg), and Vit E (100 mg/kg). Glutathione Peroxidase Activity (GPx), Reduced Glutathione (GSH), and lipid peroxidation end products in the brain were measured. Results: Subacute treatment of mice with VPA resulted in a significant increase in oxidative damage. At a dose of 100 mg/kg, both C. fontanesii and Vit E significantly reduced VPA-induced oxidative stress by inhibiting lipid peroxidation, increasing brain GSH content, and restoring the activity of GPx. Conclusion: It may be concluded that the phytoconstituents present in the n-butanol extract of aerial parts of C. fontanesii are responsible for the ameliorative effect of brain antioxidant/oxidant status affected by VPA.

scholarly journals C60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Olga O. Gonchar ◽  
Andriy V. Maznychenko ◽  
Nataliya V. Bulgakova ◽  
Inna V. Vereshchaka ◽  
Tomasz Tomiak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Expression ◽  
Restraint Stress ◽  
Stress Condition ◽  
Rat Tissues ◽  
Stress Exposure ◽  
The Brain ◽  
Nrf2 Protein

The effects of C60FAS (50 and 500 μg/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O2⋅−, H2O2, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST, γ-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes γ-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C60FAS attenuates ROS generation and O2⋅− and H2O2 releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C60FAS supplementation has dose-dependent and tissue-specific effects. C60FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C60FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an in vivo model, when C60FAS (50 and 500 μg/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the in vivo model, C60FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.

scholarly journals Changes in susceptibility of tissues to lipid peroxidation after ingestion of various levels of docosahexaenoic acid and vitamin E

1997 ◽  
Vol 78 (4) ◽  
pp. 655-669 ◽  
Author(s):  
Kazuhiro Kubo ◽  
Morio Saito ◽  
Tadahiro Tadokoro ◽  
Akio Maekawa
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Vitamin E ◽  
Liver Lipid ◽  
Lipid Peroxide ◽  
Dietary Energy ◽  
Fixed Amount ◽  
Endogenous Lipid ◽  
Liver And Kidney

To examine the effects of dietary docosahexaenoic acid (DHA) on the potential changes in endogenous lipid peroxidation in the liver and kidney, diets containing a fixed amount of vitamin E (VE; RRR-α-tocopherol equivalent; 134 mg/kg diet) and a graded amount of DHA at the levels of 0, 1.0, 3.4 and 8.7% of total dietary energy were fed to rats for 14 d (Expt 1). In Expt 2, diets containing a fixed amount of DHA (8.7% of total dietary energy) and a graded amount of VE at the levels of 54, 134 and 402 mg/kg were fed to rats for 15 d. In Expt 1 it was found that endogenous lipid peroxide contents of the liver and kidney, as measured by thiobarbituric acid value and chemiluminescence intensity, were higher, and their α-tocopherol contents lower than those of the controls, with a gradual increase and decrease in values respectively as the dietary DHA level increased (Expt 1). However, the contents of water-soluble antioxidants, i.e. ascorbic acid and non-protein-SH (glutathione), increased with increases in the dietary DHA level, while the Se-dependent glutathione peroxidase (EC 1.11.1.9) activities did not change or tended to be lower. When the graded level of VE was given to rats in Expt 2, lipid peroxide contents in the liver and kidney did not change significantly in response to the increasing levels of dietary VE, although their α-tocopherol contents were higher than control values, increasing with increases in the dietary VE levels. The lipid peroxide scavengers other than a-tocopherol changed similarly to those in Expt 1. The results obtained in Expts 1 and 2 indicate that DHA enhances the susceptibility of the liver and kidney to lipid peroxidation concomitant with higher levels of DHA in these tissues, as shown by the fatty acid composition. In addition, VE is unable to protect membranes of the liver and kidney rich in DHA from lipid peroxidation, even after ingestion of the highest level of VE. However, the liver lipid peroxide content of the group given the highest level of DHA was not as high as expected, based on the peroxidizability index which was calculated from the fatty acid composition of the liver lipid.

Effects of vitamin E supplementation on exercise-induced oxidative stress: a meta-analysis

2014 ◽  
Vol 39 (9) ◽  
pp. 1029-1037 ◽  
Author(s):  
Vahan Stepanyan ◽  
Melissa Crowe ◽  
Nagaraja Haleagrahara ◽  
Bruce Bowden
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Vitamin E ◽  
Muscle Damage ◽  
Meta Analysis ◽  
Protective Effects ◽  
Study Selection ◽  
Exercise Induced ◽  
Study Designs ◽  
Selection Of

Tocopherols (commonly referred to as “vitamin E”) are frequently studied antioxidants in exercise research. However, the studies are highly heterogeneous, which has resulted in contradicting opinions. The aim of this review is to identify similar studies investigating the effects of tocopherol supplementation on exercise performance and oxidative stress and to perform minimally biased qualitative comparisons and meta-analysis. The literature search and study selection were performed according to Cochrane guidelines. A 2-dimensional study execution process was developed to enable selection of similar and comparable studies. Twenty relevant studies were identified. The high variability of study designs resulted in final selection of 6 maximally relevant studies. Markers of lipid peroxidation (malondialdehyde) and muscle damage (creatine kinase) were the 2 most frequently and similarly measured variables. Meta comparison showed that tocopherol supplementation did not result in significant protection against either exercise-induced lipid peroxidation or muscle damage. The complex antioxidant nature of tocopherols and low accumulation rates in muscle tissues could underlie an absence of protective effects.

scholarly journals Modulatory effects of caffeine on oxidative stress and anxiety-like behavior in ovariectomized rats

2016 ◽  
Vol 94 (9) ◽  
pp. 961-972 ◽  
Author(s):  
Ionut Caravan ◽  
Alexandra Sevastre Berghian ◽  
Remus Moldovan ◽  
Nicoleta Decea ◽  
Remus Orasan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Chronic Administration ◽  
Behavioral Changes ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Plus Maze ◽  
Short Period ◽  
The Brain ◽  
And Oxidative Stress

Menopause is accompanied by enhanced oxidative stress and behavioral changes, effects attenuated by antioxidants. The aim of this study was to evaluate the effects of caffeine on behavior and oxidative stress in an experimental model of menopause. Female rats were divided into the following groups: sham-operated (CON), sham-operated and caffeine-treated (CAF), ovariectomized (OVX), ovariectomized and caffeine-treated (OVX+CAF). Caffeine (6 mg/kg) and vehicle were administered for 21 days (subchronic) and 42 days (chronic), using 2 experimental subsets. Behavioral tests and oxidative stress parameters in the blood, whole brain, and hippocampus were assessed. The subchronic administration of caffeine decreased the lipid peroxidation and improved the antioxidant defense in the blood and brain. The GSH/GGSG ratio in the brain was improved by chronic administration, with reduced activities of antioxidant enzymes and enhanced nitric oxide and malondialdehyde levels. In particular, the lipid peroxidation in the hippocampus decreased in both experiments. The rats became hyperactive after 21 days of treatment, but no effect was observed after chronic administration. In both experimental subsets, caffeine had anxiolytic effects as tested in elevated plus maze. The administration of low doses of caffeine, for a short period of time, may be a new therapeutic approach to modulating the oxidative stress and anxiety in menopause.

scholarly journals ROS Production Is Increased in the Kidney but Not in the Brain of Dahl Rats With Salt Hypertension Elicited in Adulthood

2015 ◽  
pp. 303-312 ◽  
Author(s):  
M. VOKURKOVÁ ◽  
H. RAUCHOVÁ ◽  
L. ŘEZÁČOVÁ ◽  
I. VANĚČKOVÁ ◽  
J. ZICHA
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Nadph Oxidase ◽  
Salt Intake ◽  
Renal Medulla ◽  
High Salt ◽  
Ros Production ◽  
High Salt Intake ◽  
Salt Hypertension ◽  
The Brain

Enhanced production of superoxide radicals by nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase in the brain and/or kidney of salt hypertensive Dahl rats has been proposed to participate in the pathogenesis of this form of experimental hypertension. Most information was obtained in young Dahl salt-sensitive (DS) rats subjected to high salt intake prior to sexual maturation. Therefore, the aim of our study was to investigate whether salt hypertension induced in adult DS rats is also accompanied with a more pronounced oxidative stress in the brain or kidney as compared to Dahl salt-resistant (DR) controls. NADPH oxidase activity as well as the content of thiobarbituric acid-reactive substances (TBARS) and conjugated dienes (oxidative index), which indicate a degree of lipid peroxidation, were evaluated in two brain regions (containing either hypothalamic paraventricular nucleus or rostral ventrolateral medulla) as well as in renal medulla and cortex. High salt intake induced hypertension in DS rats but did not modify blood pressure in DR rats. DS and DR rats did not differ in NADPH oxidase-dependent production of ROS, TBARS content or oxidative index in either part of the brain. In addition, high-salt diet did not change significantly any of these brain parameters. In contrast, the enhanced NADPH oxidase-mediated ROS production (without significant signs of increased lipid peroxidation) was detected in the renal medulla of salt hypertensive DS rats. Our findings suggest that there are no signs of enhanced oxidative stress in the brain of adult Dahl rats with salt hypertension induced in adulthood.

scholarly journals Curcumin Reduce Sodium Fluoride-Induced Oxidative Stress in Rat Brain

2018 ◽  
Vol 15 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Nagapuri Kiran Kumar ◽  
Mesram Nageshwar ◽  
Karnati Pratap Reddy
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Oral Administration ◽  
Rat Brain ◽  
Sodium Fluoride ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
The Brain

This study reports the ameliorative role of curcumin against sodium fluoride (NaF) induced oxidative stress in the brain of rats. The rats were divided into control, NaF (20 mg/kg), NaF+Curcumin (20mg/kg) and Curcumin (20mg/kg) groups respectively and treated at everyday interval for 60 consecutive days. Oxidative stress markers in the brain were measured at 60th day. NaF treatment significantly increased LPO content, but decreased the level of GSH and activities of SOD, GPx, and CAT the brain of rats in comparison to the control rats. Oral administration of curcumin to fluoride exposed rats significantly reversed the content of lipid peroxidation, as well as enhanced the level of GSH and SOD, GPx and CAT activities to normal compared to NaF exposed rats. Thus, curcumin showed the potential to prevent sodium fluoride induced oxidative damage in the brain of rats and curcumin may be useful agents against neurodegeneration in the brain.

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