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 Evaluation of Neuroprotective Effects of Quercetin against Aflatoxin B1-Intoxicated Mice

Animals ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 898 ◽  
Author(s):  
Enrico Gugliandolo ◽  
Alessio Filippo Peritore ◽  
Ramona D’Amico ◽  
Patrizia Licata ◽  
Rosalia Crupi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Aflatoxin B1 ◽  
Protective Effects ◽  
Behavioral Alterations ◽  
Sod Activity ◽  
Neuroprotective Effects ◽  
Oxidative Stress Pathway ◽  
Ameliorative Effect ◽  
The Brain

Aflatoxin B1 (AFB1) is a mycotoxin commonly present in feed, characterized by several toxic effects. AFB1 seems to have a neurotoxical effect that leads to memory impairment behavior. AFB1 toxicity involves the induction of the oxidative stress pathway, rising lipid peroxidation, and it decreases antioxidant enzyme levels. Hence, in our research, we wanted to evaluate the potential protective effects of quercetin 30 mg/kg in AFB1-mediated toxicity in the brain and the ameliorative effect on behavioral alterations. Oral supplementation with quercetin increased glutathione peroxidase (GSH) levels, superoxidedismutase (SOD) activity and catalase (CAT) in the brain, and it reduced lipid peroxidation in AFB1-treated mice. This antioxidant effect of quercetin in the brains of AFB1-intoxicated mice is reflected in better cognitive and spatial memory capacity, as well as a better profile of anxiety and lethargy disorders. In conclusion, our study suggests that quercetin exerts a preventive role against oxidative stress by promoting antioxidative defense systems and limiting lipid peroxidation.

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.

Rhanterium suaveolens, Vitamin E and C Pretreatment Prevents Valproic Acid Induced Renal Oxidant Damage

2020 ◽  
Vol 10 ◽  
Author(s):  
Amel Amrani ◽  
Ouahiba Benaissa ◽  
Nassima Boubekri ◽  
Fadila Benayache ◽  
Samir Benayache ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Valproic Acid ◽  
Vitamin E ◽  
Serum Creatinine ◽  
Natural Antioxidants ◽  
Control Group ◽  
Protective Effects ◽  
Butanol Extract ◽  
Renal Tubular ◽  
Vit C

Background: Long-term administration of valproic acid (VPA) is known to promote renal tubular injury mediated by increase in renal oxidative stress. Recent evidence indicates that natural antioxidants are alternative to attenuate oxidative stress and kidney damage. Objective: This study was performed to investigate the protective effects of n-butanol extract of Rhanterium suaveolens, vitamin E (Vit E) and vitamin C (Vit C) against VPA induced nephrotoxicity in mice. Methods: Mice were randomly divided into 6 groups (n: 8) and treated daily for 12 days. They received VPA (300 mg/kg intraperitoneally (ip)), buthanolic extract (100 mg/kg), Vit E (100 mg/kg), and Vit C (16.66 mg/kg) 1h prior to administration of VPA. On day 13, blood and Kidneys samples were analyzed for biomarker levels and histopathological changes. Kidneys homogenates were used for determination of oxidative stress parameters that include malondialdehyde (MDA), glutathione (GSH) level and glutathione peroxidase (GPx) activity. Result: Treatment with VPA showed a significant increase in the levels of serum creatinine, urea and malondialdehyde (MDA) and decreasing the enzymatic activity (GPx) as well as GSH levels in kidney with marked necrotic epithelial cells and infiltration in kidney sections as compared to the control group. Pretreatment with the n-butanol extract of R. suaveolens, Vit C or Vit E 1 h prior to administration of VPA showed a significant decrease in the levels of serum creatinine, urea, and MDA, as well as an improvement in the antioxidant elements and histological changes compared to those previously seen in the group treated with VPA alone. Conclusion: It is concluded that n-butanol extract of R. suaveolens, Vit C and Vit E pretreatment effectively improved renal function and tissue oxidative damage caused by VPA.

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.

scholarly journals Protective role of Limonium bonduelli extract against non-enzymatic peroxidation in brain and testes induced by iron in vitro.

2017 ◽  
Vol 9 (1) ◽  
pp. 72
Author(s):  
Amel Amrani ◽  
Nassima Boubekri ◽  
Ouahiba Benaissa ◽  
Djamila Zama ◽  
Fadila Benayache ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Rat Brain ◽  
Inhibitory Effect ◽  
Protective Role ◽  
Dependent Manner ◽  
Phytochemical Content ◽  
Butanol Extract ◽  
Aerial Parts

<p>Infertility and Neurodegerative diseases have been linked to oxidative stress arising from peroxidation of membrane biomolecules and high levels of iron have been reported to play an important role. The present study sought to determine the antioxidant activity and protective ability of <em>n</em>-butanol extract of <em>Limonium bonduelli</em> on lipid peroxidation induced by FeSO<sub>4</sub> in rat brain and testes homogenates <em>in vitro</em>. <em>n</em>-butanol extract of the aerial parts (leaves and flowers)<em> </em>was prepared, and the ability of the extract to inhibit FeSO<sub>4</sub> induced lipid peroxidation in isolated rat brain and testes was determined using spectrophotometric method. The study revealed that the extract inhibited malondialdehyde (MDA) production in FeSO<sub>4 </sub>induced lipid peroxidation in the brain and testes in a dose-dependent manner and the highest percentage of the inhibition was 89.80% similar to vitamin C in the same concentration (100 µg/mL) in brain and 82.33% in testes (200 µg/mL). <em>Limonium bonduelli</em> extract<strong> </strong>demonstrated important anti-lipid peroxidative effect, which may be useful in preventing the progress of various oxidative stress related diseases. The higher inhibitory effect of the extract could be attributed to its phytochemical content.</p>

Attenuation of erythrocyte membrane oxidative stress bySesbania grandiflorain streptozotocin-induced diabetic rats

2015 ◽  
Vol 93 (4) ◽  
pp. 385-395 ◽  
Author(s):  
Chandrabose Sureka ◽  
Thiyagarajan Ramesh ◽  
Vavamohaideen Hazeena Begum
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Blood Glucose ◽  
Erythrocyte Membrane ◽  
Osmotic Fragility ◽  
Diabetic Rats ◽  
Glycosylated Haemoglobin ◽  
Albino Rats ◽  
Enzymatic Antioxidants ◽  
Protective Effects

The aim of the present study was to investigate the protective effects of Sesbania grandiflora flower (SGF) extract on erythrocyte membrane in Streptozotocin (STZ)-induced diabetic rats. Adult male albino rats of Wistar strain, weighing 190–220 g, were made diabetic by an intraperitonial administration of STZ (45 mg/kg). Normal and diabetic rats were treated with SGF, and diabetic rats were also treated with glibenclamide as drug control, for 45 days. In this study plasma insulin and haemoglobin levels were decreased and blood glucose, glycosylated haemoglobin, protein oxidation, lipid peroxidation markers, and osmotic fragility levels were increased in diabetic rats. Moreover, erythrocytes antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxide, glutathione reductase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenase activities and non-enzymatic antioxidants such as vitamin C, vitamin E, reduced glutathione (GSH), and oxidized glutathione (GSSG) levels were altered. Similarly, the activities of total ATPases, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase were also decreased in the erythrocytes of diabetic rats. Administration of SGF to STZ-induced diabetic rats reduced blood glucose and glycosylated haemoglobin levels with increased levels of insulin and haemoglobin. Moreover, SGF reversed the protein and lipid peroxidation markers, osmotic fragility, membrane-bound ATPases activities, and antioxidant status in STZ-induced diabetic rats. These results suggest that SGF could provide a protective effect on diabetes by decreasing oxidative stress-associated diabetic complications.

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.

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