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 Effects of Panthenol and N-Acetylcysteine on Changes in the Redox State of Brain Mitochondria under Oxidative Stress In Vitro

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1699
Author(s):  
Dmitry S. Semenovich ◽  
Egor Yu. Plotnikov ◽  
Oksana V. Titko ◽  
Elena P. Lukiyenko ◽  
Nina P. Kanunnikova
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Redox Potential ◽  
Brain Mitochondria ◽  
Neuroprotective Activity ◽  
Protective Effects ◽  
Glutathione System ◽  
Mitochondrial Energy Metabolism ◽  
The Brain

The glutathione system in the mitochondria of the brain plays an important role in maintaining the redox balance and thiol–disulfide homeostasis, whose violations are the important component of the biochemical shifts in neurodegenerative diseases. Mitochondrial dysfunction is known to be accompanied by the activation of free radical processes, changes in energy metabolism, and is involved in the induction of apoptotic signals. The formation of disulfide bonds is a leading factor in the folding and maintenance of the three-dimensional conformation of many specific proteins that selectively accumulate in brain structures during neurodegenerative pathology. In this study, we estimated brain mitochondria redox status and functioning during induction of oxidative damage in vitro. We have shown that the development of oxidative stress in vitro is accompanied by inhibition of energy metabolism in the brain mitochondria, a shift in the redox potential of the glutathione system to the oxidized side, and activation of S-glutathionylation of proteins. Moreover, we studied the effects of pantothenic acid derivatives—precursors of coenzyme A (CoA), primarily D-panthenol, that exhibit high neuroprotective activity in experimental models of neurodegeneration. Panthenol contributes to the significant restoration of the activity of enzymes of mitochondrial energy metabolism, normalization of the redox potential of the glutathione system, and a decrease in the level of S-glutathionylated proteins in brain mitochondria. The addition of succinate and glutathione precursor N-acetylcysteine enhances the protective effects of the drug.

scholarly journals Pretreatment of Nicorandil Protects the Heart from Exhaustive Exercise-Induced Myocardial Injury in Rats

2022 ◽  
Vol 2022 ◽  
pp. 1-10
Author(s):  
Lei Lv ◽  
Lin Li ◽  
Yiyong Zhu ◽  
Anwar Azhar ◽  
Yao Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Structural Damage ◽  
Myocardial Injury ◽  
Protective Role ◽  
Exhaustive Exercise ◽  
High Dose ◽  
No Production ◽  
Protective Effects ◽  
Sprague Dawley

Objective. Nicorandil has been widely used for the treatment of angina pectoris and myocardial infarction. The purpose of this study was to investigate whether nicorandil plays a protective role in exhaustive exercise (EE)-induced myocardial injury. Methods. Here, we applied the rat EE model and treated them with exercise preconditioning (EP, reported to protect the heart) or different doses of nicorandil gavage, respectively, to explore whether there are protective effects of single EP or nicorandil or a combination of both and the potential mechanism. Forty-nine male Sprague Dawley rats were randomly divided into control, EE, EP + EE, nicorandil (with low, middle, and high dose) + EE, and EP + nicorandil (middle dose) + EE. Blood samples and myocardial tissues were collected to analyze the myocardial injury-related index. Results. EE induced myocardial structural damage and altered the myocardial injury markers, which were partially reversed by pretreatment of nicorandil. In addition, oxidative stress and inflammation lead to the accumulation of reactive oxygen species (ROS) products and further damage to the myocardium, while pretreatment of nicorandil reduces the oxidative stress response and inflammation. Moreover, nicorandil suppressed the myocardial apoptosis induced by EE, as indicated by a decrease of Bax and caspase-3 expression and an increase of Bcl-2 expression. Finally, the pathway in which nicorandil plays a role may be involved in the endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) pathway. Pretreatment of nicorandil increased the protein level of myocardial eNOS and NO production. Conclusion. Our result demonstrated that nicorandil has protective effects in EE-induced myocardial injury with dose-dependent effects. A combination of nicorandil and EP can further improve the protective effects. Taken together, nicorandil can be potentially used as an intervention method in EE-induced myocardial injury.

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.

Compounds from Ilex paraguariensis extracts have antioxidant effects in the brains of rats subjected to chronic immobilization stress

2017 ◽  
Vol 42 (11) ◽  
pp. 1172-1178 ◽  
Author(s):  
Ana C. Colpo ◽  
Maria Eduarda de Lima ◽  
Marisol Maya-López ◽  
Hemerson Rosa ◽  
Cristina Márquez-Curiel ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Immobilization Stress ◽  
Brain Regions ◽  
Protective Role ◽  
Ilex Paraguariensis ◽  
Protective Effects ◽  
Species Formation ◽  
Lipid And Protein Oxidation ◽  
Response To Stress ◽  
Chronic Immobilization Stress

Immobilization induces oxidative damage to the brain. Ilex paraguariensis extracts (Mate) and their major natural compound, chlorogenic acid (CGA), exert protective effects against reactive oxygen species formation. Here, the effects of Mate and CGA on oxidative damage induced by chronic immobilization stress (CIS) in the cortex, hippocampus, and striatum were investigated. For CIS, animals were immobilized for 6 h every day for 21 consecutive days. Rats received Mate or CGA by intragastric gavage 30 min before every restraint session. Endpoints of oxidative stress (levels of lipid peroxidation, protein carbonylation, and reduced (GSH) and oxidized (GSSG) forms of glutathione) were evaluated following CIS. While CIS increased oxidized lipid and carbonyl levels in all brain regions, CGA (and Mate to a lesser extent) attenuated lipid and protein oxidation as compared with control groups. GSH/GSSG balance showed a tendency to increase in all regions in response to stress and antioxidants. Taken together, our results support a protective role of dietary antioxidants against the neuronal consequences of stress.

scholarly journals Endothelial dysfunction and body mass index: is there a role for plasma peroxynitrite?

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Theresa Chikopela ◽  
Douglas C. Heimburger ◽  
Longa Kaluba ◽  
Pharaoh Hamambulu ◽  
Newton Simfukwe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Body Mass ◽  
Vascular Function ◽  
Aortic Ring ◽  
Normal Weight ◽  
Oxide Synthase ◽  
Weight Groups

Abstract Background Endothelial function is dependent on the balance between vasoconstrictive and vasodilatory substances. The endothelium ability to produce nitric oxide is one of the most crucial mechanisms in regulating vascular tone. An increase in inducible nitric oxide synthase contributes to endothelial dysfunction in overweight persons, while oxidative stress contributes to the conversion of nitric oxide to peroxynitrite (measured as nitrotyrosine in vivo) in underweight persons. The objective of this study was to elucidate the interaction of body composition and oxidative stress on vascular function and peroxynitrite. This was done through an experimental design with three weight groups (underweight, normal weight and overweight), with four treatment arms in each. Plasma nitrotyrosine levels were measured 15–20 h post lipopolysaccharide (LPS) treatment, as were aortic ring tension changes. Acetylcholine (ACh) and sodium nitroprusside (SNP) challenges were used to observe endothelial-dependent and endothelial-independent vascular relaxation after pre-constriction of aortic rings with phenylephrine. Results Nitrotyrosine levels in saline-treated rats were similar among the weight groups. There was a significant increase in nitrotyrosine levels between saline-treated rats and those treated with the highest lipopolysaccharide doses in each of the weight groups. In response to ACh challenge, Rmax (percentage reduction in aortic tension) was lowest in overweight rats (112%). In response to SNP, there was an insignificantly lower Rmax in the underweight rats (106%) compared to the normal weight rats (112%). Overweight rats had a significant decrease in Rmax (83%) in response to SNP, signifying involvement of a more chronic process in tension reduction changes. A lower Rmax accompanied an increase in peroxynitrite after acetylcholine challenge in all weight groups. Conclusions Endothelial dysfunction, observed as an impairment in the ability to reduce tension, is associated with increased plasma peroxynitrite levels across the spectrum of body mass. In higher-BMI rats, an additional role is played by vascular smooth muscle in the causation of endothelial dysfunction.

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 A Hypothesis: Hydrogen Sulfide Might Be Neuroprotective against Subarachnoid Hemorrhage Induced Brain Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yong-Peng Yu ◽  
Xiang-Lin Chi ◽  
Li-Jun Liu
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Leukocyte Adhesion ◽  
Ischemia Reperfusion ◽  
The Brain

Gases such as nitric oxide (NO) and carbon monoxide (CO) play important roles both in normal physiology and in disease. Recent studies have shown that hydrogen sulfide (H2S) protects neurons against oxidative stress and ischemia-reperfusion injury and attenuates lipopolysaccharides (LPS) induced neuroinflammation in microglia, exhibiting anti-inflammatory and antiapoptotic activities. The gas H2S is emerging as a novel regulator of important physiologic functions such as arterial diameter, blood flow, and leukocyte adhesion. It has been known that multiple factors, including oxidative stress, free radicals, and neuronal nitric oxide synthesis as well as abnormal inflammatory responses, are involved in the mechanism underlying the brain injury after subarachnoid hemorrhage (SAH). Based on the multiple physiologic functions of H2S, we speculate that it might be a promising, effective, and specific therapy for brain injury after SAH.

Abstract 814: Atorvastatin Attenuates Oxidative Stress And Improves Neuronal Nitric Oxide Synthase In The Brain Stem Of Heart Failure Mice

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Joseph Francis ◽  
Li Yu ◽  
Anuradha Guggilam ◽  
Srinivas Sriramula ◽  
Irving H Zucker
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Brain Stem ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Left Ventricular ◽  
Neuronal Nos ◽  
The Brain

3-Hydroxyl-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been shown to reduce the incidence of myocardial infarction independent of their lipid-lowering effects. Nitric oxide (NO) in the central nervous system contributes to cardiovascular regulatory mechanisms. Imbalance between nitric oxide (NO) and superoxide anion (O 2 . − ) in the brain may contribute to enhanced sympathetic drive in heart failure (HF). This study was done to determine whether treatment with atorvastatin (ATS) ameliorates the imbalance between NO and O 2 . − production in the brain stem and contributes to improvement of left ventricular (LV) function. Methods and Results: Myocardial infarction (MI) was induced by ligation of the left coronary artery or sham surgery. Subsequently, mice were treated with ATS (10 μg/kg) (MI + ATS), or vehicle (MI + V). After 5 weeks, echocardiography revealed left ventricular dilatation in MI mice. Realtime RT-PCR indicated an increase in the mRNA expression of the LV hypertrophy markers, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Neuronal NOS (nNOS) and endothelial NOS (eNOS) mRNA expression were significantly reduced, while that of NAD(P)H oxidase subunit (gp91phox) expression was elevated in the brain stem of MI mice. Compared with sham-operated mice, ATS-treated mice showed reduced cardiac dilatation, decreased ANP and BNP in the LV. ATS also reduced gp91phox expression and increased nNOS mRNA expression in the brain stem, while no changes in eNOS and iNOS were observed. Conclusion: These findings suggest that ATS reduces oxidative stress and increases neuronal NOS in the brain stem, and improves left ventricular function in heart failure.

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