scholarly journals Effect of Eclipta alba and Ocimum sanctum on haloperidol induced parkinsonism

2018 ◽  
Vol 8 (5) ◽  
pp. 288-293
Author(s):  
Harmel Singh Chahal ◽  
Shailendra Sharma
Keyword(s):  
Oxidative Stress ◽  
Protective Action ◽  
Thiobarbituric Acid ◽  
Brain Homogenate ◽  
Substantia Nigra Pars Compacta ◽  
Ocimum Sanctum ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Eclipta Alba ◽  
Tnf Α

The aim of the study is protective effect of compound Eclipta alba and Ocimum sanctum on Parkinsonism induced mice by haloperidol injection. Parkinsonism is neurodegenerative disease due to the deficiency of dopamine in brain. The pathological hallmark of Parkinson’s disease in the cell loss within substantia nigra pars compacta (SNpc) region and the disease is charactrised by bradykinesia, rigidity, postural instability, orofacial dyskinesia, muscular stiffness and tremor1. Mice were injected 1mg/kg haloperidol and then treated with test and standard substance for 15 days. The impairment in catatonia in mice were tested using catatonic activity. Biochemical analysis of brain homogenate was performed so ass to assess brain Thiobarbituric acid reactive substance (TBARS) level and reduced glutathione (GSH) and TNF-α level were measured to assess total oxidative stress. EA 300mg/kg and OS 400mg/kg show slightly change in catatonic activity in mice while EA 600mg/kg and 800mg/kg significantly change in catatonic activity. Furthermore, Eclipta alba and Ocimum sanctum prevent the haloperidol induced changes in the level of brain TBARS, GSH and TNF-α. From the results we conclude that Eclipta alba and Ocimum sanctum has protective action against impairment in catatonic activity and pathological damage due to oxidative stress induced by intraperitoneally injection of haloperidol in mice.        Keywords: Eclipta alba, Ocimum Sanctum, Parkinsonism, Anti-oxidant.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

Expression Analysis of 4-Hydroxynonenal Modified Proteins in Schizophrenia Brain; Relevance to Involvement in Redox Dysregulation

2021 ◽  
Vol 18 ◽  
Author(s):  
Sobia Manzoor ◽  
Ayesha Khan ◽  
Beena Hasan ◽  
Shamim Mushtaq ◽  
Nikhat Ahmed
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thiobarbituric Acid ◽  
Brain Regions ◽  
Protein Adducts ◽  
Antioxidant Systems ◽  
Control Group ◽  
Tbars Level ◽  
Elevated Expression ◽  
Modified Proteins

Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and activities of enzymatic and antioxidant systems in schizophrenia. Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in schizophrenia pathology due to oxidative stress, particularly lipid peroxidation. Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances (TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also estimated. Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ± 1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects an increased lipid peroxidation (LPO). Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production. Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative stress in schizophrenia pathology.

scholarly journals Biological Properties of a Citral-Enriched Fraction of Citrus limon Essential Oil

Foods ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1290
Author(s):  
Marzia Pucci ◽  
Stefania Raimondo ◽  
Chiara Zichittella ◽  
Vincenza Tinnirello ◽  
Valeria Corleone ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Essential Oil ◽  
Biological Activities ◽  
Protective Action ◽  
Biological Properties ◽  
Citrus Limon ◽  
Tnf Α ◽  
Pre Treatment ◽  
Flavoring Agent ◽  
And Oxidative Stress

Lemon essential oil (LEO) is a well-known flavoring agent with versatile biological activities. In the present study, we have isolated and characterized four citral-enriched fractions of winter LEO. We reported that in murine and human macrophages the pre-treatment with a mix of these fractions (Cfr-LEO) reduces the expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 induced by LPS. In addition, Cfr-LEO counteracts LPS-induced oxidative stress, as shown by the increase in the GSH/GSSG ratio in comparison to cells treated with LPS alone. Overall, the results reported here encourage the application of EO fractions, enriched in citral, in the nutraceutical industry, not only for its organoleptic properties but also for its protective action against inflammation and oxidative stress.

scholarly journals Sitagliptin-Dependent Differences in the Intensity of Oxidative Stress in Rat Livers Subjected to Ischemia and Reperfusion

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Małgorzata Trocha ◽  
Małgorzata Krzystek-Korpacka ◽  
Anna Merwid-Ląd ◽  
Beata Nowak ◽  
Małgorzata Pieśniewska ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Liver ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Tbars Level ◽  
Rat Livers

Purpose. Ischemia/reperfusion (IR) is the main cause of liver damage after transplantation. We evaluated the effect of sitagliptin (STG) on oxidative stress parameters in the rat liver under IR. Methods. Rats were treated with STG (5 mg/kg) (S and SIR) or saline solution (C and CIR). Livers from CIR and SIR were subjected to ischemia (60 min) and reperfusion (24 h). During reperfusion, aminotransferases (ALT and AST) were determined in blood samples. Thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), paraoxonase-1 (PON1), glutathione peroxidase (GPx), and the mRNA expression of SOD1 were determined in liver homogenates after reperfusion. Different regions of livers were also histologically evaluated. Results. The PON1 activity was higher, and the TBARS level was lower in SIR than in CIR. There was an inverse relationship between TBARS and PON1 levels in the whole cohort. The GPx activity was lower in ischemic than in nonischemic groups regardless of the STG treatment. In SIR, the SOD1 activity was higher compared to that in CIR. In S, the expression of SOD1 mRNA was the highest of all examined groups and positively correlated with the SOD1 activity in the whole animal cohort. During IR aminotransferases, the activity in the drug-treated group was lower in all examined points of time. In drug-treated groups, the percentage of steatosis was higher than that in nontreated groups regardless of IR. Conclusions. The protective effect of STG on the rat liver, especially its antioxidant properties, was revealed under IR conditions.

Chronic hypoxia and glutathione-dependent detoxication in rat small intestine

1996 ◽  
Vol 270 (4) ◽  
pp. G725-G729 ◽  
Author(s):  
T. S. LeGrand ◽  
T. Y. Aw
Keyword(s):  
Oxidative Stress ◽  
Chronic Hypoxia ◽  
Thiobarbituric Acid ◽  
Redox System ◽  
Thiobarbituric Acid Reactive Substance ◽  
Sprague Dawley ◽  
Distal Intestine ◽  
Key Enzyme ◽  
Cysteine Synthetase ◽  
Glucose 6 Phosphate Dehydrogenase

It has previously been found that chronic O2 deficiency decreases activity of the enzymes of the glutathione (GSH) redox system in the liver. To study the effects of O2 deficiency on intestinal detoxication capacity, pair-fed (16 g food/day) Sprague-Dawley rats were exposed to air (20.9% O2; n = 4) or 10% O2 (n = 4) for 10 days. Animals were killed, and intestinal mucosal homogenate (20% wt/vol) was obtained and assayed for activities of glucose-6-phosphate dehydrogenase (G6PD), GSH peroxidase (GSHPx), GSH disulfide reductase (GSSGRd), and gamma-glutamyl cysteine synthetase (gamma-GCS). Hypoxia decreases activities of GSHPx, GSSGRd, and gamma-GCS by approximately 50%, which suggests compromised detoxication. A proximal-to-distal reduction in enzymatic capacity indicates impairment of detoxication may be more pronounced in the distal intestine. G6PD, a key enzyme in NADPH production, remains unchanged. Urinary malondialdehyde was also monitored. Hypoxic rats exhibited a threefold increase in thiobarbituric acid-reactive substance, consistent with a generalized oxidative stress in these animals. Taken together, the results indicate that chronic hypoxia promotes tissue oxidative stress and impairs the ability of the enterocyte to metabolize ingested oxidants.

scholarly journals Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Julie Chao ◽  
Youming Guo ◽  
Pengfei Li ◽  
Lee Chao
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Animal Models ◽  
Hypoxia Inducible Factor ◽  
Thiobarbituric Acid ◽  
Organ Injury ◽  
Thiobarbituric Acid Reactive Substance ◽  
Bacterial Killing ◽  
Antioxidant Genes ◽  
Pkc Activation

Oxidative stress has both detrimental and beneficial effects. Kallistatin, a key component of circulation, protects against vascular and organ injury. Serum kallistatin levels are reduced in patients and animal models with hypertension, diabetes, obesity, and cancer. Reduction of kallistatin levels is inversely associated with elevated thiobarbituric acid-reactive substance. Kallistatin therapy attenuates oxidative stress and increases endothelial nitric oxide synthase (eNOS) and NO levels in animal models. However, kallistatin administration increases reactive oxygen species formation in immune cells and bacterial killing activity in septic mice. High oxygen inhibits kallistatin expression via activating the JNK-FOXO1 pathway in endothelial cells. Conversely, mild oxygen/hyperoxia stimulates kallistatin, eNOS, and hypoxia-inducible factor-1 (HIF-1) expression in endothelial cells and in the kidney of normal mice. Likewise, kallistatin stimulates eNOS and HIF-1, and kallistatin antisense RNA abolishes oxygen-induced eNOS and HIF-1 expression, indicating a role of kallistatin in mediating mild oxygen’s stimulation on antioxidant genes. Protein kinase C (PKC) activation mediates HIF-1-induced eNOS synthesis in response to hyperoxia/exercise; thus, mild oxygen through PKC activation stimulates kallistatin-mediated HIF-1 and eNOS synthesis. In summary, oxidative stress induces down- or upregulation of kallistatin expression, depending on oxygen concentration, and kallistatin plays a novel role in mediating oxygen/exercise-induced HIF-1-eNOS-NO pathway.

Degradation of oxidative stress-induced denatured albumin in rat liver endothelial cells

2005 ◽  
Vol 289 (3) ◽  
pp. C531-C542 ◽  
Author(s):  
Ryuji Bito ◽  
Sayaka Hino ◽  
Atsushi Baba ◽  
Miharu Tanaka ◽  
Haruka Watabe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Rat Liver ◽  
Laser Scanning ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Endocytic Pathway ◽  
Thiobarbituric Acid Reactive Substance ◽  
Liver Endothelial Cells

We previously identified conformationally denatured albumin (D2 and D3 albumin) in rats with endotoxicosis (Bito R, Shikano T, and Kawabata H. Biochim Biophys Acta 1646: 100–111, 2003). In the present study, we attempted first to confirm whether the denatured albumins generally increase in conditions of oxidative stress and second to characterize the degradative process of the denatured albumin using primary cultured rat liver endothelial cells. We used five models of oxidative stress, including endotoxicosis, ischemic heart disease, diabetes, acute inflammation, and aging, and found that serum concentrations of D3 albumin correlate with the serum levels of thiobarbituric acid-reactive substance ( R = 0.87), whereas the concentrations of D2 albumin are 0.52. Ligand blot analysis showed that the D3 albumin binds to gp18 and gp30, which are known endothelial scavenger receptors for chemically denatured albumin. Primary cultured rat liver endothelial cells degraded the FITC-D3 albumin, and the degradation rate decreased to ∼60% of control levels in response to anti-gp18 and anti-gp30 antibodies, respectively. An equimolar mixture of these antibodies produced an additive inhibitory effect on both uptake and degradation, resulting in levels ∼20% those of the control. Furthermore, filipin and digitonin, inhibitors of the caveolae-related endocytic pathway, reduced the FITC-D3 albumin uptake and degradation to <20%. Laser-scanning confocal microscopic observation supported these data regarding the uptake and degradation of D3 albumin. These results indicate that conformationally denatured D3 albumin occurs generally under oxidative stress and is degraded primarily via gp18- and gp30-mediated and caveolae-related endocytosis in liver endothelial cells.

scholarly journals COMPARATIVE ANALYSIS OF THE EFFECT OF WHITE AND RED TABLE WINES ON THE BRAIN OF WISTER RATS

2020 ◽  
Vol 1 (1) ◽  
pp. 28-35
Author(s):  
A. J. Kukoyi ◽  
T. A. Coker ◽  
K. A. Arowora ◽  
J. E. Ukperoro ◽  
M. A. Alabi ◽  
...  
Keyword(s):  
Body Weight ◽  
Red Wine ◽  
Hdl Cholesterol ◽  
Thiobarbituric Acid ◽  
Brain Homogenate ◽  
White Wine ◽  
Thiobarbituric Acid Reactive Substance ◽  
Water Control ◽  
The University ◽  
The Brain

The aim of this research was to investigate the possible effects of white and red table wine on the brain using Wister rats. Twenty-four (24) Wister rats weighing an average of 193g were purchased and identified at the zoological department of the University of Ibadan, Ibadan, Nigeria. The rats were randomly assigned to four groups of six rats each. Red wine (12% alcoholic content), white wine (12% alcoholic content), ethanol+H2O (12%) and distilled water (control), were administered orally and respectively for 10 days. Administration was done using syringe and tourniquets to each rat according to the kg body weight (10ml/kg body weight). The rats were later sacrificed and subjected to biochemical and brain homogenate analysis. The results show that the plasma and brain homogenate of rats administered White wines were significantly lower (p<0.05) than control for Total Cholesterol determination. Similarly, the plasma and brain homogenate of rats administered White wine were significantly lower (p<0.05) than control for Thiobarbituric Acid Reactive Substance (TBARS) determination. Meanwhile, other parameters like HDL-cholesterol, LDL-Cholesterol, Glutathione, Triglyceride, Total Protein, Uric acid and Creatinine were not significantly different from the control for plasma and homogenate analysis. In all, White wine was not found to express any trace of toxicity on the brain as opposed to Red wine. The study therefore shows that White wine are more healthy than red wines and as such when given an option between red and white, white wine should be preferred. Kukoyi, A. J. | Department of Biochemistry, Faculty of Pure and Applied Sciences, Federal University Wukari, P.M.B. 1020, Wukari, Taraba State, Nigeria

Exercise-induced oxidative stress leads hemolysis in sedentary but not trained humans

2005 ◽  
Vol 99 (4) ◽  
pp. 1434-1441 ◽  
Author(s):  
Ümit Kemal Şentürk ◽  
Filiz Gündüz ◽  
Oktay Kuru ◽  
Günnur Koçer ◽  
Yaşar Gül Özkaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Osmotic Fragility ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Antioxidant Vitamin ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protein Carbonyl Content ◽  
Trained Subjects ◽  
Exercise Induced ◽  
Sedentary Subjects

Intravascular hemolysis is one of the most emphasized mechanisms for destruction of erythrocytes during and after physical activity. Exercise-induced oxidative stress has been proposed among the different factors for explaining exercise-induced hemolysis. The validity of oxidative stress following exhaustive cycling exercise on erythrocyte damage was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 mo. Exercise induced a significant increase in thiobarbituric acid-reactive substance and protein carbonyl content levels in sedentary subjects and resulted in an increase of osmotic fragility and decrease in deformability of erythrocytes, accompanied by signs for intravascular hemolysis (increase in plasma hemoglobin concentration and decrease in haptoglobulin levels). Administration of antioxidant vitamins for 2 mo prevented exercise-induced oxidative stress (thiobarbituric acid-reactive substance, protein carbonyl content) and deleterious effects of exhaustive exercise on erythrocytes in sedentary subjects. Trained subjects' erythrocyte responses to exercise were different from those of sedentary subjects before antioxidant vitamin treatment. Osmotic fragility and deformability of erythrocytes, plasma hemoglobin concentration, and haptoglobulin levels were not changed after exercise, although the increased oxidative stress was observed in trained subjects. After antioxidant vitamin treatment, functional and structural parameters of erythrocytes were not altered in the trained group, but exercise-induced oxidative stress was prevented. Increased percentage of young erythrocyte populations was determined in trained subjects by density separation of erythrocytes. These findings suggest that the exercise-induced oxidative stress may contribute to exercise-induced hemolysis in sedentary humans.

scholarly journals Exposure of precision-cut rat liver slices to ethanol accelerates fibrogenesis

2010 ◽  
Vol 299 (3) ◽  
pp. G661-G668 ◽  
Author(s):  
Courtney S. Schaffert ◽  
Michael J. Duryee ◽  
Robert G. Bennett ◽  
Amy L. DeVeney ◽  
Dean J. Tuma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cytokine Production ◽  
Smooth Muscle Actin ◽  
Thiobarbituric Acid ◽  
Ethanol Metabolism ◽  
Thiobarbituric Acid Reactive Substance ◽  
Ethanol Treatment ◽  
Liver Slices

Ethanol metabolism in the liver induces oxidative stress and altered cytokine production preceding myofibroblast activation and fibrogenic responses. The purpose of this study was to determine how ethanol affects the fibrogenic response in precision-cut liver slices (PCLS). PCLS were obtained from chow-fed male Wistar rats (200–300 g) and were cultured up to 96 h in medium, 25 mM ethanol, or 25 mM ethanol and 0.5 mM 4-methylpyrazole (4-MP), an inhibitor of ethanol metabolism. Slices from every time point (24, 48, 72, and 96 h) were examined for glutathione (GSH) levels, lipid peroxidation [thiobarbituric acid-reactive substance (TBARS) assay], cytokine production (ELISA and RT-PCR), and myofibroblast activation [immunoblotting and immunohistochemistry for smooth muscle actin (SMA) and collagen]. Treatment of PCLS with 25 mM ethanol induced significant oxidative stress within 24 h, including depletion of cellular GSH and increased lipid peroxidation compared with controls ( P < 0.05). Ethanol treatment also elicited a significant and sustained increase in interleukin-6 (IL-6) production ( P < 0.05). Importantly, ethanol treatment accelerates a fibrogenic response after 48 h, represented by significant increases in SMA and collagen 1α(I) production ( P < 0.05). These ethanol-induced effects were prevented by the addition of 4-MP. Ethanol metabolism induces oxidative stress (GSH depletion and increased lipid peroxidation) and sustained IL-6 expression in rat PCLS. These phenomena precede and coincide with myofibroblast activation, which occurs within 48 h of treatment. These results indicate the PCLS can be used as in vitro model for studying multicellular interactions during the early stages of ethanol-induced liver injury and fibrogenesis.

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