scholarly journals Modafinil Effects on Behavior and Oxidative Damage Parameters in Brain of Wistar Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Felipe Ornell ◽  
Samira S. Valvassori ◽  
Amanda V. Steckert ◽  
Pedro F. Deroza ◽  
Wilson R. Resende ◽  
...  

The effects of modafinil (MD) on behavioral and oxidative damage to protein and lipid in the brain of rats were evaluated. Wistar rats were given a single administration by gavage of water or MD (75, 150, or 300 mg/kg). Behavioral parameters were evaluated in open-field apparatus 1, 2, and 3 h after drug administration. Thiobarbituric acid reactive substances (TBARS) and protein carbonyl formation were measured in the brain. MD increased locomotor activity at the highest dose 1 and 3 h after administration. MD administration at the dose of 300 mg/kg increased visits to the center of open-field 1 h after administration; however, 3 h after administration, all administered doses of MD increased visits to the open-field center. MD 300 mg/kg increased lipid damage in the amygdala, hippocampus, and striatum. Besides, MD increased protein damage in the prefrontal cortex, amygdala, and hippocampus; however, this effect varies depending on the dose administered. In contrast, the administration of MD 75 and 300 mg/kg decreased the protein damage in the striatum. This study demonstrated that the MD administration induces behavioral changes, which was depending on the dose used. In addition, the effects of MD on oxidative damage parameters seemed to be in specific brain region and doses.

2003 ◽  
Vol 89 (1) ◽  
pp. 89-96 ◽  
Author(s):  
S. L. de Oliveira ◽  
D. B. Diniz ◽  
J. Amaya-Farfan

Chronic energy restriction, α-tocopherol supplementation and their interaction with exhaustive exercise were investigated. Eleven-week-old male Wistar rats (n 6×10) were fed either a control (C), a 30 % carbohydrate-energy-restricted control (R) or an α-tocopherol-supplemented (S) diet for 5 months. The animals in each diet were divided into exercised (E) and non-exercised (NE) groups. Before killing, the exercised rats were required to run to exhaustion (39 (SE 6), 69 (se 11) and 18 (se 2) min for the C, R and S groups, respectively). Lipid peroxidation (thiobarbituric acid-reactive substances; TBARS), protein damage (reactive carbonyls) and α-tocopherol were determined in gastrocnemius, liver, brain an/r plasma. There was no difference in lipid peroxidation between the R and C groups, but in liver and muscle peroxidation appeared significantly lower in the S than the other two diets. TBARS in the brain were similar in all groups. On the other hand, reactive carbonyls showed that both the R and S diets reduced protein damage in the brain, while exhaustive exercise increased it. For liver and muscle, however, reactive carbonyl levels were similar in all groups. α-Tocopherol supplementation increased the vitamin concentrations in liver, muscle and plasma, but exercise decreased them in plasma and brain. Carbohydrate-energy restriction increased (P=0·0025) resistance to exhaustive exercise considerably without depleting stores of α-tocopherol or exacerbating oxidative damage in monitored tissues. It is concluded that while exhaustive exercise promotes a tissue-specific oxidative damage detectable only in brain proteins, both experimental diets tended to ameliorate this condition.


2020 ◽  
Vol 16 ◽  
Author(s):  
Anupama Sharma ◽  
Renu Bist ◽  
Hemant Pareek

Background:: Current study evaluated the protective potential of quercetin against lindane induced toxicity in mice brain. For investigation, mice were allocated into four groups; First group was control. Second group was administered with oral dose of lindane (25 mg/kg bw) for 4 consecutive days. Third group was exposed to quercetin (40 mg/kg bw) and in fourth group, quercetin was administered 1 hour prior to the exposure of lindane. Objective:: Two major objectives were decided for study. First was to create lesions in the brain by lindane and; second was to evaluate the neuroprotective potential of quercetin. Methods:: To study oxidative responses, level of thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCC), reduced glutathione (GSH), superoxide dismutase (SOD), Catalase (CAT), and glutathione peroxidase (GPx) were measured in brain homogenates. Three key step regulating enzymes of tricarboxylic acid (TCA) cycle viz citrate synthase (CS), pyruvate dehydrogenase (PDH) and fumarase were also assayed. Results:: Lindane treatment significantly enhanced the levels of TBARS (P<0.001),PCC (P<0.001), GPx (P<0.001), SOD (P<0.05), PDH (P<0.05) and fumarase (P<0.001) in brains of mice compared to control. Meanwhile, it alleviated GSH, CAT and CS (P<0.05) activity. Conclusion:: Pretreatment with quercetin in lindane treated group not only restored, previously altered biochemical parameters after lindane treatment and also significantly improved them too which suggests that quercetin is not only invulnerable rather neuroprotective against lindane intoxication.


2020 ◽  
Vol 71 (3) ◽  
pp. 197-204
Author(s):  
Dragana Javorac ◽  
Aleksandra Buha Đorđević ◽  
Milena Anđelković ◽  
Simona Tatović ◽  
Katarina Baralić ◽  
...  

AbstractMost Pb and Cd neurotoxicity studies investigate exposure to either of the toxic metals alone, while data on co-exposure are scarce. The aim of our study was to fill that gap by investigating acute combined effects of Pb and Cd on redox and essential metal status in the brain of Wistar rats. Animals were randomised in four groups of six to eight rats, which received 15 or 30 mg/kg of Cd, 150 mg/kg of Pb, or 150 mg/kg of Pb + 15 mg/kg of Cd by gavage. The fifth, control, group received distilled water only. Co-treatment with Pb and Cd induced significant increase in malondialdehyde (MDA) and thiobarbituric acid-reactive substances (TBARS) compared to control and groups receiving either metal alone. This is of special importance, as MDA presence in the brain has been implicated in many neurodegenerative disorders. The groups did not significantly differ in Zn, Cu, Mn, and Fe brain levels. Our findings highlight the importance of metal mixture studies. Neurotoxicity assessments of single chemicals do not provide a real insight into exposure to mixtures in real life. Further research should look into interactions between these metals to reveal complex molecular mechanisms of their neurotoxicity.


2016 ◽  
Vol 94 (10) ◽  
pp. 1074-1082 ◽  
Author(s):  
Dragan Hrncic ◽  
Jelena Mikić ◽  
Aleksandra Rasic-Markovic ◽  
Milica Velimirović ◽  
Tihomir Stojković ◽  
...  

The aim of this study was to examine the effects of a methionine-enriched diet on anxiety-related behavior in rats and to determine the role of the brain oxidative status in these alterations. Adult male Wistar rats were fed from the 30th to 60th postnatal day with standard or methionine-enriched diet (double content comparing with standard diet: 7.7 g/kg). Rats were tested in open field and light–dark tests and afterwards oxidative status in the different brain regions were determined. Hyperhomocysteinemia induced by methionine-enriched diet in this study decreased the number of rearings, as well as the time that these animals spent in the center of the open field, but increased index of thigmotaxy. Oxidative status was selectively altered in the examined regions. Lipid peroxidation was significantly increased in the cortex and nc. caudatus of rats developing hyperhomocysteinemia, but unaltered in the hippocampus and thalamus. Based on the results of this research, it could be concluded that hyperhomocysteinemia induced by methionine nutritional overload increased anxiety-related behavior in rats. These proanxiogenic effects could be, at least in part, a consequence of oxidative stress in the rat brain.


2021 ◽  
Vol 11 ◽  
Author(s):  
Anand Thirupathi ◽  
Ricardo A. Pinho ◽  
Ukadike C. Ugbolue ◽  
Yuhuan He ◽  
Yao Meng ◽  
...  

Background: Exercise induced health benefits are limited by the overaccumulation of reactive oxygen species (ROS). ROS and further oxidative stress could potentially induce muscle damage which could result in poor exercise performance. However, predicting ROS induced oxidative stress in response to endurance training has several limitations in terms of selecting biomarkers that are used to measure oxidative stress.Objective: The purpose of this study was to systematically investigate the suitable biomarkers that predict oxidative stress status among runners.Methods: According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, a search for relevant articles was carried out on PubMed/Medline, ISI Web of Science, and Google Scholar using related search terms such as oxidative damage, ROS, exercise, physical training, running, marathon, and ultramarathon.Results: Outcomes included (1) running programs like a half-marathon, ultramarathon, and iron-man race, (2) measuring biochemical assessment of oxidative damage markers such as malondialdehyde (MDA), protein carbonyl (PC), total antioxidant capacity (TAC), thiobarbituric acid reactive substances (TBARS), 8-Oxo-2'-deoxyguanosine (8-OH-dG), 4-hydroxynonenal (HNE), and F1-isoprostones, and enzymatic and non-enzymatic antioxidants level.Conclusions: This study concluded that a running exercise does not elicit a response to specific biomarkers of oxidative stress, instead, oxidative damage markers of lipids, proteins, and various enzymatic and non-enzymatic antioxidants are expressed according to the training status of the individual.


2007 ◽  
Vol 26 (6) ◽  
pp. 527-534 ◽  
Author(s):  
P. Murugavel ◽  
L. Pari

The protective efficacy of diallyl tetrasulfide (DTS) from garlic on liver injury induced by cadmium (Cd) was investigated. In this study, Cd (3 mg/kg body weight) was administered subcutaneously for 3 weeks to induce toxicity. DTS was administered orally (10, 20 and 40 mg/kg body weight) for 3 weeks with subcutaneous (sc) injection of Cd. Cd-induced liver damage was evidenced from increased activities of serum hepatic enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase, with significant elevation of lipid peroxidation indices (thiobarbituric acid reactive substances and hydroperoxides) and protein carbonyl groups in the liver. Rats subjected to Cd toxicity also showed a decline in the levels of total thiols, reduced glutathione (GSH), vitamin C and vitamin E, accompanied by an increased accumulation of Cd, and significantly decreased activities of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione-S-transferase (GST), glutathione reductase, and glucose-6-phosphate dehydrogenase in the liver. Administration of DTS at 40 mg/kg body weight significantly normalised the activities of hepatic marker enzymes, compared to other doses of DTS (10 and 20 mg/kg body weight). In addition, DTS (40 mg/kg body weight) significantly reduced the accumulation of Cd and the level of lipid peroxidation, and restored the level of antioxidant defense in the liver. Histological studies also showed that administration of DTS to Cd-treated rats resulted in a marked improvement of hepatocytes morphology with mild portal inflammation. Our results suggest that DTS might play a vital role in protecting Cd-induced oxidative damage in the liver. Human & Experimental Toxicology(2007) 26, 527—534


2015 ◽  
pp. 263-267 ◽  
Author(s):  
V. RILJAK ◽  
D. MAREŠOVÁ ◽  
J. POKORNÝ ◽  
K. JANDOVÁ

Kainic acid (KA) is a potent neurotoxic substance valuable in research of temporal lobe epilepsy. We tested how subconvulsive dose of KA influences spontaneous behavior of adult Wistar rats. Animals were treated with 5 mg/kg of KA and tested in Laboras open field test for one hour in order to evaluate various behavioral parameters. Week after the KA treatment animals were tested again in Laboras open field test. Finally, rat’s brains were sliced and stained with Fluoro-Jade B to detect possible neuronal degeneration. Treatment with KA increased the time spent by locomotion (p<0.01), exploratory rearing (p<0.05) and animals traveled longer distance (p<0.01). These parameters tended to increase thirty minutes after KA administration. Week after the treatment we did not found differences in any measured behavioral parameter. Histology in terms of Fluoro-Jade B staining did not reveal any obvious neuronal damage in hippocampus. These results demonstrate that subconvulsive KA dose changes the behavioral parameters only transiently. Clarification of timing of the KA induced changes may contribute to understand mutual relationship between non-convulsive seizures and behavioral/cognitive consequences.


Author(s):  
Djemli Samir

Objective: The present study shows the beneficial effect of (zinc 10mg / kg + magnesium 10mg / kg) against cadmium poisoning at a dose of 15mg / kg on biochemical parameters and neurobehavioral functions in Wistar rats during a period of 45 days. Methods: The experiment was carried out on 20 Wistar rats, weighing 180 to 232g for an initial weight before starting treatment with cadmium. The rats are grouped in cages at a rate of 5 in groups:Group (1) control: was supplied only with waterGroup (2) contaminated with cadmium (Cd):  water plus oral administration cadmium dose 15mg / Kg / l.Group (3) contaminated with (Cd) dose 15mg / Kg / l in water plus magnesium (Mg) dose 10mg / Kg / l oral administration.Group (4) contaminated with (Cd) dose 15mg / Kg / l in water plus zinc (Zn) dose 10mg / Kg / l oral administration.Results: The rats exposure to cadmium showed a very highly significant decrease in body weight of cadmium-contaminated rats (P <0.001) compared with the control group. Regarding the biochemical parameters, there was a very highly significant increase (P <0.001) in the cadmium group blood glucose level compared to the control group, a highly significant increase (P <0.01) in the group urea level. cadmium compared to the control, a very highly significant increase (P <0.001) in the creatinine level of the cadmium lot compared to the control, a very highly significant increase (P <0.001) of transaminases (GOT, GPT) of the group cadmium relative to the control, complete blood  count (CBC) demonstrated a very highly significant increase (P <0.001) in the white blood cell count, the hematocrit of the cadmium lot compared to the control, a very highly significant decrease (P <0.001). ) the red blood cell and hemoglobin levels of the cadmium group compared to the control. A significant improvement (P <0.001) (P <0.01) (P <0.05) of lots: zinc, magnesium, cadmium + zinc and cadmium + zinc compared to cadmium. However, the results obtained from the neurobehavioral tests reveal a significant elevation (P <0.001) (P <0.01) (P <0.05) in the number of cells crossed, the number of straightening in the test. Open field in the group exposed to cadmium resulting in locomotors hyperactivity compared to the control and it is minimal in other groups treated with zinc and magnesium. On the other hand, the plus maze (labyrinth test) revealed a very highly significant increase (P <0.001) (P <0.01) (P <0.05) of the time spent in the closed arms of the cadmium group compared to the control, a significant improvement (P <0.001) (P <0.01) (P <0.05) of the lots: zinc, magnesium, cadmium + zinc and cadmium + zinc compared with cadmium. Conclusion: Subchronic cadmium toxicity has harmful effects on the biochemical, hematological and neuro-behavioral parameters of  Wistar rats, with the installation of an anxiety that will lead to a depressive state, which will be reduced and improved by the antioxidant effect of zinc + magnesium. Keywords: Cadmium-zinc-magnesium-subchronic toxicity-Wistar-Open field-plus maze 


2018 ◽  
Vol 118 ◽  
pp. 784-794 ◽  
Author(s):  
P. Merino ◽  
J.A. Santos-López ◽  
C.J. Mateos ◽  
I. Meseguer ◽  
A. Garcimartín ◽  
...  

1986 ◽  
Vol 64 (6) ◽  
pp. 745-747 ◽  
Author(s):  
Shinji Itoh ◽  
Goro Katsuura

Cholecystokinin octapeptide (CCK-8) was administered intracerebroventricularly (icv) or subcutaneously (sc) into subdiaphragmatically vagotomized and sham-operated rats, and the behavioral effects were quantified by an open-field test. Intracerebroventricularly injection of CCK-8 decreased locomotion and rearing to the same extent in both vagotomized and sham-operated rats, while sc injection produced behavioral changes only in sham-operated rats but not in vagotomized ones. The results indicate that CCK-8 affects both central and peripheral receptors, and the vagal nerve may be the major pathway causing behavioral effects from the visceral organs to the brain.


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