scholarly journals Hyperlipidemia Diet Reduces Superoxide Dismutase Inhibition Rate in the Brain Organ of Rattus norvegicus

2022 ◽  
Vol 22 (1) ◽  
pp. 14-19
Author(s):  
Muhammad Luthfi Adnan ◽  
Miranti Dewi Pramaningtyas ◽  
Dini Islamiana ◽  
Hilmi Ardian Sudarto
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Defense Mechanism ◽  
Egg Yolk ◽  
Stress Effect ◽  
Inhibition Rate ◽  
Coturnix Coturnix ◽  
Male Wistar Rats ◽  
Ad Libitum ◽  
The Brain

Quail (Coturnix coturnix japonica L.) egg yolk is one of the high-fat foods which can trigger hyperlipidemia. The condition of hyperlipidemia can have an oxidative stress effect on the brain. Superoxide dismutase (SOD) is a natural antioxidant that acts as a defense mechanism against oxidative stress. The inhibition rate of SOD decreases when oxidative stress occurs. This study aims to determine the effect of quail egg yolk on the SOD inhibition rate of brain organs on a rat. This study used male Wistar rats aged 2-3 months with 200-300 grams of weight. The rats were divided into two groups. Each group was fed with ad libitum for two weeks. The A groups as control continued ad libitum consumption, and the B group was given additional quail egg yolk 5 ml / 200 g BW for 2 weeks. At the end of the study, the rats were terminated. The brain organs were examined for SOD inhibition rate with spectrophotometry. The mean SOD inhibition rate in the A and B groups was 74.14% ± 6.16 and 24.14% ± 5.65, respectively. The independent t-test showed significant differences in SOD inhibition rate between groups (p 0.001). Furthermore, quail egg yolk significantly reduced the SOD inhibition rate in the brain organ of the rat.

Cellular Cysteine Network and Neurodegeneration

2020 ◽  
pp. 303-325
Author(s):  
Shubhangi H. Pawar ◽  
Vishal S. Gulecha ◽  
Manoj S. Mahajan ◽  
Aman B Upaganiawar ◽  
Chandrashekhar D. Upasani
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanism ◽  
Free Radical Scavenger ◽  
Cellular Damage ◽  
Radical Scavenger ◽  
Post Translational Modifications ◽  
Cellular Defense ◽  
Brain Antioxidants ◽  
The Brain ◽  
Oxidative Species

Oxidative stress is strongly linked to neurodegeneration and oxidative species can modify many amino acids and proteins in the brain. Cysteine amino acid is most susceptible to oxidative post-translational modifications (PTMs). Reversible or irreversible cysteine PTMs can cause dyshomeostasis, which further continued to cellular damage. Many cysteine dependent proteins and many non-proteins using cysteine as their structural components are affected by oxidative stress. Several cysteine dependent enzymes are acting as antioxidants. Cysteine is a major contributor to glutathione (GSH) and superoxide dismutase (SOD) synthesis. Cysteine precursor N-acetylcysteine (NAC) supplementation is proven as a potent free radical scavenger and increase brain antioxidants and subsequently potentiates the natural antioxidant cellular defense mechanism. Thus, in this chapter, the authors explore the linkage of cellular cysteine networks and neurodegenerative disorders.

Anxiety-related behavior in hyperhomocysteinemia induced by methionine nutritional overload in rats: role of the brain oxidative stress

2016 ◽  
Vol 94 (10) ◽  
pp. 1074-1082 ◽  
Author(s):  
Dragan Hrncic ◽  
Jelena Mikić ◽  
Aleksandra Rasic-Markovic ◽  
Milica Velimirović ◽  
Tihomir Stojković ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Open Field ◽  
Wistar Rats ◽  
Brain Regions ◽  
Oxidative Status ◽  
Standard Diet ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
The Brain

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.

Differential oxidative stress and DNA damage in rat brain regions and blood following chronic arsenic exposure

2008 ◽  
Vol 24 (4) ◽  
pp. 247-256 ◽  
Author(s):  
D Mishra ◽  
SJS Flora
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Drinking Water ◽  
Wistar Rats ◽  
Arsenic Exposure ◽  
Brain Regions ◽  
Single Strand ◽  
Male Wistar Rats ◽  
Chronic Arsenic Exposure ◽  
The Brain

Chronic arsenic poisoning caused by contaminated drinking water is a wide spread and worldwide problem particularly in India and Bangladesh. One of the possible mechanisms suggested for arsenic toxicity is the generation of reactive oxygen species (ROS). The present study was planned 1) to evaluate if chronic exposure to arsenic leads to oxidative stress in blood and brain – parts of male Wistar rats and 2) to evaluate which brain region of the exposed animals was more sensitive to oxidative injury. Male Wistar rats were exposed to arsenic (50 ppm sodium arsenite in drinking water) for 10 months. The brain was dissected into five major parts, pons medulla, corpus striatum, cortex, hippocampus, and cerebellum. A number of biochemical variables indicative of oxidative stress were studied in blood and different brain regions. Single-strand DNA damage using comet assay was also assessed in lymphocytes. We observed a significant increase in blood and brain ROS levels accompanied by the depletion of GSH/GSSG ratio and glucose-6-phosphate dehydrogenase (G6PD) activity in different brain regions of arsenic-exposed rats. Chronic arsenic exposure also caused significant single-strand DNA damage in lymphocytes as depicted by comet with a tail in arsenic-exposed cells compared with the control cells. On the basis of results, we concluded that the cortex region of the brain was more sensitive to oxidative injury compared with the other regions studied. The present study, thus, leads us to suggest that arsenic induces differential oxidative stress in brain regions with cortex followed by hippocampus and causes single-strand DNA damage in lymphocytes.

scholarly journals Riboceine Regimen Attenuates Ethanol-induced Neuronal Damage in the Cerebellum of Adult Male Wistar Rats

2021 ◽  
Vol 15 (4) ◽  
pp. 249-256
Author(s):  
Taiwo Adekemi Abayomi ◽  
◽  
Olorunfemi Samuel Tokunbo ◽  
Moyinoluwa Ajayi ◽  
Olawale Ayobami Abayomi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Neuronal Damage ◽  
Motor Impairment ◽  
Stress Profile ◽  
Stress Markers ◽  
Ethanol Toxicity ◽  
Male Wistar Rats ◽  
Cerebellar Astrocytes ◽  
The Brain

Background: Although ethanol exerts its neurotoxic effect on the brain through inflammatory and oxidative processes, the effect of Riboceine on the brain following ethanol neurotoxicity is yet to be elucidated. Therefore, this study was designed to evaluate the effects of riboceine on the cellular, behavioral, and molecular impairments induced by ethanol toxicity in rats. Methods: A total of 24 male Wistar rats weighing between 160-170 grams were used for the study, and were divided into four groups of six rats each. After completion of the administration of ethanol and riboceine, and testing for motor impairment, the rats were sacrificed. The cerebellum was excised and processed for oxidative stress analyses, based on oxidative stress markers and histological examinations. The immunohistochemical expression of astrocytes in the cerebellum was examined, using Glial Fibrillary Acidic Protein (GFAP) stain. Results: This study demonstrated that ethanol-induced neurotoxicity in the cerebellum, characterized by increased oxidative stress profile, astrocyte activation, and neuronal death in the cerebellum, especially the Purkinje layer. Necrosis, significant decrease in Superoxide Dismutase (SOD), Catalase (CAT) and Gluathione (GSH) activities (P<0.05) as well as astrogliosis was associated with ethanol treatment. However, riboceine was observed to significantly increase the cerebellar SOD, CAT and GSH activities with significantly reduced Malondialdehyde (MDA) levels (P<0.05). It also attenuated the histomorphological alteration of the cerebellum and reduced the cerebellar astrocytes activation following ethanol-induced neurotoxicity, thus leading to the attenuation of motor impairment. Conclusion: Riboceine attenuated motor impairment caused by chronic ethanol-induced neurotoxicity, suggestive of its anti-oxidative and anti-inflammatory properties.

scholarly journals Effect of Nandrolone Treatment with And Without Resistance Training on Superoxide Dismutase Concentration and Pathology of Kidney Tissue in Rats

2020 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Esfandiyar Heidari ◽  
Seyed Ali Hosseini ◽  
Mohammad Ali Azarbayjani
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Resistance Training ◽  
Anabolic Steroids ◽  
Kidney Tissue ◽  
Sod Activity ◽  
Significant Difference ◽  
Stress Levels ◽  
Sh Group ◽  
Male Wistar Rats

Background: The prevalence of anabolic steroids abuse in athletes and non-athletes is associated with the risk of injury to various organs, but there are limited studies of oxidative changes in kidney tissue following nandrolone (N) administration. Objectives: the aim of this study was to investigate the effect of N treatment with and without resistance training (RT) on superoxide dismutase (SOD) concentration and tissue pathology of kidney tissue in rats. Methods: In this experimental study, 20 male Wistar rats were randomly divided into four groups of five rats including 1) control (C), 2) sham (normal saline) (Sh), 3) N, and 4) N + RT. Groups 3 and 4 received 10 mg/kg N peritoneally, and the N + RT group performed 1 m ladder climbing for eight weeks and three sessions per week. SOD levels of kidney tissue were measured by ELISA and radioimmunoassay. Hematoxylin-eosin (H&E) staining was used to evaluate oxidative stress levels in kidney tissue. One-way ANOVA with Bonferroni’s post- hoc tests were used for analysis of research findings in SPSS version 22 (P ≤ 0.05). Results: SOD levels in the C group were higher than the Sh (P = 0.001), N (P = 0.001), and N + RT (P = 0.001) groups. SOD levels were lower in the Sh group than in the N (P = 0.049) and N + RT (P = 0.001) groups. However, there was no significant difference in SOD levels in the N + RT group and N group (P = 0.28). Also, oxidative stress levels were normal in tissue studies in all groups. Conclusions: It seems that Ntreatment with and without RT reduces SOD activity in kidney tissue, but more studies are needed in this regard given the normality of tissue oxidative stress results.

scholarly journals Reversal effect of Solanum dasyphyllum against rotenone-induced neurotoxicity

2020 ◽  
Vol 33 (4) ◽  
pp. 191-196
Author(s):  
Omotayo B. Ilesanmi ◽  
Obade Efe ◽  
Temitope T. Odewale ◽  
Frances O. Atanu ◽  
Esther F. Adeogun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
In Vivo Model ◽  
Respiratory Enzymes ◽  
Reversal Effect ◽  
Male Wistar Rats ◽  
Markers Of Oxidative Stress ◽  
The Brain ◽  
Rotenone Exposure

Abstract We earlier reported the protective effect of Solanum dasyphyllum against cyanide neurotoxicity. In furtherance to this, we investigated the protective effect of S. dasyphyllum against rotenone, a chemical toxin that causes brain-related diseases. Mitochondria fraction obtained from the brain of male Wistar rats was incubated with various solvents (hexane, dichloromethane, ethylacetate, and methanol) extracts of S. dasyphyllum before rotenone exposure. Mitochondria respiratory enzymes (MRE) were evaluated along with markers of oxidative stress. The inhibition of MRE by rotenone was reversed by treatment with various fractions of S. dasyphyllum. The oxidative stress induced by rotenone was also reversed by fractions of S. dasyphyllum. In addition, the ethylacetate fraction of S. dasyphyllum was most potent against rotenone-induced neurotoxicity. In conclusion, S. dasyphyllum is rich in active phytochemicals that can prevent some neurotoxic effects of rotenone exposure. Further study can be done in an in vivo model to substantiate our results.

scholarly journals Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

Molecules ◽  
2020 ◽  
Vol 25 (8) ◽  
pp. 1807 ◽  
Author(s):  
Juste Baranauskaite ◽  
Ilona Sadauskiene ◽  
Arunas Liekis ◽  
Arturas Kasauskas ◽  
Robertas Lazauskas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Phenolic Compounds ◽  
Rosmarinic Acid ◽  
Sod Activity ◽  
Mice Brain ◽  
Aluminum Accumulation ◽  
Liver Homogenates ◽  
The Brain

Aluminum accumulation, glutathione (GSH) and malondialdehyde (MDA) concentrations as well as catalase (CAT) and superoxide dismutase (SOD) activities were determined in erythrocytes and brain and liver homogenates of BALB/c mice treated with Al3+ (7.5 mg/kg/day (0.15 LD50) as AlCl3 (37.08 mg/kg/day), whereas HCl (30.41 mg/kg/day) was used as Cl− control, the treatments were performed for 21 days, i.p., in the presence and absence of rosmarinic acid (0.2805 mg/kg/day (0.05 LD50), 21 days, i.g.) or carvacrol (0.0405 mg/kg/day (0.05 LD50), 21 days, i.g.). The treatment with AlCl3 increased GSH concentration in erythrocytes only slightly and had no effect on brain and liver homogenates. Rosmarinic acid and carvacrol strongly increased GSH concentration in erythrocytes but decreased it in brain and liver homogenates. However, AlCl3 treatment led to Al accumulation in mice blood, brain, and liver and induced oxidative stress, assessed based on MDA concentration in the brain and liver. Both rosmarinic acid and carvacrol were able to counteract the negative Al effect by decreasing its accumulation and protecting tissues from lipid peroxidation. AlCl3 treatment increased CAT activity in mice brain and liver homogenates, whereas the administration of either rosmarinic acid or carvacrol alone or in combination with AlCl3 had no significant effect on CAT activity. SOD activity remained unchanged after all the treatments in our study. We propose that natural herbal phenolic compounds rosmarinic acid and carvacrol could be used to protect brain and liver against aluminum induced oxidative stress leading to lipid peroxidation.

Role of Catalase and Superoxide Dismutase Activities on Oxidative Stress in the Brain of a Phenylketonuria Animal Model and the Effect of Lipoic Acid

2012 ◽  
Vol 33 (2) ◽  
pp. 253-260 ◽  
Author(s):  
Tarsila Barros Moraes ◽  
Carlos Eduardo Diaz Jacques ◽  
Andrea Pereira Rosa ◽  
Giovana Reche Dalazen ◽  
Melaine Terra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Superoxide Dismutase ◽  
Lipoic Acid ◽  
The Brain

Atorvastatin inhibits brain oxidative stress of Streptozotocininduced diabetic rat

2013 ◽  
Vol 1 (1) ◽  
pp. 35
Author(s):  
Mohammad Taghi Mohammadi ◽  
Mojtaba Gaedniaye Jahromi ◽  
Mohammad Hossein Mirjalili ◽  
Mehdi Ramezani Binabaj ◽  
Mahvash Jafari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Atorvastatin Treatment ◽  
Increase Blood Glucose ◽  
Increase Blood Glucose Level ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
The Brain

It is well known that production of ROS compounds and generation of oxidative stress during diabetes are the most important mechanisms of tissue damage. The aim of this study was to examine the effects of atorvastatin treatment, as an antioxidant, to prevent the brain tissue oxidative stress in streptozotocin-induced diabetic rats. Male Wistar rats were randomly divided into four groups (five rats in each group) as followed: normal, normal treated was orally received 20 mg/kg/day atorvastatin for 30 days, diabetic group was given 40 mg/kg streptozotocin by intravenous injection and diabetic treated similar to normal treated rats. After 30 days of treatment, rats were sacrificed under deep anesthesia to remove the brain. After tissue homogenization, superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) and malondialdehyde (MDA) levels were determined by biochemical methods. In addition to increase blood glucose level in diabetic rats (78%), brain SOD and CAT activities were significantly increased compared with normal rats. Also, diabetes significantly decreased the GSH content of brain tissue by 57%, and increased the brain MDA level by 35%. Finally treatment with atorvastatin significantly decreased the augmented brain CAT activity and the MDA level during diabetes. Based on the finding of this study, diabetes-induced hyperglycemia provoked the production of free radicals in the brain tissue that leading to oxidative stress. Also, treatment with atorvastatin may have prevented from hyperglycemia-induced oxidative stress in the brain of diabetic rat.

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