scholarly journals Melatonin Pretreatment Protects Against Status Epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish

2021 ◽  
Author(s):  
Ana Caroline Salvador de Farias ◽  
Karolyne de Pieri Pickler ◽  
Henrique Teza Bernardo ◽  
Samira Leila Baldin ◽  
Eduardo Ronconi Dondossola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Kainic Acid ◽  
Neuronal Damage ◽  
Glutamate Uptake ◽  
Radical Scavenging ◽  
Antioxidant Enzyme Activities ◽  
Melatonin Treatment ◽  
Zebrafish Brain ◽  
And Oxidative Stress

Abstract Status epilepticus (SE) develops from abnormal electrical discharges, resulting in neuronal damage. Current treatments include antiepileptic drugs. However, the most common drugs used to treat seizures may sometimes be ineffective and have many side effects. Melatonin is an endogenous physiological hormone that is considered an alternative treatment for neurological disorders because of its free radical scavenging property. Thus, this study aimed to determine the effects of melatonin pretreatment on SE by inducing glutamatergic hyperstimulation in zebrafish. Seizures were induced in zebrafish using kainic acid (KA), a glutamate analog, and the seizure intensity was recorded for 60 min. Melatonin treatment for 7 days showed a decrease in seizure intensity (28%), latency to reach score 5 (14 min), and duration of SE (29%). In addition, melatonin treatment attenuated glutamate transporter levels, which significantly decreased in the zebrafish brain after 12 h of KA-induced seizures. Melatonin treatment reduced the increase in oxidative stress by reactive oxygen species formation through thiobarbituric acid reactive substances and 2‘,7‘-dichiorofluorescin, induced by KA-seizure. An imbalance of antioxidant enzyme activities such as superoxide dismutase and catalase was influenced by melatonin and KA-induced seizures. Our study indicates that melatonin promotes a neuroprotective response against the epileptic profile in zebrafish. These effects could be related to the modulation of glutamatergic neurotransmission, recovery of glutamate uptake, and oxidative stress parameters in the zebrafish brain.

scholarly journals Melatonin Pretreatment Protects Against Status epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish

2021 ◽  
Author(s):  
Ana Caroline Salvador de Farias ◽  
Karolyne de Pieri Pickler ◽  
Henrique Teza Bernardo ◽  
Samira Leila Baldin ◽  
Eduardo Ronconi Dondossola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Kainic Acid ◽  
Glutamate Transport ◽  
And Oxidative Stress

scholarly journals Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Computational Models ◽  
Neuronal Damage ◽  
Living Organism ◽  
The Body ◽  
Mitochondrial Functions ◽  
A Cell ◽  
The Brain ◽  
And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

scholarly journals 57 Carnosine prevents oxidative damage in myoblast cells derived from porcine skeletal muscle

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 59-59
Author(s):  
Marie-France Palin ◽  
Jérôme Lapointe ◽  
Claude Gariépy ◽  
Danièle Beaudry ◽  
Claudia Kalbe
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Metal Ion ◽  
Antioxidant Activities ◽  
Radical Scavenging ◽  
Biochemical Properties ◽  
Antioxidant Enzyme Activities ◽  
Antioxidant Genes ◽  
Mitochondrial Functions ◽  
Myoblast Cells

Abstract Carnosine (β-alanyl-L-histidine) is a molecule naturally and exclusively present in muscle food with the highest concentrations found in skeletal muscles and brain of the animal. Among its numerous biochemical properties, carnosine has antioxidant activity which include metal ion chelation and free radical scavenging. We have recently reported that high muscle carnosine content in pig is associated with better meat quality. Moreover, supplementing pigs with β-alanine reduced oxidative damage to Longissimus muscle (LM) lipids and proteins. Among previously reported antioxidant activities, carnosine was found to limit the production of reactive oxygen species (ROS) and increase antioxidant enzyme activities. However, these studies were mainly conducted in rodents and cell lines and mechanisms in play remain to be characterized. To determine the effect of carnosine in preventing oxidative damage and characterize the mechanisms in play, we have undertaken experiments using the progeny (myoblasts) of satellite cells isolated from the LM of newborn piglets. Cells were treated with carnosine (0, 10, 25 and 50 mM) for 48 h and were then either collected immediately or treated with H2O2 (0.3 mM, 1 h) to induce an oxidative stress. Our results showed that carnosine prevents oxidative stress through the reduction of total intracellular ROS and by modulating the antioxidant system in myoblasts.Carnosine increased the mRNA abundance of NEF2L2, a transcription factor activated by oxidative stress, and several of its downstream regulated antioxidant genes. Western blot analyses further suggest that the protective effect of carnosine on H2O2-induced oxidative stress is mediated through the p38 MAPK intracellular pathway. Finally, the addition of carnosine to H2O2-treated myoblasts increased the basal cellular oxygen consumption rate (OCR), the ATP-linked OCR and proton leaks, thus suggesting an effect of carnosine on mitochondrial functions. Taken together, these findings demonstrate the important role of carnosine in preventing oxidative damage in porcine muscle cells.

Antioxidant enzyme activities and oxidative stress in human breast cancer

1994 ◽  
Vol 120 (6) ◽  
pp. 374-377 ◽  
Author(s):  
K. Punnonen ◽  
M. Ahotupa ◽  
K. Asaishi ◽  
M. Hy�ty ◽  
R. Kudo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Human Breast Cancer ◽  
Antioxidant Enzyme Activities ◽  
Human Breast ◽  
And Oxidative Stress

scholarly journals Protective Role of UCP2 in Oxidative Stress and Apoptosis during the Silent Phase of an Experimental Model of Epilepsy Induced by Pilocarpine

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Marina Rascio Henriques Dutra ◽  
Regiane dos Santos Feliciano ◽  
Kalil Ribeiro Jacinto ◽  
Telma Luciana Furtado Gouveia ◽  
Eduardo Brigidio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Role ◽  
Negative Regulator ◽  
Antioxidant Enzyme Activities ◽  
Ucp2 Expression ◽  
Silent Phase ◽  
Ros Formation ◽  
Neuroprotective Actions ◽  
And Oxidative Stress

Neuroprotection is a desirable process in many neurological disorders, yet complex mechanisms involved in this field are not completely understood. The pilocarpine epilepsy model causes potent, seizure-induced excitotoxicity cell death and mitochondria impairment. The present study is aimed at investigating the role of UCP2, a ROS negative regulator, in the neuroprotection after cholinergic insult. Our data demonstrated that UCP2 expression was augmented in the rat hippocampus 3 days after status epilepticus (SE), reaching a peak on the fifth day, then returning to basal levels. Concomitantly, phospho-AKT expression levels were higher in the hippocampus during the early silent phase (5 days after SE). Additionally, it was demonstrated that the blockade of UCP2 by antisense oligonucleotides (ASO) in SE rats successfully diminished both UCP2 mRNA and protein contents. SE ASO rats presented increased mitochondrial proapoptotic factor expression, caspase-3 activity, inflammatory cytokine expression, and ROS formation. Moreover, ASO treatment diminished p-AKT expression and antioxidant enzyme activities after pilocarpine insult. In conclusion, the present results highlight the neuroprotective actions of UCP2, acting in the inhibition of apoptotic factors and oxidative stress, to increase neuron survival after SE onset.

Combined Low-Intensity Exercise and Ascorbic Acid Attenuates Kainic Acid-Induced Seizure and Oxidative Stress in Mice

2015 ◽  
Vol 41 (5) ◽  
pp. 1035-1041 ◽  
Author(s):  
Hee-jae Kim ◽  
Wook Song ◽  
Eun Hee Jin ◽  
Jongkyu Kim ◽  
Yoonseok Chun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Kainic Acid ◽  
Low Intensity ◽  
Low Intensity Exercise ◽  
And Oxidative Stress

Silibinin mitigates zidovudine-induced hepatocellular degenerative changes, oxidative stress and hyperlipidaemia in rats

2015 ◽  
Vol 34 (11) ◽  
pp. 1031-1042 ◽  
Author(s):  
R Raghu ◽  
B Jesudas ◽  
G Bhavani ◽  
D Ezhilarasan ◽  
S Karthikeyan
Keyword(s):  
Oxidative Stress ◽  
Liver Toxicity ◽  
Parenchymal Cell ◽  
Radical Scavenging ◽  
Simultaneous Treatment ◽  
Protein Thiols ◽  
Radical Scavenging Properties ◽  
Withdrawal Of Therapy ◽  
Inflammatory Changes ◽  
And Oxidative Stress

Prolonged zidovudine (AZT) treatment in HIV-infected and AIDS patients is shown to induce liver toxicity leading to complications. Therapeutic regimen that could encounter this adverse effect is unavailable and management of toxicity is often symptomatic or is limited to withdrawal of therapy. In the present investigation, we evaluated the alleviating properties of silibinin (SBN), a flavanolignan obtained from Silybum marianum against subacute AZT-induced hepatotoxicity and oxidative stress in rats. AZT treatment (50 mg/kg body weight (b.w.) periorally (p.o.), daily for 45 days) caused highly significant increases in alanine transaminase, alkaline phosphatase, argininosuccinic acid lyase and bilirubin in serum. Oxidative stress is shown by a highly significant increase in lipid peroxidase and total carbonyl content and decrease in catalase and protein thiols in the liver tissue. Hyperlipidaemia is indicated by highly significant increase in total lipids and free fatty acid in serum. Evaluation of liver by haematoxylin and eosin staining shows parenchymal cell enlargement, inflammatory changes and increase in sinusoidal spaces. Simultaneous treatment of SBN (100 mg/kg b.w. p.o., daily for 45 days) significantly protected the liver against hepatotoxicity, oxidative stress and hyperlipidaemia induced by AZT, and this alleviating property is attributed to hepatoprotective, membrane-stabilizing, antioxidant and free radical scavenging properties of SBN.

Gastrodia elata BL Mediates the Suppression of nNOS and Microglia Activation to Protect Against Neuronal Damage in Kainic Acid-Treated Rats

2005 ◽  
Vol 33 (04) ◽  
pp. 599-611 ◽  
Author(s):  
Ching-Liang Hsieh ◽  
Chi-Long Chen ◽  
Nou-Ying Tang ◽  
Chin-Min Chuang ◽  
Ching-Tou Hsieh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Kainic Acid ◽  
Neuronal Damage ◽  
Radical Scavenging ◽  
Microglia Activation ◽  
Physiological Mechanisms ◽  
Gastrodia Elata ◽  
The Right ◽  
Oxide Synthase

Our previous studies showed that Gastrodia elata (GE), an herb used in traditional Chinese medicine, has both anti-convulsive and free radical-scavenging activities in kainic acid (KA)-treated rats. The aim of the present study was to further investigate possible physiological mechanisms of GE against activities of neuronal nitric oxide synthase (nNOS) and microglia in KA-treated rats; 0.5 g/kg and 1.0 g/kg of GE extract were administered orally, whereas 20 mg/kg of N-nitro-L-arginine methyl ester (L-NAME) was administered intraperitoneally (ip), both at 30 minutes prior to KA (2 μg/2 μl) being injected into the right hippocampus region of rats. ED1-staining, apoptotic, inducible nitric oxide synthase (iNOS), and nNOS-staining cells were observed in the hippocampus region. The results indicated that 1.0 g/kg of GE and 20 mg/kg of L-NAME reduced the counts of ED1-stained cells, and 0.5 g/kg and 1.0 g/kg of GE, and 20 mg/kg of L-NAME reduced the numbers of apoptotic cells and nNOS-staining cells. In addition, 20 mg/kg of L-NAME also reduced the numbers of iNOS-staining cells, but 0.5 g/kg and 1.0 g/kg of GE did not. This study demonstrated that GE was able to reduce nNOS, microglia activation and apoptosis, suggesting that GE has a protective effect against neuronal damage in KA-treated rats.

Beneficial effect of melatonin treatment on inflammation, apoptosis and oxidative stress on pancreas of a senescence accelerated mice model

2011 ◽  
Vol 132 (11-12) ◽  
pp. 573-582 ◽  
Author(s):  
Sara Cuesta ◽  
Roman Kireev ◽  
Cruz García ◽  
Katherine Forman ◽  
Germaine Escames ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beneficial Effect ◽  
Mice Model ◽  
Melatonin Treatment ◽  
And Oxidative Stress ◽  
Senescence Accelerated Mice
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