Preventive effect of melatonin against brain mitochondria DNA damage, lipid peroxidation and seizures induced by kainic acid

Mohanan, P.V.; Yamamoto, Hiroaki

doi:10.1016/s0378-4274(01)00475-1

Cited by 70 publications

(53 citation statements)

References 26 publications

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“…It was reported that acute latency for onset of the first seizure, lipid peroxidation in the hippocampus, and mitochondrial Mn SOD were decreased in rats with KAinduced status epilepticus by long periods (10 mg/kg per day for 14 days) of melatonin treatment but the melatonin treatment did not prevent the development of a chronic epileptic state in the rats . High dosage, but for a short period (20 mg/kg for single dose), of melatonin treatment decreased the seizures and attenuated lipid peroxidation in the brain cortex and mitochondrial DNA injury in KA-induced epileptic mice (Mohanan and Yamamoto, 2002;Yamamoto and Mohanan, 2003). Anxiogenic activity of diazinon and the level of brain lipid peroxidation were decreased in rats by oral melatonin (10 mg/kg) treatment, although GSH-Px activity was increased by the treatment (Ahmed et al, 2013).…”

Section: Methodsmentioning

confidence: 96%

“…Value and effect Reference Rats Cytosolic SOD/CuZn and mitochondrial SOD Mn increased but seizures and lipid peroxidation levels decreased in KA-induced epileptic rats Atanasova et al (2013) Mice Antioxidant role of agomelatine and melatonin through modulation of GABAergic systems and MT2 receptor in brain of pilocarpine and strychnine-induced epileptic mice Aguiar et al (2013) Mice Seizures, brain cortex lipid peroxidation, and mitochondrial DNA injury in KA-induced epileptic mice were decreased by melatonin treatment Mohanan and Yamamoto (2002) Rats Epileptic seizures were not decreased in PTZ-and KA-induced epileptic rats by the melatonin treatment Xu and Stringer (2008) Rats Latency development and nitroxyl radical level did not decrease in rats with flurothyl-induced seizure by melatonin treatment, although lipid peroxidation level was decreased in the rats Mareš et al (2013) Children (1-16 years old) Occurrences of epileptiform discharges were decreased in the children by melatonin treatment Gustafsson et al (2014) PTZ, pentylentetrazol. SOD, superoxide dismutase.…”

Section: Methodsmentioning

confidence: 99%

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Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

Nazıroğlu¹

2015

Turk J Biol

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Calcium ion (Ca 2+ ) accumulation and excessive oxidative stress in the hippocampus and brain cortex have long been known as major contributors to the etiology of epilepsy. I have reviewed the role of Ca 2+ signaling through cation channels and mitochondriamediated oxidative stress on epilepsy in human and animals. A review of the relevant papers and results from recent studies were obtained from PubMed and the Science Citation Index. Current literature findings indicate that melatonin and agomelatine reduce activation of hippocampal transient receptor potential (TRP), glutamate receptors, and voltage-gated calcium channels that are critical for the development of abnormal Ca 2+ homeostasis and oxidative stress and associated mitochondrial dysfunction. In addition, low doses of melatonin induce anticonvulsant action through increase of GABA levels in the hippocampus and brain cortex. The accumulating evidence implicates a modulator role of melatonin on excessive oxidative stress products, plus mitochondrial and Ca 2+ dysregulations in epilepsy. The evidence indicates that modulation of oxidative stress and neuronal Ca 2+ handling occurs through effects on TRP channels, suggesting an increasingly viable approach for therapeutic interventions against epilepsy.

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Section: Methodsmentioning

confidence: 96%

Section: Methodsmentioning

confidence: 99%

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

Nazıroğlu¹

2015

Turk J Biol

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“…This observation contradicts results of some other studies were no protective effect of vitamin E on epileptic attacks created by PTZ and other chemical convulsants was found [24,25]. These contradictions are probably related to the fact that antioxidants manifest dissimilar anticonvulsant effects depending on the type of the convulsant or subeffective doses.…”

Section: Discussionmentioning

confidence: 56%

Effect of Vitamin E on Blood-Brain Barrier Permeability in Aged Rats with PTZ-Induced Convulsions

2011

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The effect of vitamin E on the blood-brain barrier (BBB) permeability was studied under conditions of pentylenetetrazole (PTZ)-induced convulsions in aged (23-to 24-month-old) male albino rats; Evans Blue was used as a tracer. The BBB permeability was found to considerably increase in rats with PTZ-evoked seizures; the Evans Blue contents in the left and right hemispheres and cerebellum + brainstem region were significantly higher than those in the control. Vitamin E used in the dose of 70 mg/kg exerted practically no beneficial effect on the increased BBB permeability in rats with seizures, while a greater dose of vitamin E (700 mg/kg) exerted a significant protective effect, especially with respect to the cerebellum + brainstem regions (P < 0.01). The seizure-related rise in the arterial blood pressure was also smaller in the latter experimental group. Thus, our observations confirm the importance of the dose of vitamin E as a protective factor for the BBB permeability and demonstrate that the dose dependence of this antioxidant in aged animals differs from that in younger organisms.

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“…Briefly, single cell suspension of splenic lymphocytes was divided in to several groups; each group contained 1 ml of the splenic lymphocytes single cell suspension in triplicate. The concentration of kainic acid and melatonin were fixed according to the authors earlier studies [20][21][22][23][24][25][26][27][28][29][30][31][32][33]. First group I was kept as normal control 9 without any treatment); group II was treated with 1 mM of kainic acid alone (KA); group III was treated with 1 mM melatonin alone (MLT); group IV was treated with KA (1 mM)+MLT (0.25 mM) in combination; groups V was treated with KA (1 mM)+MLT (0.5 mM) in combination, groups VI was treated with KA (1 mM)+MLT (1 mM) in combination.…”

Section: Experimental Designmentioning

confidence: 99%

“…First group I was kept as normal control 9 without any treatment); group II was treated with 1 mM of kainic acid alone (KA); group III was treated with 1 mM melatonin alone (MLT); group IV was treated with KA (1 mM)+MLT (0.25 mM) in combination; groups V was treated with KA (1 mM)+MLT (0.5 mM) in combination, groups VI was treated with KA (1 mM)+MLT (1 mM) in combination. In all the combination groups of KA and MLT, MLT was added simultaneously together with the KA [20][21][22][23][24][25][26][27][28][29][30][31][32][33].…”

Section: Experimental Designmentioning

confidence: 99%

Protective Mechanism of Melatonin on Kainic Acid Induced Immune Modulatory Effect on Lymphocytes Derived from Mouse Spleen

Gayathri¹

2013

J Clin Cell Immunol

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Toxicity occurs when cells develop inflammation due to exposure to several toxic substances. The study was aimed to assess the damage (toxicity) induced by kainic acid on splenic lymphocyte and enriched T lymphocyte under in vitro conditions and the protective role of exogenous melatonin against this damage (toxicity). The study included assessment of inflammatory mechanism by the expression of immune modulatory cytokine mediators using real time PCR. Oxidative stress (reactive oxygen species) and nitrosative stress (reactive nitrogen species) were also studied to determine the free radical production. Interestingly, kainic acid caused severe splenic lymphocytes and enriched T lymphocyte damage which was evident from deleterious alterations in various parameters. Kainic acid treatment (1 mM) resulted in increased mRNA expression of cytokines like tumour necrosis factor-beta, interleukin 6, interleukin 1, interferon gamma, mitogen-activated protein kinase gene-14, inducible nitric oxide synthase and decreased interleukin 10 mRNA expression. Tritiated ( 3 H) Thymidine Incorporation study signifies that kainic acid treatment (1 mM) increased the proliferation of splenic and enriched T lymphocytes. These changes were normalized by exogenous administration of melatonin (0.25-1.0 mM) in combination with kainic acid. Flow Cytometry Analysis using Annexin V apoptosis assay kit revealed an increase in apoptotic and necrosis (double positive cells) in splenic lymphocytes treated with kainic acid alone. However, melatonin treated in combination with kainic acid, showed attenuation to apoptosis and necrosis on splenic lymphocytes. This study depicts that kainic acid induced inflammatory toxicity could be attenuated by exogenous melatonin treatment as evident by the decreased levels of the inflammatory cytokines, immune reactions and free radical production.

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Preventive effect of melatonin against brain mitochondria DNA damage, lipid peroxidation and seizures induced by kainic acid

Cited by 70 publications

References 26 publications

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

Effect of Vitamin E on Blood-Brain Barrier Permeability in Aged Rats with PTZ-Induced Convulsions

Protective Mechanism of Melatonin on Kainic Acid Induced Immune Modulatory Effect on Lymphocytes Derived from Mouse Spleen

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