Ganglioside GT1B and melatonin inhibit brain mitochondrial DNA damage and seizures induced by kainic acid in mice

Yamamoto, Hiroaki; Mohanan, P.V.

doi:10.1016/s0006-8993(02)04083-0

Cited by 51 publications

(39 citation statements)

References 43 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: 99%

“…At the cellular level, a large Ca 2+ influx via VGCCs and NMDA-dependent calcium channels results in huge seizure activities (Nazıroğlu, 2009;Vimala et al, 2014). Following melatonin treatment in epilepsy, decrease in intracellular Ca 2+ concentration through inhibition of VGCCs, TRP channels, and NMDA receptors promotes biochemical antioxidant cascades, resulting in decreased neuronal cell death (Yamamoto and Mohanan, 2003;. This latter aspect will be the focus of the remaining sections of this review.…”

Section: +mentioning

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: 99%

Section: +mentioning

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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“…After E16, the concentration of GD3 and GM3 markedly decreased, and the concentration of a-series gangliosides, including GD1a, increased (Ngamukote et al, 2007). Yamamoto and Mohanan (2003) reported that ganglioside GT1b inhibits mitochondrial DNA damage in the brain during embryonic development. GD3-expressing cells sorted from embryonic, postnatal, and adult mouse brains were shown to have high proliferative potential, the ability to self-renew, marker expression, and multipotency for differentiation into neurons, astrocytes, or oligodendrocytes.…”

Section: Gangliosides In Mouse Embryonic Developmentmentioning

confidence: 99%

Roles of gangliosides in mouse embryogenesis and embryonic stem cell differentiation

et al. 2011

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Gangliosides have been suggested to play important roles in various functions such as adhesion, cell differentiation, growth control, and signaling. Mouse follicular development, ovulation, and luteinization during the estrous cycle are regulated by several hormones and cell-cell interactions. In addition, spermatogenesis in seminiferous tubules of adult testes is also regulated by several hormones, including follicle-stimulating hormone (FSH) and luteinizing hormone (LH) and cell-cell interactions. The regulation of these processes by hormones and cell-cell interactions provides evidence for the importance of surface membrane components, including gangliosides. During preimplantation embryo development, a mammalian embryo undergoes a series of cleavage divisions whereby a zygote is converted into a blastocyst that is sufficiently competent to be implanted in the maternal uterus and continue its development. Mouse embryonic stem (mES) cells are pluripotent cells derived from mouse embryo, specifically, from the inner cell mass of blastocysts. Differentiated neuronal cells are derived from mES cells through the formation of embryonic bodies (EBs). EBs recapitulate many aspects of lineage-specific differentiation and temporal and spatial gene expression patterns during early embryogenesis. Previous studies on ganglioside expression during mouse embryonic development (including during in vitro fertilization, ovulation, spermatogenesis, and embryogenesis) reported that gangliosides were expressed in both undifferentiated and differentiated (or differentiating) mES cells. In this review, we summarize some of the advances in our understanding of the functional roles of gangliosides during the stages of mouse embryonic development, including ovulation, spermatogenesis, and embryogenesis, focusing on undifferentiated and differentiated mES cells (neuronal cells).

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“…35 Their mode of action varies in different cell types, including altering the activity of several enzymes and specific proteins, [36][37][38][39][40] membrane stabilisation and fluidity, 34,35 scavenging hydroxyl radicals. 41 Even if there were a consensus on the protective effects of gangliosides against cellular damage, the mechanism(s) underlying these effects and the models in which gangliosides are protective would still require precise evaluation. If oxidative stress and apoptosis are chemically induced in cultures of hepatocytes and rat liver epithelial cells, Figure 1 Structure of the monoganglioside GM1 and the trisialoganglioside GT1b.…”

Section: Introductionmentioning

confidence: 99%

“…35 In vivo, GT1b prevents chemically induced DNA damage in mice. 41 There is evidence that the antioxidative properties of GM1 are dependent on its effect on iron ion exchange 35,42 because iron ions are involved in ROS and LPO product formation in many cell types.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of exogenous gangliosides on ROS-induced changes in human spermatozoa

Gavella¹,

Lipovac²

2013

Asian J Androl

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This article summarizes the available evidence on the efficacy of gangliosides to reduce the degree of reactive oxygen species (ROS)-mediated damage. The antioxidative efficacy of exogenous gangliosides in protecting different cells encouraged us to examine their ability to protect human spermatozoa. Gangliosides are sialic acid-containing glycosphingolipids with strong amphiphilic character due to the bulky headgroup made of several sugar rings with sialic acid residues and the double-tailed hydrophobic lipid moiety. The amphiphilicity of gangliosides allows them to exist as micelles in aqueous media when they are present at a concentration above their critical micellar concentration. The protective effect of ganglioside micelles on spermatozoa is believed to stem from their ability to scavenge free radicals and prevent their damaging effects. In our study, we particularly focused our attention on the protective effect of ganglioside micelles on DNA in human spermatozoa exposed to cryopreservation. The results indicate that ganglioside micelles can modulate the hydrophobic properties of the sperm membrane to increase tolerance to DNA fragmentation, thus protecting the DNA from cryopreservation-induced damage. Further actions of ganglioside micelles, which were documented by biochemical and biophysical studies, included (i) the modulation of superoxide anion generation by increasing the diffusion barrier for membrane events responsible for signal translocation to the interior of the cell; (ii) the inhibition of iron-catalysed hydroxyl radical formation due to the iron chelation potential of gangliosides; and (iii) inhibition of hydrogen peroxide diffusion across the sperm membrane.

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Ganglioside GT1B and melatonin inhibit brain mitochondrial DNA damage and seizures induced by kainic acid in mice

Cited by 51 publications

References 43 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

Roles of gangliosides in mouse embryogenesis and embryonic stem cell differentiation

Protective effects of exogenous gangliosides on ROS-induced changes in human spermatozoa

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