Excitotoxicity and Oxidative Stress in Acute Ischemic Stroke

Bretón, Ramón Rama

doi:10.5772/28300

Cited by 11 publications

(11 citation statements)

References 171 publications

(326 reference statements)

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“…57,58 During reperfusion phase of stroke, the excessive amount of O 2 is delivered to the ischemic neurons to maintain their viability, this impairs mitochondrial respiratory chain via elevation of O 2 to supra-physiologic levels. 59 Besides, a deficit in brain antioxidant enzymes could result in macromolecular damages and apoptotic cell death. 5,60,61 Fanaei et al demonstrated that TES attenuated oxidative stress in mice model of MCAO.…”

Section: Neuroprotective Mechanisms Of Testosteronementioning

confidence: 99%

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Testosterone May Hold Therapeutic Promise for the Treatment ofIschemic Stroke in Aging: A Closer Look at Laboratory Findings

et al. 2019

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Male sex is more prone to cerebrovascular disorders, yet the exact role of androgens in cerebralischemia remains unclear. Here we reviewed current understanding of testosterone (TES)neuroprotective activity against ischemic stroke and mechanisms underlying these effects inaging. TES may exert a neuroprotective effect in aging through pathways including inhibition ofoxidant molecules production, enhancing the enzymatic antioxidant capacity of the brain andmodulation of apoptotic cell death. Given this, a better understanding of the neuroprotectiveroles of TES may propose an effective therapeutic strategy to improve the quality of life anddecrease androgen-related cerebrovascular problems in the aging men.

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Section: Neuroprotective Mechanisms Of Testosteronementioning

confidence: 99%

“…63 Penumbra or periinfarct zone comprises nearly half of the total lesion volume during the initial stages of stroke which represent that the area may be recovered by early re-occlusion. 59…”

Section: Neuroprotective Mechanisms Of Testosteronementioning

confidence: 99%

Testosterone May Hold Therapeutic Promise for the Treatment ofIschemic Stroke in Aging: A Closer Look at Laboratory Findings

et al. 2019

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“…In summary, numerous studies report the important involvement of excitotoxicity and oxidative stress in the complex processes that cause neuronal death in acute ischemic stroke [139]. The hypoxia and the low glucose levels caused by the blood flow reduction in the penumbra zone lead to oxidative stress and excessive release of glutamate.…”

Section: Apoptosismentioning

confidence: 99%

Excitotoxicity and Oxidative Stress in Acute Stroke

Rama¹,

García²

2016

Ischemic Stroke - Updates

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Excitotoxicity, defined as cell death resulting from the toxic actions of excitatory amino acids, is actually considered as a major factor contributing to the early stage of ischemic cell death in stroke. In stroke, once vessel occlusion is produced, the disruptions to the blood flow in the affected areas decrease the delivery of oxygen and metabolic substrates to neurons. Consequently, the lack of oxygen interrupts oxidative phosphorylation by the mitochondria and drastically reduces cellular ATP production, which results in a rapid decline in cellular ATP. After several minutes, inhibition of the Na + /K +-ATPase function causes a profound loss of ionic gradients and depolarization of regulated neurons, which leads to excessive release of excitatory amino acids-particularly glutamate-to the extracellular compartment. The presence of excessive amounts of glutamate into the synapses and extrasynaptic sites can lead eventually to neuronal death. Excitotoxicity leads to a number of deleterious consequences, including impairment of cellular calcium homeostasis, generation of free radicals and oxidative stress, mitochondrial damage, and activation of several transcription factors and their genes expression. All these mechanisms' acting synergy can cause neuron death by apoptosis. Oxidative stress induced by excitotoxicity is considered to be the main event leading to brain damage after stroke. On the basis of experimental models, there is ample evidence of the role of oxidative stress in ischemic brain damage.

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“…Both channels play critical roles in Ca 2+ and Mg 2+ homeostasis (Fliniaux et al, 2017;Sun, 2017;Cook et al, 2009;Komiya et al, regulation of cellular processes ranging from neurotransmission to cell stress responses (Romani, 2007;Rama and García, 2016;Nazıroğlu, 2011a;Abiria et al, 2017;Sun, 2017). Homeostatic disruptions of either cation is associated with numerous human disorders (Zündorf and Reiser, 2011;De Baaij et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

“…

and TRPM2 are non-specific cation channels of the Transient Receptor Potential channel superfamily. Each channel has gained attention for their potential to mediate oxidative and anoxic cell death (Rama and García, 2016;Nazıroğlu, 2011a;Abiria et al, 2017;Sun, 2017), however their physiological expression and roles in the developing brain remain poorly defined. We employed real-time reverse transcription PCR to examine mRNA expression of TRPM7 and TRPM2 in the developing rat brain and brain-specific cell types.

…”

mentioning

confidence: 99%

mRNA expression of transient receptor potential melastatin (TRPM) channels 2 and 7 in perinatal brain development

Ratnam¹,

Chan

Lesani³

et al. 2018

Intl J of Devlp Neuroscience

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TRPM7 and TRPM2 are non-specific cation channels of the Transient Receptor Potential channel superfamily. Each channel has gained attention for their potential to mediate oxidative and anoxic cell death (Rama and García, 2016; Nazıroğlu, 2011a; Abiria et al., 2017; Sun, 2017), however their physiological expression and roles in the developing brain remain poorly defined. We employed real-time reverse transcription PCR to examine mRNA expression of TRPM7 and TRPM2 in the developing rat brain and brain-specific cell types. We determined the temporal and spatial expression patterns at four developmental time points (postnatal day 7, 14, 21, and 90) in four critical regions of the brain (cortex, hippocampus, striatum, and cerebellum) and examined gene expression in neuronal, astrocytic, and microglial primary cell cultures. Our results revealed that TRPM7 mRNA expression peaks in the cortex at 2-weeks after birth, and thus correlates most closely with a period of rat brain development associated with neurite outgrowth, which is heightened at 2-weeks after birth. Our cell-specific gene expression assays revealed that TRPM7 was expressed at equivalent levels in neurons, astrocytes, and microglia. Conversely, TRPM2 was most highly expressed in microglia with little expression in neurons and astrocytes. In the hippocampus and striatum, the expression profile of TRPM2 parallels the perinatal expression timeline for microglial infiltration and maturation in the rat brain. Microglial maturation is highest from the time of birth, up to 7-days, but subsequently declines. The latter developmental expression profiles indicate a role for TRPM2 in microglial activation.

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Excitotoxicity and Oxidative Stress in Acute Ischemic Stroke

Cited by 11 publications

References 171 publications

Testosterone May Hold Therapeutic Promise for the Treatment ofIschemic Stroke in Aging: A Closer Look at Laboratory Findings

Testosterone May Hold Therapeutic Promise for the Treatment ofIschemic Stroke in Aging: A Closer Look at Laboratory Findings

Excitotoxicity and Oxidative Stress in Acute Stroke

mRNA expression of transient receptor potential melastatin (TRPM) channels 2 and 7 in perinatal brain development

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