Protective effect of glutathione on kainic acid-induced neuropathological changes in the rat brain

Saija, Antonella; Princi, Pietro; Pisani, Antonina; Lanza, Marcos R. V.; Scalese, M.; Aramnejad, E.; Ceserani, R.; Costa, Giovanni

doi:10.1016/0306-3623(94)90016-7

Cited by 34 publications

(8 citation statements)

References 29 publications

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“…KA-induced neurotoxicity is linked with an imbalance of neuronal GSH, and melatonin administration is capable of restoring tissue GSH homeostasis. Treatment with GSH may also protect against KA-dependent neuropathological changes in rat brain, 55 suggesting the value of pharmacological strategies directed toward the regulation of endogenous melatonin levels. Melatonin has the capability of entering cells because of its high lipophilicity and it readily crosses all morphophysiological barriers.…”

Section: Discussionmentioning

confidence: 99%

Excitotoxicity, Oxidative Stress, and the Neuroprotective Potential of Melatonin

Skaper

Floreani

Ceccon

et al. 1999

Annals of the New York Academy of Sciences

120

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The brain consumes large quantities of oxygen relative to its contribution to total body mass. This, together with its paucity of oxidative defense mechanisms, places this organ at risk for damage mediated by reactive oxygen species. The pineal secretory product melatonin possesses broad-spectrum free radical scavenging and antioxidant activities, and prevents kainic acid-induced neuronal lesions, glutathione depletion, and reactive oxygen species-mediated apoptotic nerve cell death. Melatonin's action is thought to involve electron donation to directly detoxify free radicals such as the highly toxic hydroxyl radical, which is a probable end-product of the reaction between NO. and peroxynitrite. Moreover, melatonin limits NO.-induced lipid peroxidation, inhibits cerebellar NO. synthase, scavenges peroxynitrite, and alters the activities of enzymes that improve the total antioxidative defense capacity of the organism. Melatonin function as a free radical scavenger and antioxidant is likely facilitated by the ease with which it crosses morphophysiological barriers, e.g., the blood-brain barrier, and enters cells and subcellular compartments. Pinealectomy, which eliminates the nighttime rise in circulating and tissue melatonin levels, worsens both reactive oxygen species-mediated tissue damage and brain damage after focal cerebral ischemia and excitotoxic seizures. That melatonin protects against hippocampal neurodegeneration linked to excitatory synaptic transmission is fully consistent with the last study. Conceivably, the decreased melatonin secretion that is documented to accompany the aging process may be exaggerated in populations with dementia.

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Section: Discussionmentioning

confidence: 99%

Excitotoxicity, Oxidative Stress, and the Neuroprotective Potential of Melatonin

Skaper

Floreani

Ceccon

et al. 1999

Annals of the New York Academy of Sciences

120

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“…In addition to the increase in lipid peroxidation, systemic administration of KA also caused a decrease in reduced form of glutathione (GSH) levels in the hippocampus (Shin et al, 2008b). Intravenous GSH administration protected against KA-induced neuronal loss in the hippocampus and subsequent development of edema (Saija et al, 1994). Melatonin also prevented the neurotoxic effects of ROS generated by KA receptor activation through an increase in intracellular GSH (Floreani et al, 1997).…”

Section: Seizure-induced Oxidative Damagementioning

confidence: 99%

Role of oxidative stress in epileptic seizures

Shin

Jeong

Chung

et al. 2011

Neurochemistry International

360

218

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Oxidative stress resulting from excessive free-radical release is likely implicated in the initiation and progression of epilepsy. Therefore, antioxidant therapies aimed at reducing oxidative stress have received considerable attention in epilepsy treatment. However, much evidence suggests that oxidative stress does not always have the same pattern in all seizures models. Thus, this review provides an overview aimed at achieving a better understanding of this issue. We summarize work regarding seizure models (i.e., genetically epilepsy-prone rats, kainic acid, pilocarpine, pentylenetetrazol, and trimethyltin), oxidative stress as an etiologic factor in epileptic seizures (i.e., impairment of antioxidant systems, mitochondrial dysfunction, involvement of redox-active metals, arachidonic acid pathway activation, and aging), and antioxidant strategies for seizure treatment. Combined, this review highlights pharmacological mechanisms associated with oxidative stress in epileptic seizures and the potential for neuroprotection in epilepsy that targets oxidative stress and is supported by effective antioxidant treatment.

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“…An intravenous administration of GSH protects the KA‐induced neuronal loss in hippocampus and subsequent development of edema (Saija et al . 1994).…”

Section: Discussionmentioning

confidence: 99%

Effects of glutathione depletion by 2‐cyclohexen‐1‐one on excitatory amino acids‐induced enhancement of activator protein‐1 DNA binding in murine hippocampus

Ogita

Kitayama

Okuda

et al. 2001

Journal of Neurochemistry

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We have investigated the role of glutathione in mechanisms associated with excitatory amino acid signaling to the nuclear transcription factor activator protein-1 (AP1) in the brain using mice depleted of endogenous glutathione by prior treatment with 2-cyclohexen-1-one (CHX). In the hippocampus of animals treated with CHX 2 h before, a signi®cant increase was seen in enhancement of AP1 DNA binding when determined 2 h after the injection of kainic acid (KA) at low doses. The sensitization to KA was not seen in animals injected with CHX 24 h before, in coincidence with the recovery of glutathione contents to the normal levels. By contrast, CHX did not signi®cantly affect the potentiation by NMDA of AP1 binding under any experimental conditions. Prior treatment with CHX resulted in facilitation of behavioral changes induced by KA without affecting those induced by NMDA. These results suggest that endogenous glutathione may be at least in part involved in molecular mechanisms underlying transcriptional control by KA, but not by NMDA, signals of cellular functions.

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Protective effect of glutathione on kainic acid-induced neuropathological changes in the rat brain

Cited by 34 publications

References 29 publications

Excitotoxicity, Oxidative Stress, and the Neuroprotective Potential of Melatonin

Excitotoxicity, Oxidative Stress, and the Neuroprotective Potential of Melatonin

Role of oxidative stress in epileptic seizures

Effects of glutathione depletion by 2‐cyclohexen‐1‐one on excitatory amino acids‐induced enhancement of activator protein‐1 DNA binding in murine hippocampus

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