Effect of <i>γ</i>-glutamylcysteine ethylester on the levels of <i>c-fos</i> mRNA expression, glutathione and reactive oxygen species formation in kainic acid excitotoxicity

Turunç, Ezgi; Kanıt, Lütfiye; Yalçın, Ayfer

doi:10.1111/j.2042-7158.2010.01122.x

Cited by 8 publications

(5 citation statements)

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“…Brain cells are particularly vulnerable to oxidative stress because of their high oxygen consumption, high content of unsaturated fatty acids and iron and decreased activities of antioxidant enzymes. Thus, effective antioxidant defence is vital for neuroprotection in the brain . Our previous study showed that intrahippocampal A β (1–42) injection caused significant increases in oxidative stress markers, and NA treatments provided a protection supporting antioxidant defence against the elevation of lipid peroxidation, protein oxidation and ROS production induced by A β (1–42) in vivo .…”

Section: Discussionmentioning

confidence: 61%

“…Thus, effective antioxidant defence is vital for neuroprotection in the brain. [45][46][47][48] Our previous study showed that intrahippocampal A(1-42) injection caused significant increases in oxidative stress markers, and NA treatments provided a protection supporting antioxidant defence against the elevation of lipid peroxidation, protein oxidation and ROS production induced by A in vivo. 49 This study reveals the effects of A(1-42) on oxidative stress and mitochondrial reduction capacity and whether there are possible neuroprotective effects of 3-AB and NA in synaptosomes with an ex vivo experimental approach because the changes in these parameters might be relevant to synaptic loss that has been proposed as an early event in AD neuropathogenesis.…”

Section: Discussionmentioning

confidence: 98%

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Ex vivo protective effects of nicotinamide and 3‐aminobenzamide on rat synaptosomes treated with Aβ(1–42)

Turunç

Armağan

Uyanıkgil

et al. 2014

Cell Biochemistry & Function

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Alzheimer's disease (AD) is the most common form of dementia and is characterized by the presence of senile plaques and neurofibrillary tangles, along with synaptic loss. The underlying mechanisms of AD are not clarified yet, but oxidative stress and mitochondrial dysfunction are important factors. Overactivation of poly(adenosine diphosphate ribose) polymerase-1 (PARP-1) enzyme has been known to cause neuroinflammation and cell death in neurodegenerative processes. The aim of the present study was to investigate the protective effects of the PARP-1 inhibitors, 3-aminobenzamide (3-AB) and nicotinamide (NA), against amyloid β peptide (1-42) (Aβ(1-42))-induced oxidative damage and mitochondrial reduction capacity on isolated synaptosomes. Rats were injected intraperitoneally with 3-AB (30-100 mg kg(-1)), NA (100-500 mg kg(-1)) or with saline for 7 days. Synaptosomes were incubated with 10-30 μM Aβ(1-42) or saline for 6 h at 37 °C. Ex vivo Aβ(1-42) treatment significantly induced oxidative stress and mitochondrial dysfunction in synaptosomes of the saline group, while synaptosomes of 3-AB and NA groups showed significant decreases in lipid peroxidation, reactive oxygen species production and protein oxidation. Moreover, both NA and 3-AB were able to improve the mitochondrial reduction capacity against Aβ(1-42). These data suggest that NA and 3-AB may have protective effects in neurodegenerative processes because of the reduced levels of oxidative stress and the improvement of mitochondrial function.

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 98%

Ex vivo protective effects of nicotinamide and 3‐aminobenzamide on rat synaptosomes treated with Aβ(1–42)

Turunç

Armağan

Uyanıkgil

et al. 2014

Cell Biochemistry & Function

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“…Since GCEE has been proven to be effective in vivo at doses of 10 mg/kg [25] and 150 mg/kg b.wt. [21], we selected a dose of 100 mg/kg to be tested in our study.…”

Section: Methodsmentioning

confidence: 99%

Gamma‐Glutamylcysteine Ethyl Ester Protects against Cyclophosphamide‐Induced Liver Injury and Hematologic Alterations via Upregulation of PPARγ and Attenuation of Oxidative Stress, Inflammation, and Apoptosis

Alqahtani

Mahmoud

2016

Oxidative Medicine and Cellular Longevity

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Gamma-glutamylcysteine ethyl ester (GCEE) is a precursor of glutathione (GSH) with promising hepatoprotective effects. This investigation aimed to evaluate the hepatoprotective effects of GCEE against cyclophosphamide- (CP-) induced toxicity, pointing to the possible role of peroxisome proliferator activated receptor gamma (PPARγ). Wistar rats were given GCEE two weeks prior to CP. Five days after CP administration, animals were sacrificed and samples were collected. Pretreatment with GCEE significantly alleviated CP-induced liver injury by reducing serum aminotransferases, increasing albumin, and preventing histopathological and hematological alterations. GCEE suppressed lipid peroxidation and nitric oxide production and restored GSH and enzymatic antioxidants in the liver, which were associated with downregulation of COX-2, iNOS, and NF-κB. In addition, CP administration significantly increased serum proinflammatory cytokines and the expression of liver caspase-3 and BAX, an effect that was reversed by GCEE. CP-induced rats showed significant downregulation of PPARγ which was markedly upregulated by GCEE treatment. These data demonstrated that pretreatment with GCEE protected against CP-induced hepatotoxicity, possibly by activating PPARγ, preventing GSH depletion, and attenuating oxidative stress, inflammation, and apoptosis. Our findings point to the role of PPARγ and suggest that GCEE might be a promising agent for the prevention of CP-induced liver injury.

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“…Recently, i.p. injections of GCEE protected against kainic acid induced ROS and downregulated c-fos mRNA in the cortex and hippocampus of rats [85]. GCEE may react directly with ROS due to the cysteine residue and/or increase GSH, which can protect against ROS and nucleophilic compounds.…”

Section: γ-Glutamylcysteine Ethyl Ester (Gcee)mentioning

confidence: 99%

Elevation of glutathione as a therapeutic strategy in Alzheimer disease

Pocernich

Butterfield

2012

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

293

149

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Oxidative stress has been associated with the onset and progression of mild cognitive impairment (MCI) and Alzheimer disease (AD). AD and MCI brain and plasma display extensive oxidative stress as indexed by protein oxidation, lipid peroxidation, free radical formation, DNA oxidation, and decreased antioxidants. The most abundant endogenous antioxidant, glutathione, plays a significant role in combating oxidative stress. The ratio of oxidized to reduced glutathione is utilized as a measure of intensity of oxidative stress. Antioxidants have long been considered as an approach to slow down AD progression. In this review, we focus on the elevation on glutathione through N-acytl-cysteine (NAC) and γ-glutamylcysteine ethyl ester (GCEE) as a potential therapeutic approach for Alzheimer disease.

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Effect of γ-glutamylcysteine ethylester on the levels of c-fos mRNA expression, glutathione and reactive oxygen species formation in kainic acid excitotoxicity

Abstract: The increased levels of glutathione and the reduced levels of reactive oxygen species formation lead us to conclude that GCEE may be beneficial as a potential antioxidant against neurodegenerative processes where excitotoxicity is involved.

Cited by 8 publications

References 66 publications

Ex vivo protective effects of nicotinamide and 3‐aminobenzamide on rat synaptosomes treated with Aβ(1–42)

Ex vivo protective effects of nicotinamide and 3‐aminobenzamide on rat synaptosomes treated with Aβ(1–42)

Gamma‐Glutamylcysteine Ethyl Ester Protects against Cyclophosphamide‐Induced Liver Injury and Hematologic Alterations via Upregulation of PPARγ and Attenuation of Oxidative Stress, Inflammation, and Apoptosis

Elevation of glutathione as a therapeutic strategy in Alzheimer disease

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