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Behl, Christian; Manthey, Dieter

doi:10.1023/a:1007109222673

Cited by 93 publications

(20 citation statements)

References 63 publications

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“…While the exact mechanism of estrogen neuroprotection is currently unclear, there is mounting evidence that the protective effects of estrogen-related compounds may occur in cells in a nongenomic manner, independent of estrogen receptor activation and subsequent gene expression [24], [46], [47], [48], [49]. The antioxidant properties of estrogens [50] are due to the presence of a phenol at position 3 on the A-ring of estrogens [49], [51].…”

Section: Discussionmentioning

confidence: 99%

Estrogen Prevents Oxidative Damage to the Mitochondria in Friedreich's Ataxia Skin Fibroblasts

Richardson¹,

Yu²,

Yi³

et al. 2012

PLoS ONE

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Estrogen and estrogen-related compounds have been shown to have very potent cytoprotective properties in a wide range of disease models, including an in vitro model of Friedreich's ataxia (FRDA). This study describes a potential estrogen receptor (ER)-independent mechanism by which estrogens act to protect human FRDA skin fibroblasts from a BSO-induced oxidative insult resulting from inhibition of de novo glutathione (GSH) synthesis. We demonstrate that phenolic estrogens, independent of any known ER, are able to prevent lipid peroxidation and mitochondrial membrane potential (ΔΨm) collapse, maintain ATP at near control levels, increase oxidative phosphorylation and maintain activity of aconitase. Estrogens did not, however, prevent BSO from depleting GSH or induce an increased expression level of GSH. The cytoprotective effects of estrogen appear to be due to a direct overall reduction in oxidative damage to the mitochondria, enabling the FRDA fibroblast mitochondria to generate sufficient ATP for energy requirements and better survive oxidative stress. These data support the hypothesis that phenol ring containing estrogens are possible candidate drugs for the delay and/or prevention of FRDA symptoms.

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Section: Discussionmentioning

confidence: 99%

Estrogen Prevents Oxidative Damage to the Mitochondria in Friedreich's Ataxia Skin Fibroblasts

Richardson¹,

Yu²,

Yi³

et al. 2012

PLoS ONE

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“…-induced cellular death, but does not modulate ER-a and ER-b or DAT, supporting its role as a powerful antioxidant (Gelinas and Martinoli 2002;Dore 2005;Alvira et al 2007;Robb et al 2008). Indeed, the neuroprotective potential of certain natural polyphenols is based on their antioxidant action and is independent of their estrogenic properties (Behl et al 1997;Behl and Manthey 2000). Resveratrol, is known to protect neuronal cells against MPP ?…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Resveratrol and Quercetin Against MPP+ -Induced Oxidative Stress Act by Modulating Markers of Apoptotic Death in Dopaminergic Neurons

2009

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Reactive oxygen species produced by oxidative stress may participate in the apoptotic death of dopamine neurons distinctive of Parkinson's disease. Resveratrol, a red wine extract, and quercetin, found mainly in green tea, are two natural polyphenols, presenting antioxidant properties in a variety of cellular paradigms. The aim of this study was to evaluate the effect of resveratrol and quercetin on the apoptotic cascade induced by the administration of 1-methyl-4-phenylpyridinium ion (MPP(+)), a Parkinsonian toxin, provoking the selective degeneration of dopaminergic neurons. Our results show that a pre-treatment for 3 h with resveratrol or quercetin before MPP(+) administration could greatly reduce apoptotic neuronal PC12 death induced by MPP(+). We also demonstrated that resveratrol or quercetin modulates mRNA levels and protein expression of Bax, a pro-apoptotic gene, and Bcl-2, an anti-apoptotic gene. We then evaluated the release of cytochrome c and the nuclear translocation of the apoptosis-inducing factor (AIF). Altogether, our results indicate that resveratrol and quercetin diminish apoptotic neuronal cell death by acting on the expression of pro- and anti-apoptotic genes. These findings support the role of these natural polyphenols in preventive and/or complementary therapies for several human neurodegenerative diseases caused by oxidative stress and apoptosis.

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“…There is substantial biologic evidence for the importance of the role of estrogen and progesterone in the development, growth, differentiation, maturation, and function of various tissues throughout the body, including the peripheral and central nervous systems [131]. These hormones have been found to possess significant neuroprotective properties in various neurodegenerative conditions [132–135].…”

Section: The Contribution Of Blood Glutamate Reduction To Neuropromentioning

confidence: 99%

Blood Glutamate Scavenging: Insight into Neuroprotection

Leibowitz

Boyko

Shapira

et al. 2012

IJMS

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Brain insults are characterized by a multitude of complex processes, of which glutamate release plays a major role. Deleterious excess of glutamate in the brain’s extracellular fluids stimulates glutamate receptors, which in turn lead to cell swelling, apoptosis, and neuronal death. These exacerbate neurological outcome. Approaches aimed at antagonizing the astrocytic and glial glutamate receptors have failed to demonstrate clinical benefit. Alternatively, eliminating excess glutamate from brain interstitial fluids by making use of the naturally occurring brain-to-blood glutamate efflux has been shown to be effective in various animal studies. This is facilitated by gradient driven transport across brain capillary endothelial glutamate transporters. Blood glutamate scavengers enhance this naturally occurring mechanism by reducing the blood glutamate concentration, thus increasing the rate at which excess glutamate is cleared. Blood glutamate scavenging is achieved by several mechanisms including: catalyzation of the enzymatic process involved in glutamate metabolism, redistribution of glutamate into tissue, and acute stress response. Regardless of the mechanism involved, decreased blood glutamate concentration is associated with improved neurological outcome. This review focuses on the physiological, mechanistic and clinical roles of blood glutamate scavenging, particularly in the context of acute and chronic CNS injury. We discuss the details of brain-to-blood glutamate efflux, auto-regulation mechanisms of blood glutamate, natural and exogenous blood glutamate scavenging systems, and redistribution of glutamate. We then propose different applied methodologies to reduce blood and brain glutamate concentrations and discuss the neuroprotective role of blood glutamate scavenging.

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Untitled

Cited by 93 publications

References 63 publications

Estrogen Prevents Oxidative Damage to the Mitochondria in Friedreich's Ataxia Skin Fibroblasts

Estrogen Prevents Oxidative Damage to the Mitochondria in Friedreich's Ataxia Skin Fibroblasts

Protective Effects of Resveratrol and Quercetin Against MPP+ -Induced Oxidative Stress Act by Modulating Markers of Apoptotic Death in Dopaminergic Neurons

Blood Glutamate Scavenging: Insight into Neuroprotection

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