Glutathione elevation by γ‐glutamyl cysteine ethyl ester as a potential therapeutic strategy for preventing oxidative stress in brain mediated by in vivo administration of adriamycin: Implication for chemobrain

@article{Joshi2007GlutathioneEB,
  title={Glutathione elevation by $\gamma$‐glutamyl cysteine ethyl ester as a potential therapeutic strategy for preventing oxidative stress in brain mediated by in vivo administration of adriamycin: Implication for chemobrain},
  author={Gururaj Joshi and Sarita S. Hardas and Rukhsana Sultana and Daret K. St. Clair and Mary Vore and David Allan Butterfield},
  journal={Journal of Neuroscience Research},
  year={2007},
  volume={85}
}
Oxidative stress in heart and brain by the cancer chemotherapeutic drug adriamycin (ADR), used for treating solid tumors, is well established. Long‐term treatment with ADR in breast cancer patients has led to symptoms of cardiomyopathy. Less well recognized, but increasingly well documented, is cognitive dysfunction. After chemotherapy, free radical‐mediated oxidative stress has been reported in both heart and brain. We recently showed a significant increase in protein oxidation and lipid… 
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115 Citations

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Alterations in brain antioxidant enzymes and redox proteomic identification of oxidized brain proteins induced by the anti-cancer drug adriamycin: implications for oxidative stress-mediated chemobrain
In vivo amelioration of adriamycin induced oxidative stress in plasma by gamma-glutamylcysteine ethyl ester (GCEE).
Doxorubicin-induced elevated oxidative stress and neurochemical alterations in brain and cognitive decline: protection by MESNA and insights into mechanisms of chemotherapy-induced cognitive impairment (“chemobrain”)
TLDR
This study is the first to demonstrate the protective effects of MESNA on Dox-related protein oxidation, cognitive decline, phosphocholine (PCho) levels, and PC-PLC activity in brain and suggests novel potential therapeutic targets and strategies to mitigate CICI.
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Supplementation with γ-glutamylcysteine (γ-GC) lessens oxidative stress, brain inflammation and amyloid pathology and improves spatial memory in a murine model of AD
DOXORUBICIN-INDUCED, TNF-α-MEDIATED BRAIN OXIDATIVE STRESS, NEUROCHEMICAL ALTERATIONS, AND COGNITIVE DECLINE: INSIGHTS INTO MECHANISMS OF CHEMOTHERAPY INDUCED COGNITIVE IMPAIRMENT AND ITS PREVENTION
TLDR
Results provide strong evidence that TNF-α is strongly associated, if not responsible for CICI, with central nervous system toxicity including mitochondrial dysfunction, neuronal death, and cognitive impairment.
The triangle of death of neurons: Oxidative damage, mitochondrial dysfunction, and loss of choline-containing biomolecules in brains of mice treated with doxorubicin. Advanced insights into mechanisms of chemotherapy induced cognitive impairment ("chemobrain") involving TNF-α.
The Precursor to Glutathione (GSH), γ-Glutamylcysteine (GGC), Can Ameliorate Oxidative Damage and Neuroinflammation Induced by Aβ40 Oligomers in Human Astrocytes
TLDR
This study examined the potential beneficial effects of GGC against exogenous Aβ40 oligomers on biomarkers of apoptosis and cell death, oxidative stress, and neuroinflammation, in human astrocytes and identifies yet another potential therapeutic strategy to attenuate the cytotoxic effects of Aβ oligomers in AD.
Oxidative Stress and Neurodegenerative Disorders
TLDR
The source, balance maintenance and physiologic functions of ROS, oxidative stress and its toxic mechanisms underlying a number of neurodegenerative diseases, and the possible involvement of ROS in chemotherapy-induced toxicity to the CNS and PNS are summarized.
Glutamate cysteine ligase and the age-related decline in cellular glutathione: The therapeutic potential of γ-glutamylcysteine.
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References

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TLDR
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