2017年10月22日 星期日

Professional medical papers related to cysteine or glutathione;_WJD_2017-1023_V001R01_IR00_

Professional medical papers related to cysteine or glutathione;_WJD_2017-1023_V001R01_IR00_
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Oxidative stress and ageing is ageing a cysteine deficiency syndrome [2005];_WJD_2017-1023_V001R01_IR93_
Source (資訊來源):
(e) Everybody is likely to experience a cysteine deficiency sooner or later
As everybody beyond the fifth decade of life will experience sooner or later a decrease in muscle function, a decrease in immune function, a decrease in plasma albumin concentration, and/or an increase in TNF-α concentration, it is hypothesized that practically everybody experiences sooner or later an ageing-related deficit in the body cysteine and glutathione reservoirs that warrants cysteine supplementation. This hypothesis implies that ageing may be postponed and frailty be avoided to some extent by supplementation of the ‘paravitamin’ cysteine. It is emphasized, however, that several details still require more systematic investigation. Although substantial negative side effects have not been observed in previous studies on cysteine supplementation, it is felt that the treatment protocols ought to be further improved to achieve maximum safety and efficacy over long periods of time. Properly done, cysteine supplementation can reasonably be expected to improve the quality of life in old age. With the availability of novel cysteine delivery systems with minimum amounts of calories, which are superior to any of the naturally available cysteine sources, it is conceivable that even the maximum human life span may be increased beyond the previous limit.
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Elevation of Glutathione as a Therapeutic Strategy in Alzheimer Disease [2011];_WJD_2017-1023_V001R01_IR93_
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Glutathione Synthesis Is Diminished in Patients With Uncontrolled Diabetes and Restored by Dietary Supplementation With Cysteine and Glycine [2010];_WJD_2017-1023_V001R01_IR93_
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Crosstalk between cystine and glutathione is critical for the regulation of amino acid signaling pathways and ferroptosis [2016];_WJD_2017-1023_V001R01_IR93_
Source (資訊來源):
The ability of cells to sense and respond to nutrient availability is critical for cell survival. It is well-established that essential amino acids are required for the regulation of protein translation and growth. Although cysteine is not considered an essential amino acid, cysteine deficiency is associated with various diseases including metabolic disorders, immune dysfunction, and cancer.
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Zinc-Binding Cysteines: Diverse Functions and Structural Motifs [2014];_WJD_2017-1016_V001R01_IR93_
Source (資訊來源):
Info cited on 2017-10-16-WD1 (資訊引用於 中華民國1061016) by 湯偉晉 (WeiJin Tang)
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Cysteine residues are known to perform essential functions within proteins, including binding to various metal ions. In particular, cysteine residues can display high affinity toward zinc ions (Zn2+), and these resulting Zn2+-cysteine complexes are critical mediators of protein structure, catalysis and regulation.
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Glutathione a molecular whistleblower for Alzheimer’s disease [2015];_WJD_2017-1013_V001R01_IR93_
Source (資訊來源):
Info cited on 2017-10-13-WD5 (資訊引用於 中華民國1061013) by 湯偉晉 (WeiJin Tang)
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Depletion of reduced glutathione, ascorbic acid, vitamin E and antioxidant defence enzymes in a healing cutaneous wound. [1997];_WJD_2017-1023_V001R01_IR92_
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DNA recognition by Cys2His2 zinc finger proteins. [2000];_WJD_2017-1023_V001R01_IR93_
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Endogenous Glutathione Conjugates Occurrence and Biological Functions [1998];_WJD_2017-1023_V001R01_IR93_
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The role of glutathione in copper metabolism and toxicity. [1989];_WJD_2017-1023_V001R01_IR92_
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Central nervous system uptake of intranasal glutathione in Parkinson’s disease [2016];_WJD_2017-1023_V001R01_IR93_
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Neuroprotection against neuroblastoma cell death induced by depletion of mitochondrial glutathione [2013];_WJD_2017-1023_V001R01_IR93_
Source (資訊來源):
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Mitochondrial glutathione pool is vital in protecting cells against oxidative stress as the majority of the cellular reactive oxygen species are generated in mitochondria. Oxidative stress is implicated as a causative factor in neuronal death in neurodegenerative disorders. We hypothesized that depletion of mitochondrial glutathione leads to mitochondrial dysfunction and apoptotic death of SK-N-SH (human neuroblastoma) cells and investigated the neuroprotective strategies against GSH depletion.
Our data suggest that depletion of mitochondrial glutathione leads to mitochondrial dysfunction and apoptosis. The study indicates that preventing mitochondrial glutathione depletion could become a novel strategy for the development of neuroprotective therapeutics in neurodegenerative disorders.
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Glutathione as a Redox Biomarker in Mitochondrial Disease—Implications for Therapy [2017];_WJD_2017-1023_V001R01_IR93_
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2017-10-23
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Glutathione in Parkinson's Disease [2016]; Ph.D. dissertation, University of Washington_WJD_2017-1023_V001R01_IR93_
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