---
- - --- - - ---
2020-09-26
Reduced Glutathione as an Effector of Phosphoenolpyruvate Carboxylase of the
Crassulacean Acid Metabolism Plant Sedum praealtum D.C; PY1983; Please select a
University Name.;_WJD_2020-0926_V001R01_IR93_RvD20200926_
Source (資訊來源):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1066010/
Info cited on 2020-09-26-WD6 (資訊引用於 中華民國109年9月26日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
Plant Physiol. 1983 Jan; 71(1): 187–189.
doi: 10.1104/pp.71.1.187
PMCID: PMC1066010
PMID: 16662783
Reduced Glutathione
as an Effector of Phosphoenolpyruvate Carboxylase of the Crassulacean Acid
Metabolism Plant Sedum praealtum D.C
Yiannis Manetas and Nikos A. Gavalas
Laboratory of Plant Physiology, University of Patras, Patras, Greece
Abstract
Reduced glutathione, but not mercaptoethanol or dithiothreitol, inhibits
phosphoenolpyruvate carboxylase (PEPC) in desalted leaf extracts from Sedum
praealtum D.C. The
inhibition is more evident at low pH values (< 7.2) and becomes increasingly
smaller at higher pH. In the presence of the inhibitor, the hyperbolic
rate curve of night PEPC is transformed to sigmoid and the S0.5 is increased.
When the enzyme is extracted during the day, the rate curve is sigmoid and it
is not changed by the inhibitor, though the S0.5 is further increased. Oxidized
glutathione is completely inactive. Levels of reduced glutathione in leaf tissue are distinctly higher in the
light. A role of photosynthetically reduced glutathione in the
regulation of PEPC in Crassulacean acid metabolism species appears probable.
- - - - -- -- - -
--- --- - - --- ---
2020年9月26日 星期六
2020年8月4日 星期二
Inhibitory effects of glutathione on dengue virus production; PY2010; PR China (中華人民共和國);_WJD_2020-0804_IR94_
---
- - --- - - ---
2020-08-04
Inhibitory effects of glutathione on dengue virus production; PY2010; PR China (中華人民共和國);_WJD_2020-0804_V001R01_IR94_RvD20200804_
Source (資訊來源):
https://www.sciencedirect.com/science/article/abs/pii/S0006291X10010235
Info cited on 2020-08-04-WD2 (資訊引用於 中華民國109年8月4日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
Biochemical and Biophysical Research Communications
Volume 397, Issue 3, 2 July 2010, Pages 420-424
Inhibitory effects of glutathione on dengue virus production
Abstract
Reduced glutathione (GSH) is the most powerful intracellular antioxidant and also involved in viral infections. The pathogenesis of dengue virus (DV) infection has not been completely clarified. This study investigated the relationship between DV serotype 2 (DV2) infections and host intracellular GSH content. Results showed infection with DV2 resulted in a decrease in intracellular GSH, which caused NF-κB activation and increased DV2 production. Supplemental GSH significantly inhibited activation of NF-κB, resulting in a decreased production of DV2 in HepG2 cells. Furthermore, high activity of NF-κB and increased production of DV2 was observed in HepG2 cells treated with buthionine sulfoximine (BSO), an inhibitor of GSH synthesis. In conclusion, DV2 infection could reduce host intracellular GSH concentration and benefited from this process. Supplemental GSH could inhibit viral production, indicating GSH might be valuable in the prevention and treatment of DV2 infection.
Keywords
Dengue virus, Redox stage, GSH, NF-κB
- - - - -- -- - -
--- --- - - --- ---
2020-08-04
Inhibitory effects of glutathione on dengue virus production; PY2010; PR China (中華人民共和國);_WJD_2020-0804_V001R01_IR94_RvD20200804_
Source (資訊來源):
https://www.sciencedirect.com/science/article/abs/pii/S0006291X10010235
Info cited on 2020-08-04-WD2 (資訊引用於 中華民國109年8月4日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
Biochemical and Biophysical Research Communications
Volume 397, Issue 3, 2 July 2010, Pages 420-424
Inhibitory effects of glutathione on dengue virus production
Abstract
Reduced glutathione (GSH) is the most powerful intracellular antioxidant and also involved in viral infections. The pathogenesis of dengue virus (DV) infection has not been completely clarified. This study investigated the relationship between DV serotype 2 (DV2) infections and host intracellular GSH content. Results showed infection with DV2 resulted in a decrease in intracellular GSH, which caused NF-κB activation and increased DV2 production. Supplemental GSH significantly inhibited activation of NF-κB, resulting in a decreased production of DV2 in HepG2 cells. Furthermore, high activity of NF-κB and increased production of DV2 was observed in HepG2 cells treated with buthionine sulfoximine (BSO), an inhibitor of GSH synthesis. In conclusion, DV2 infection could reduce host intracellular GSH concentration and benefited from this process. Supplemental GSH could inhibit viral production, indicating GSH might be valuable in the prevention and treatment of DV2 infection.
Keywords
Dengue virus, Redox stage, GSH, NF-κB
- - - - -- -- - -
--- --- - - --- ---
2020年6月1日 星期一
Important Components of the UW Solution; PY1990; University of Wisconsin;_WJD_2020-0601_IR94_
---
- - --- - - ---
2020-06-01
Important Components of the UW Solution; PY1990; University of Wisconsin;_WJD_2020-0601_V001R01_IR94_RvD20200601_
Source (資訊來源):
https://pubmed.ncbi.nlm.nih.gov/1689516/
Info cited on 2020-06-01-WD1 (資訊引用於 中華民國109年6月1日) by 湯偉晉 (WeiJin Tang)
#
UW Solution
University of Wisconsin solution (威斯康辛大學溶液)
- - - - - - - -
Transplantation
1990 Feb;49(2):251-7. doi: 10.1097/00007890-199002000-00004.
Important Components of the UW Solution
J H Southard 1, T M van Gulik, M S Ametani, P K Vreugdenhil, S L Lindell, B L Pienaar, F O Belzer
Affiliation
1Department of Surgery, University of Wisconsin, Madison 53792.
PMID: 1689516 DOI: 10.1097/00007890-199002000-00004
Abstract
The UW solution for preservation of the liver, kidney, and pancreas contains a number of components, and the importance of each of these has not been fully resolved. In the studies reported here the importance of glutathione and adenosine is demonstrated in isolated cell models (rabbit renal tubules and rat liver hepatocytes) of hypothermic preservation and reperfusion and in dog renal transplantation. Glutathione in the UW solution is necessary for the preservation of the capability of the cell to regenerate ATP and maintain membrane integrity. Adenosine in the UW solution provides the preserved cell with substrates for the regeneration of ATP during the reperfusion period following cold storage. The omission of GHS from the UW solution results in poorer renal function in the 48 hr dog kidney preservation-transplant model. The role of other components of the UW solution is discussed including lactobionic acid; other impermeants; and the colloid, hydroxyethyl starch. It is concluded that the development of improved preservation solutions will require a more detailed understanding of the mechanism of injury due to cold storage and, once obtained, solutions more complex than the UW solution may be required for improved long-term storage of organs.
- - - - -- -- - -
--- --- - - --- ---
2020-06-01
Important Components of the UW Solution; PY1990; University of Wisconsin;_WJD_2020-0601_V001R01_IR94_RvD20200601_
Source (資訊來源):
https://pubmed.ncbi.nlm.nih.gov/1689516/
Info cited on 2020-06-01-WD1 (資訊引用於 中華民國109年6月1日) by 湯偉晉 (WeiJin Tang)
#
UW Solution
University of Wisconsin solution (威斯康辛大學溶液)
- - - - - - - -
Transplantation
1990 Feb;49(2):251-7. doi: 10.1097/00007890-199002000-00004.
Important Components of the UW Solution
J H Southard 1, T M van Gulik, M S Ametani, P K Vreugdenhil, S L Lindell, B L Pienaar, F O Belzer
Affiliation
1Department of Surgery, University of Wisconsin, Madison 53792.
PMID: 1689516 DOI: 10.1097/00007890-199002000-00004
Abstract
The UW solution for preservation of the liver, kidney, and pancreas contains a number of components, and the importance of each of these has not been fully resolved. In the studies reported here the importance of glutathione and adenosine is demonstrated in isolated cell models (rabbit renal tubules and rat liver hepatocytes) of hypothermic preservation and reperfusion and in dog renal transplantation. Glutathione in the UW solution is necessary for the preservation of the capability of the cell to regenerate ATP and maintain membrane integrity. Adenosine in the UW solution provides the preserved cell with substrates for the regeneration of ATP during the reperfusion period following cold storage. The omission of GHS from the UW solution results in poorer renal function in the 48 hr dog kidney preservation-transplant model. The role of other components of the UW solution is discussed including lactobionic acid; other impermeants; and the colloid, hydroxyethyl starch. It is concluded that the development of improved preservation solutions will require a more detailed understanding of the mechanism of injury due to cold storage and, once obtained, solutions more complex than the UW solution may be required for improved long-term storage of organs.
- - - - -- -- - -
--- --- - - --- ---
2020年5月3日 星期日
Glutathione depletion inhibits dendritic cell maturation and delayed-type hypersensitivity： Implications for systemic disease and immunosenescence; PY2007; USA (美國);_WJD_2020-0504_V001R01_IR94_IR95_
--- - - --- - - ---
2020-05-04
Glutathione depletion inhibits dendritic cell maturation and delayed-type hypersensitivity: Implications for systemic disease and immunosenescence
Source (資訊來源):
https://www.jacionline.org/article/S0091-6749(07)00177-7/fulltext
Info cited on 2020-05-04-WD1 (資訊引用於 中華民國109年5月4日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
BASIC AND CLINICAL IMMUNOLOGY| VOLUME 119, ISSUE 5, P1225-1233, MAY 01, 2007
Glutathione depletion inhibits dendritic cell maturation and delayed-type hypersensitivity: Implications for systemic disease and immunosenescence
2020-05-04
Glutathione depletion inhibits dendritic cell maturation and delayed-type hypersensitivity: Implications for systemic disease and immunosenescence
Source (資訊來源):
https://www.jacionline.org/article/S0091-6749(07)00177-7/fulltext
Info cited on 2020-05-04-WD1 (資訊引用於 中華民國109年5月4日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
BASIC AND CLINICAL IMMUNOLOGY| VOLUME 119, ISSUE 5, P1225-1233, MAY 01, 2007
Glutathione depletion inhibits dendritic cell maturation and delayed-type hypersensitivity: Implications for systemic disease and immunosenescence
Begin_電腦自動翻譯的內容_Y2020m05d04h03m52Rn5980_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
穀胱甘肽耗竭抑制樹突狀細胞成熟和遲髮型超敏反應：對全身性疾病和免疫衰老的影響
End_電腦自動翻譯的內容_Y2020m05d04h03m52Rn5980_
Hyon-Jeen Kim, PhD
Berenice Barajas, BS
Ray Chun-Fai Chan, PhD
Andre E. Nel, MD, PhD
Published:March 10, 2007DOI:https://doi.org/10.1016/j.jaci.2007.01.016
Background
Dendritic cells (DCs) play a key role as antigen-presenting cells in the immune system. There is growing evidence that the redox equilibrium of these cells influences their ability to induce T-cell activation and to regulate the polarity of the immune response. This could affect the outcome of the immune response during systemic diseases and aging.
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
穀胱甘肽耗竭抑制樹突狀細胞成熟和遲髮型超敏反應：對全身性疾病和免疫衰老的影響
End_電腦自動翻譯的內容_Y2020m05d04h03m52Rn5980_
Hyon-Jeen Kim, PhD
Berenice Barajas, BS
Ray Chun-Fai Chan, PhD
Andre E. Nel, MD, PhD
Published:March 10, 2007DOI:https://doi.org/10.1016/j.jaci.2007.01.016
Background
Dendritic cells (DCs) play a key role as antigen-presenting cells in the immune system. There is growing evidence that the redox equilibrium of these cells influences their ability to induce T-cell activation and to regulate the polarity of the immune response. This could affect the outcome of the immune response during systemic diseases and aging.
Begin_電腦自動翻譯的內容_Y2020m05d04h03m56Rn2887_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
背景
樹突狀細胞（DC）在免疫系統中作為抗原呈遞細胞發揮著關鍵作用。越來越多的證據表明，這些細胞的氧化還原平衡會影響它們誘導T細胞活化和調節免疫應答極性的能力。這可能會影響全身性疾病和衰老過程中免疫反應的結果。
End_電腦自動翻譯的內容_Y2020m05d04h03m56Rn2887_
Objective
Our aim was to elucidate the mechanism by which the redox equilibrium of antigen-presenting DCs affects the delayed-type hypersensitivity (DTH) response during experimental modification of glutathione levels, as well as during aging.
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
背景
樹突狀細胞（DC）在免疫系統中作為抗原呈遞細胞發揮著關鍵作用。越來越多的證據表明，這些細胞的氧化還原平衡會影響它們誘導T細胞活化和調節免疫應答極性的能力。這可能會影響全身性疾病和衰老過程中免疫反應的結果。
End_電腦自動翻譯的內容_Y2020m05d04h03m56Rn2887_
Objective
Our aim was to elucidate the mechanism by which the redox equilibrium of antigen-presenting DCs affects the delayed-type hypersensitivity (DTH) response during experimental modification of glutathione levels, as well as during aging.
Begin_電腦自動翻譯的內容_Y2020m05d04h03m58Rn5158_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
目的
我們的目的是闡明在穀胱甘肽水平的實驗性修飾以及衰老過程中，抗原呈遞DC的氧化還原平衡影響延遲型超敏反應（DTH）的機制。
End_電腦自動翻譯的內容_Y2020m05d04h03m58Rn5158_
Methods
We looked at the effect of glutathione depletion by diethyl maleate in DCs as well as during systemic administration on the DTH response to the contact-sensitizing antigens, oxazolone, and 2,4-dinitro-1-fluorobenzene. We also determined whether glutathione repletion with N-acetyl cysteine could influence the decline of the DTH response in aged mice.
Results
Glutathione depletion in bone marrow–derived DCs interfered in their ability to mount a DTH response on adoptive transfer into recipient mice. Glutathione depletion interfered in IL-12 production and costimulatory receptor expression in DCs, leading to decreased IFN-γ production in the skin of recipient mice. Systemic diethyl maleate treatment exerted similar effects on the DTH response and IFN-γ production, whereas N-acetyl cysteine administration reversed the decline of the DTH response in aged animals.
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
目的
我們的目的是闡明在穀胱甘肽水平的實驗性修飾以及衰老過程中，抗原呈遞DC的氧化還原平衡影響延遲型超敏反應（DTH）的機制。
End_電腦自動翻譯的內容_Y2020m05d04h03m58Rn5158_
Methods
We looked at the effect of glutathione depletion by diethyl maleate in DCs as well as during systemic administration on the DTH response to the contact-sensitizing antigens, oxazolone, and 2,4-dinitro-1-fluorobenzene. We also determined whether glutathione repletion with N-acetyl cysteine could influence the decline of the DTH response in aged mice.
Results
Glutathione depletion in bone marrow–derived DCs interfered in their ability to mount a DTH response on adoptive transfer into recipient mice. Glutathione depletion interfered in IL-12 production and costimulatory receptor expression in DCs, leading to decreased IFN-γ production in the skin of recipient mice. Systemic diethyl maleate treatment exerted similar effects on the DTH response and IFN-γ production, whereas N-acetyl cysteine administration reversed the decline of the DTH response in aged animals.
Begin_電腦自動翻譯的內容_Y2020m05d04h03m57Rn7867_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
結果
骨髓來源的DC中的穀胱甘肽耗竭會干擾它們在過繼轉移到受體小鼠中時引起DTH反應的能力。穀胱甘肽耗竭會干擾DC中IL-12的產生和共刺激受體的表達，從而導致受體小鼠皮膚中IFN-γ的產生減少。全身性馬來酸二乙酯治療對DTH反應和IFN-γ產生具有相似的作用，而N-乙酰半胱胺酸的給藥可以逆轉衰老動物DTH反應的下降。
End_電腦自動翻譯的內容_Y2020m05d04h03m57Rn7867_
Conclusion
Glutathione depletion downregulates TH1 immunity through a perturbation of DC maturation and IL-12 production.
Clinical implications
These data show that the induction of oxidative stress in the immune system, under disease conditions and aging, interferes in TH1 immunity.
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
結果
骨髓來源的DC中的穀胱甘肽耗竭會干擾它們在過繼轉移到受體小鼠中時引起DTH反應的能力。穀胱甘肽耗竭會干擾DC中IL-12的產生和共刺激受體的表達，從而導致受體小鼠皮膚中IFN-γ的產生減少。全身性馬來酸二乙酯治療對DTH反應和IFN-γ產生具有相似的作用，而N-乙酰半胱胺酸的給藥可以逆轉衰老動物DTH反應的下降。
End_電腦自動翻譯的內容_Y2020m05d04h03m57Rn7867_
Conclusion
Glutathione depletion downregulates TH1 immunity through a perturbation of DC maturation and IL-12 production.
Clinical implications
These data show that the induction of oxidative stress in the immune system, under disease conditions and aging, interferes in TH1 immunity.
Begin_電腦自動翻譯的內容_Y2020m05d04h03m57Rn0875_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
結論
穀胱甘肽耗竭通過乾擾DC成熟和IL-12產生而下調TH1免疫力。
臨床的意義
這些數據表明，在疾病條件和衰老過程中，免疫系統中氧化壓力的誘導會干擾TH1免疫。
End_電腦自動翻譯的內容_Y2020m05d04h03m57Rn0875_
Key words
Dendritic cells
TH1
glutathione
delayed-type hypersensitivity
skin dermatitis
aging
antigen-presenting cells
redox
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
結論
穀胱甘肽耗竭通過乾擾DC成熟和IL-12產生而下調TH1免疫力。
臨床的意義
這些數據表明，在疾病條件和衰老過程中，免疫系統中氧化壓力的誘導會干擾TH1免疫。
End_電腦自動翻譯的內容_Y2020m05d04h03m57Rn0875_
Key words
Dendritic cells
TH1
glutathione
delayed-type hypersensitivity
skin dermatitis
aging
antigen-presenting cells
redox
Abbreviations used:
APC (Antigen-presenting cell), BM-DC (Bone marrow–derived dendritic cell), CON (Vehicle-treated control), DC (Dendritic cell), DEM (Diethyl maleate), DEP (Diesel exhaust particle), DNBS (2,4-Dinitrobenzene sulfonic acid), DNFB (2,4-Dinitro-1-fluorobenzene), DTH (Delayed-type hypersensitivity), FITC (Fluorescein isothiocyanate), MBB (Monobromobimane), MLR (Mixed-leukocyte reaction), NAC (N-acetyl cysteine), OXA (Oxazolone), PE (Phycoerythrin), ROS (Reactive oxygen species), Treg (Regulatory T)
APC (Antigen-presenting cell), BM-DC (Bone marrow–derived dendritic cell), CON (Vehicle-treated control), DC (Dendritic cell), DEM (Diethyl maleate), DEP (Diesel exhaust particle), DNBS (2,4-Dinitrobenzene sulfonic acid), DNFB (2,4-Dinitro-1-fluorobenzene), DTH (Delayed-type hypersensitivity), FITC (Fluorescein isothiocyanate), MBB (Monobromobimane), MLR (Mixed-leukocyte reaction), NAC (N-acetyl cysteine), OXA (Oxazolone), PE (Phycoerythrin), ROS (Reactive oxygen species), Treg (Regulatory T)
Oxidative stress is a state of redox
disequilibrium that is defined as a depletion of intracellular glutathione and
an accumulation of glutathione disulfide. A decline
of the cellular glutathione/glutathione disulfide ratio initiates a series of
biological responses that are relevant to normal physiology as well as the
pathophysiology of disease. According to the hierarchical oxidative stress hypothesis, low levels of oxidative stress
initiate cellular antioxidant responses through nuclear factor-erythroid
2 (NF-E2)–related factor 2 (Nrf2)-mediated phase II enzyme (eg, catalase and
superoxide dismutase) expression.1 At higher levels of oxidative stress, activation
of the mitogen-activated protein kinase and NF-κB signaling cascades culminate
in proinflammatory effects, whereas
at the highest level of oxidative stress, interference in mitochondrial
function leads to ATP depletion and programmed cell death.1 This dynamic interplay between protective
and injurious oxidative stress responses could modulate the immune
response in asthma, AIDS, diabetes mellitus, contact dermatitis, and
cancer.2, 3, 4, 5, 6 Moreover, several of the biological effects of aging have been
ascribed to altered redox equilibrium and generation of excessive reactive
oxygen species (ROSs).6
Oxidative stress is of key
importance in the effector as well as the induction phases of the immune
response.5, 6, 7 It is well known that immune activation generates inflammatory states in
which ROS production by immune cells contributes to protective as well as
tissue damaging effects. Less appreciated is that ROS and oxidative stress also regulate the
induction of the immune response by controlling signal transduction pathways in
antigen-presenting cells (APCs) and lymphocytes.8 ROSs not only regulate T-cell
activation but also interfere in the polarity of the immune response as
evidenced by the finding that oxidative stress favors TH2 skewing of the immune
response while suppressing TH1 differentiation.8, 9 Accordingly, glutathione depletion in vivo results in lowered TH1 but
increased TH2 responses, whereas glutathione repletion has the opposite effect.8
The elucidation of the mechanisms by which oxidative stress changes APC
function is of key importance in studying the pathophysiology of disease as
well as understanding immune senescence.8,
9, 10
Although under disease conditions it is difficult to regulate the level of oxidative stress independent from pathological events, it is experimentally possible to obtain glutathione depletion with the thiol-alkylating agent, diethyl maleate (DEM).11 We used this agent to treat dendritic cells (DCs) ex vivo as well as deplete glutathione levels in mice to study the effects of oxidative stress on the delayed-type hypersensitivity (DTH) response and cytokine profiles in the skin. Adjustable levels of oxidative stress could be achieved in DCs as well as the lymph nodes and spleens of DEM-treated animals. Glutathione depletion interferes in the expression of costimulatory receptors and IL-12 production in bone marrow–derived DCs (BM-DCs), making these cells less capable of supporting a DTH response and TH1 immunity after adoptive transfer in vivo. DEM also interfered in DTH responses in intact animals, whereas the glutathione precursor, N-acetyl cysteine (NAC), reversed the decline in the DTH response in aged mice.
- - - - -- -- - -
--- --- - - --- ---
Although under disease conditions it is difficult to regulate the level of oxidative stress independent from pathological events, it is experimentally possible to obtain glutathione depletion with the thiol-alkylating agent, diethyl maleate (DEM).11 We used this agent to treat dendritic cells (DCs) ex vivo as well as deplete glutathione levels in mice to study the effects of oxidative stress on the delayed-type hypersensitivity (DTH) response and cytokine profiles in the skin. Adjustable levels of oxidative stress could be achieved in DCs as well as the lymph nodes and spleens of DEM-treated animals. Glutathione depletion interferes in the expression of costimulatory receptors and IL-12 production in bone marrow–derived DCs (BM-DCs), making these cells less capable of supporting a DTH response and TH1 immunity after adoptive transfer in vivo. DEM also interfered in DTH responses in intact animals, whereas the glutathione precursor, N-acetyl cysteine (NAC), reversed the decline in the DTH response in aged mice.
- - - - -- -- - -
--- --- - - --- ---
Blood glutathione decreases in chronic diseases; PY2000; University of Louisville School of Medicine, USA (美國);_WJD_2020-0504_V001R01_IR94_
---
- - --- - - ---
2020-05-04
Blood glutathione decreases in chronic diseases.
Source (資訊來源):
https://www.ncbi.nlm.nih.gov/pubmed/10811055
Info cited on 2020-05-04-WD1 (資訊引用於 中華民國109年5月4日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
J Lab Clin Med. 2000 May;135(5):402-5.
Blood glutathione decreases in chronic diseases.
Lang CA1, Mills BJ, Mastropaolo W, Liu MC.
Author information
1
Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, KY 40292, USA.
Abstract
Previously a high blood glutathione level was correlated with long life span in the mouse and rat and in healthy elderly human beings. This raised the question of whether low glutathione levels occur in unhealthy subjects. To this end, 74 consecutive patients newly admitted to the hospital, with ages ranging from 21 to 89 years and diagnosed with chronic diseases, were studied along with 32 healthy control subjects. Blood samples were analyzed for reduced (GSH) and oxidized (GSSG) glutathione with a high-performance liquid chromatography-dual electrochemical method. The data were integrated with the clinical diagnoses and statistically analyzed. Marked total glutathione decreases from the control levels occurred in over 36% of the patients with chronic diseases including cancer and genitourinary, gastrointestinal, cardiovascular, and musculoskeletal diseases (P < .001). The deficit was due to low GSH concentrations and not to GSSG, which was the same as that in the control subjects. The conclusion is that a decrease in GSH is a risk factor for chronic diseases that may be used to monitor the severity and progress of the diseases. Future work is necessary to elucidate the mechanism of action.
Begin_電腦自動翻譯的內容_Y2020m05d04h03m21Rn6560_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
以前，高穀胱甘肽水平與小鼠和大鼠以及健康老年人的壽命長有關。這就提出了一個問題，即在不健康的受試者中是否發生了低穀胱甘肽水平。為此，與32名健康對照受試者一起研究了74名新入院的連續患者，年齡在21至89歲之間，並被診斷出患有慢性疾病。使用高效液相色譜-雙電化學方法分析血樣中的還原型（GSH）和氧化型（GSSG）穀胱甘肽。數據與臨床診斷整合併進行統計分析。超過36％的慢性疾病患者（包括癌症和泌尿生殖系統，胃腸道，心血管和肌肉骨骼疾病）的總穀胱甘肽水平明顯低於對照組（P <.001）。缺乏症是由於GSH濃度低而不是GSSG引起的，與對照組相同。結論是，穀胱甘肽降低是慢性疾病的危險因素，可用於監測疾病的嚴重程度和進展。為了闡明作用機理，未來的工作是必要的。
End_電腦自動翻譯的內容_Y2020m05d04h03m21Rn6560_
PMID: 10811055 DOI: 10.1067/mlc.2000.105977
- - - - -- -- - -
--- --- - - --- ---
2020-05-04
Blood glutathione decreases in chronic diseases.
Source (資訊來源):
https://www.ncbi.nlm.nih.gov/pubmed/10811055
Info cited on 2020-05-04-WD1 (資訊引用於 中華民國109年5月4日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
J Lab Clin Med. 2000 May;135(5):402-5.
Blood glutathione decreases in chronic diseases.
Lang CA1, Mills BJ, Mastropaolo W, Liu MC.
Author information
1
Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, KY 40292, USA.
Abstract
Previously a high blood glutathione level was correlated with long life span in the mouse and rat and in healthy elderly human beings. This raised the question of whether low glutathione levels occur in unhealthy subjects. To this end, 74 consecutive patients newly admitted to the hospital, with ages ranging from 21 to 89 years and diagnosed with chronic diseases, were studied along with 32 healthy control subjects. Blood samples were analyzed for reduced (GSH) and oxidized (GSSG) glutathione with a high-performance liquid chromatography-dual electrochemical method. The data were integrated with the clinical diagnoses and statistically analyzed. Marked total glutathione decreases from the control levels occurred in over 36% of the patients with chronic diseases including cancer and genitourinary, gastrointestinal, cardiovascular, and musculoskeletal diseases (P < .001). The deficit was due to low GSH concentrations and not to GSSG, which was the same as that in the control subjects. The conclusion is that a decrease in GSH is a risk factor for chronic diseases that may be used to monitor the severity and progress of the diseases. Future work is necessary to elucidate the mechanism of action.
Begin_電腦自動翻譯的內容_Y2020m05d04h03m21Rn6560_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
以前，高穀胱甘肽水平與小鼠和大鼠以及健康老年人的壽命長有關。這就提出了一個問題，即在不健康的受試者中是否發生了低穀胱甘肽水平。為此，與32名健康對照受試者一起研究了74名新入院的連續患者，年齡在21至89歲之間，並被診斷出患有慢性疾病。使用高效液相色譜-雙電化學方法分析血樣中的還原型（GSH）和氧化型（GSSG）穀胱甘肽。數據與臨床診斷整合併進行統計分析。超過36％的慢性疾病患者（包括癌症和泌尿生殖系統，胃腸道，心血管和肌肉骨骼疾病）的總穀胱甘肽水平明顯低於對照組（P <.001）。缺乏症是由於GSH濃度低而不是GSSG引起的，與對照組相同。結論是，穀胱甘肽降低是慢性疾病的危險因素，可用於監測疾病的嚴重程度和進展。為了闡明作用機理，未來的工作是必要的。
End_電腦自動翻譯的內容_Y2020m05d04h03m21Rn6560_
PMID: 10811055 DOI: 10.1067/mlc.2000.105977
- - - - -- -- - -
--- --- - - --- ---
2020年4月25日 星期六
Low glutathione and glutathione S-transferase levels in Barrett’s esophagus as compared to normal esophageal epithelium; PY1999; Netherlands;_WJD_2020-0426_V001R01_IR94_
---
- - --- - - ---
2020-04-26
Low glutathione and glutathione S-transferase levels in Barrett’s esophagus as compared to normal esophageal epithelium; PY1999; Netherlands;_WJD_2020-0426_V001R01_IR94_RvD20200426_
Source (資訊來源):
https://www.ncbi.nlm.nih.gov/pubmed/10076569
Info cited on 2020-04-26-WD7 (資訊引用於 中華民國109年4月26日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
Jpn J Cancer Res. 1999 Jan;90(1):81-5.
Low glutathione and glutathione S-transferase levels in Barrett’s esophagus as compared to normal esophageal epithelium.
van Lieshout EM1, Tiemessen DM, Witteman BJ, Jansen JB, Peters WH.
Author information
1
Department of Gastroenterology and Hepatology, University Hospital St. Radboud, Nijmegen, The Netherlands.
Abstract
Patients with Barrett’s esophagus, wherein squamous epithelium has been replaced by columnar epithelium, have an increased risk for developing esophageal adenocarcinoma as compared to the general population. Glutathione S-transferase (GST), a family of detoxification enzymes consisting of class alpha, mu, pi, and theta isoforms, is involved in detoxification of carcinogens and low levels of these enzymes correlated with high cancer risk. We have now compared GST enzyme activity, GST isoenzyme composition and glutathione (GSH) content of Barrett’s mucosa with that of adjacent normal squamous epithelium. Biopsy specimens of 98 patients with Barrett’s esophagus were taken from both Barrett’s and adjacent normal squamous epithelium. GST enzyme activity towards 1-chloro-2,4-dinitrobenzene was measured, and GST isoenzyme levels were determined by densitometrical analyses of western blots after immunodetection with monoclonal antibodies. Total GSH content was determined by high-performance liquid chromatography after conjugation with monobromobimane. Wilcoxon’s signed rank test and Spearman correlation analyses were used for statistical evaluation. As compared with adjacent normal squamous epithelium, GST enzyme activity in Barrett’s epithelium was reduced by 35%, and GST mu, GST pi and GSH levels were reduced by 24%, 30%, and 63%, respectively. However, the minor GST alpha and GST theta levels were higher in Barrett’s epithelium (by 625% and 33%, respectively). High levels of GSH and GSTs in general are correlated with protection against cellular or cytogenetic damage. The observed reduction in GSTs and GSH in Barrett’s epithelium may therefore contribute to the increased cancer risk in this tissue.
Begin_電腦自動翻譯的內容_Y2020m04d26h08m01Rn5532_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
與普通人群相比，Barrett食管患者的鱗狀上皮已被柱狀上皮所代替，患食管腺癌的風險增加。穀胱甘肽S-轉移酶（GST）是由α，mu，pi和theta亞型組成的排毒酶家族，與致癌物的排毒有關，這些酶的水平低與癌症風險高相關。現在，我們比較了Barrett粘膜與鄰近正常鱗狀上皮的GST酶活性，GST同工酶組成和穀胱甘肽（GSH）含量。取自Barrett食管和鄰近正常鱗狀上皮的98例Barrett食管患者的活檢標本。測量了對1-氯-2,4-二硝基苯的GST酶活性，並在用單克隆抗體免疫檢測後通過western印蹟的光密度分析確定了GST同工酶水平。在與一溴二苯胺偶聯後，通過高效液相色譜法測定總GSH含量。Wilcoxon的符號秩檢驗和Spearman相關分析用於統計評估。與鄰近的正常鱗狀上皮相比，巴雷特上皮中的GST酶活性降低了35％，GST mu，GST pi和GSH含量分別降低了24％，30％和63％。但是，巴雷特上皮中的次要GSTα和GST theta水平較高（分別為625％和33％）。通常，高水平的GSH和GST與防止細胞或細胞遺傳學損害相關。因此，觀察到的Barrett上皮中GST和GSH的減少可能導致該組織中癌症風險的增加。
End_電腦自動翻譯的內容_Y2020m04d26h08m01Rn5532_
PMID:
10076569 PMCID: PMC5925975 DOI: 10.1111/j.1349-7006.1999.tb00669.x
[Indexed for MEDLINE] Free PMC Article
- - - - -- -- - -
--- --- - - --- ---
2020-04-26
Low glutathione and glutathione S-transferase levels in Barrett’s esophagus as compared to normal esophageal epithelium; PY1999; Netherlands;_WJD_2020-0426_V001R01_IR94_RvD20200426_
Source (資訊來源):
https://www.ncbi.nlm.nih.gov/pubmed/10076569
Info cited on 2020-04-26-WD7 (資訊引用於 中華民國109年4月26日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
Jpn J Cancer Res. 1999 Jan;90(1):81-5.
Low glutathione and glutathione S-transferase levels in Barrett’s esophagus as compared to normal esophageal epithelium.
van Lieshout EM1, Tiemessen DM, Witteman BJ, Jansen JB, Peters WH.
Author information
1
Department of Gastroenterology and Hepatology, University Hospital St. Radboud, Nijmegen, The Netherlands.
Abstract
Patients with Barrett’s esophagus, wherein squamous epithelium has been replaced by columnar epithelium, have an increased risk for developing esophageal adenocarcinoma as compared to the general population. Glutathione S-transferase (GST), a family of detoxification enzymes consisting of class alpha, mu, pi, and theta isoforms, is involved in detoxification of carcinogens and low levels of these enzymes correlated with high cancer risk. We have now compared GST enzyme activity, GST isoenzyme composition and glutathione (GSH) content of Barrett’s mucosa with that of adjacent normal squamous epithelium. Biopsy specimens of 98 patients with Barrett’s esophagus were taken from both Barrett’s and adjacent normal squamous epithelium. GST enzyme activity towards 1-chloro-2,4-dinitrobenzene was measured, and GST isoenzyme levels were determined by densitometrical analyses of western blots after immunodetection with monoclonal antibodies. Total GSH content was determined by high-performance liquid chromatography after conjugation with monobromobimane. Wilcoxon’s signed rank test and Spearman correlation analyses were used for statistical evaluation. As compared with adjacent normal squamous epithelium, GST enzyme activity in Barrett’s epithelium was reduced by 35%, and GST mu, GST pi and GSH levels were reduced by 24%, 30%, and 63%, respectively. However, the minor GST alpha and GST theta levels were higher in Barrett’s epithelium (by 625% and 33%, respectively). High levels of GSH and GSTs in general are correlated with protection against cellular or cytogenetic damage. The observed reduction in GSTs and GSH in Barrett’s epithelium may therefore contribute to the increased cancer risk in this tissue.
Begin_電腦自動翻譯的內容_Y2020m04d26h08m01Rn5532_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
與普通人群相比，Barrett食管患者的鱗狀上皮已被柱狀上皮所代替，患食管腺癌的風險增加。穀胱甘肽S-轉移酶（GST）是由α，mu，pi和theta亞型組成的排毒酶家族，與致癌物的排毒有關，這些酶的水平低與癌症風險高相關。現在，我們比較了Barrett粘膜與鄰近正常鱗狀上皮的GST酶活性，GST同工酶組成和穀胱甘肽（GSH）含量。取自Barrett食管和鄰近正常鱗狀上皮的98例Barrett食管患者的活檢標本。測量了對1-氯-2,4-二硝基苯的GST酶活性，並在用單克隆抗體免疫檢測後通過western印蹟的光密度分析確定了GST同工酶水平。在與一溴二苯胺偶聯後，通過高效液相色譜法測定總GSH含量。Wilcoxon的符號秩檢驗和Spearman相關分析用於統計評估。與鄰近的正常鱗狀上皮相比，巴雷特上皮中的GST酶活性降低了35％，GST mu，GST pi和GSH含量分別降低了24％，30％和63％。但是，巴雷特上皮中的次要GSTα和GST theta水平較高（分別為625％和33％）。通常，高水平的GSH和GST與防止細胞或細胞遺傳學損害相關。因此，觀察到的Barrett上皮中GST和GSH的減少可能導致該組織中癌症風險的增加。
End_電腦自動翻譯的內容_Y2020m04d26h08m01Rn5532_
[Indexed for MEDLINE] Free PMC Article
- - - - -- -- - -
--- --- - - --- ---
訂閱：
文章 (Atom)