2025-10-13
Repression of the antiporter SLC7A11/glutathione/glutathione
peroxidase 4 axis drives ferroptosis of vascular smooth muscle cells to
facilitate vascular calcification
Repression of the antiporter SLC7A11／glutathione／glutathione peroxidase 4 axis drives ferroptosis of
vascular smooth muscle cells to facilitate vascular calcification PY2022 IR95教材
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/36063875/
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
2025年10月12日 星期日
Melatonin as a Potent and Inducible Endogenous Antioxidant： Synthesis and Metabolism (褪黑激素作為強效且可誘導的內源性抗氧化劑：其合成與代謝) PY2015 Glutathione IR95教材
Melatonin as a Potent and Inducible Endogenous Antioxidant： Synthesis and Metabolism (褪黑激素作為強效且可誘導的內源性抗氧化劑：其合成與代謝)
PY2015 Glutathione IR95教材
Melatonin： the placental antioxidant and anti-inflammatory (褪黑激素：胎盤中的抗氧化與抗發炎因子) PY2024 IR95 Glutathione教材
2025-10-13
Melatonin: the placental antioxidant and anti-inflammatory
Melatonin： the placental antioxidant and anti-inflammatory (褪黑激素：胎盤中的抗氧化與抗發炎因子) PY2024 IR95 Glutathione教材
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/38361952/
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
Melatonin: the placental antioxidant and anti-inflammatory
Melatonin： the placental antioxidant and anti-inflammatory (褪黑激素：胎盤中的抗氧化與抗發炎因子) PY2024 IR95 Glutathione教材
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/38361952/
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
Choroid plexus glutathione peroxidases are instrumental in protecting the brain fluid environment from hydroperoxides during postnatal development
Choroid plexus glutathione peroxidases are instrumental in protecting the brain fluid environment from hydroperoxides during postnatal development
Glucose toxicity in beta-cells： type 2 diabetes, good radicals gone bad, and the glutathione connection PY2003 IR95 教材
--- - - --- - - ---
2025-10-13
Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection
Glucose toxicity in beta-cells： type 2 diabetes, good radicals gone bad, and the glutathione connection PY2003 IR95 教材
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/12606496/
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
Review Diabetes
. 2003 Mar;52(3):581-7. doi: 10.2337/diabetes.52.3.581.
Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection
R Paul Robertson 1, Jamie Harmon, Phuong Oanh Tran, Yoshito Tanaka, Hiroki Takahashi
Affiliations collapse
Affiliation
1Pacific Northwest Research Institute, 720 Broadway, Seattle, WA 98122, USA.
PMID: 12606496 DOI: 10.2337/diabetes.52.3.581
Abstract
Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over time, a process that is termed glucose toxicity. Our perspective about glucose toxicity as it pertains to the pancreatic beta-cell is that the characteristic decreases in insulin synthesis and secretion are caused by decreased insulin gene expression. The responsible metabolic lesion appears to involve a posttranscriptional defect in pancreas duodenum homeobox-1 (PDX-1) mRNA maturation. PDX-1 is a critically important transcription factor for the insulin promoter, is absent in glucotoxic islets, and, when transfected into glucotoxic beta-cells, improves insulin promoter activity. Because reactive oxygen species are produced via oxidative phosphorylation during anaerobic glycolysis, via the Schiff reaction during glycation, via glucose autoxidation, and via hexosamine metabolism under supraphysiological glucose concentrations, we hypothesize that chronic oxidative stress is an important mechanism for glucose toxicity. Support for this hypothesis is found in the observations that high glucose concentrations increase intraislet peroxide levels, that islets contain very low levels of antioxidant enzyme activities, and that adenoviral overexpression of antioxidant enzymes in vitro in islets, as well as exogenous treatment with antioxidants in vivo in animals, protect the islet from the toxic effects of excessive glucose levels. Clinically, consideration of antioxidants as adjunct therapy in type 2 diabetes is warranted because of the many reports of elevated markers of oxidative stress in patients with this disease, which is characterized by imperfect management of glycemia, consequent chronic hyperglycemia, and relentless deterioration of beta-cell function.
glucose toxicity
葡萄糖毒性
glucose toxicity (葡萄糖毒性)
葡萄糖毒性 (glucose toxicity)
Abstract
摘要
Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over time, a process that is termed glucose toxicity.
長期暴露於高血糖環境可導致細胞功能障礙，且此損傷可能隨時間而不可逆，這一過程被稱為葡萄糖毒性（glucose toxicity）。
Our perspective about glucose toxicity as it pertains to the pancreatic beta-cell is that the characteristic decreases in insulin synthesis and secretion are caused by decreased insulin gene expression.
我們對於葡萄糖毒性在胰臟 β 細胞中的看法是，其特徵性胰島素合成與分泌下降，主要是由胰島素基因表現降低所導致。
The responsible metabolic lesion appears to involve a posttranscriptional defect in pancreas duodenum homeobox-1 (PDX-1) mRNA maturation.
造成此現象的代謝異常似乎涉及胰臟十二指腸同源盒基因-1（pancreas duodenum homeobox-1，PDX-1）mRNA 成熟過程中的轉錄後缺陷。
PDX-1 is a critically important transcription factor for the insulin promoter, is absent in glucotoxic islets, and, when transfected into glucotoxic beta-cells, improves insulin promoter activity.
PDX-1 是調控胰島素啟動子的關鍵轉錄因子，在受到葡萄糖毒性影響的胰島中缺乏；然而，當其被轉染入葡萄糖毒性的 β 細胞中時，可恢復胰島素啟動子活性。
Because reactive oxygen species are produced via oxidative phosphorylation during anaerobic glycolysis, via the Schiff reaction during glycation, via glucose autoxidation, and via hexosamine metabolism under supraphysiological glucose concentrations, we hypothesize that chronic oxidative stress is an important mechanism for glucose toxicity.
由於在超出生理濃度的葡萄糖條件下，反應性氧化物（ROS）可經由厭氧糖解過程中的氧化磷酸化、糖化反應中的席夫反應（Schiff reaction）、葡萄糖自動氧化，以及己糖胺代謝途徑產生，因此我們推測慢性氧化壓力是葡萄糖毒性的主要機制之一。
Support for this hypothesis is found in the observations that high glucose concentrations increase intraislet peroxide levels, that islets contain very low levels of antioxidant enzyme activities, and that adenoviral overexpression of antioxidant enzymes in vitro in islets, as well as exogenous treatment with antioxidants in vivo in animals, protect the islet from the toxic effects of excessive glucose levels.
此假說的支持來自以下觀察結果：高葡萄糖濃度會提升胰島內過氧化物水平；胰島內抗氧化酵素活性極低；而在體外以腺病毒過表達抗氧化酵素的胰島模型，或在動物體內以外源性抗氧化劑處理時，皆能保護胰島免受過量葡萄糖的毒性影響。
Clinically, consideration of antioxidants as adjunct therapy in type 2 diabetes is warranted because of the many reports of elevated markers of oxidative stress in patients with this disease, which is characterized by imperfect management of glycemia, consequent chronic hyperglycemia, and relentless deterioration of beta-cell function.
在臨床上，考慮將抗氧化劑作為第二型糖尿病的輔助治療具有合理性，因為許多研究報告指出此類患者普遍存在氧化壓力標誌物升高的現象，而該疾病特徵為血糖控制不完全、慢性高血糖，以及 β 細胞功能持續惡化。
PubMed Disclaimer
Similar articles
Role of oxidative stress in pancreatic beta-cell dysfunction.
Kajimoto Y, Kaneto H.
Ann N Y Acad Sci. 2004 Apr;1011:168-76. doi: 10.1007/978-3-662-41088-2_17.
PMID: 15126294
Chronic oxidative stress as a mechanism for glucose toxicity of the beta cell in type 2 diabetes.
Robertson R, Zhou H, Zhang T, Harmon JS.
Cell Biochem Biophys. 2007;48(2-3):139-46. doi: 10.1007/s12013-007-0026-5.
PMID: 17709883
IPF1/PDX1 deficiency and beta-cell dysfunction in Psammomys obesus, an animal With type 2 diabetes.
Leibowitz G, Ferber S, Apelqvist A, Edlund H, Gross DJ, Cerasi E, Melloul D, Kaiser N.
Diabetes. 2001 Aug;50(8):1799-806. doi: 10.2337/diabetes.50.8.1799.
PMID: 11473041
Diabetes, glucose toxicity, and oxidative stress: A case of double jeopardy for the pancreatic islet beta cell.
Robertson RP, Harmon JS.
Free Radic Biol Med. 2006 Jul 15;41(2):177-84. doi: 10.1016/j.freeradbiomed.2005.04.030. Epub 2006 May 4.
PMID: 16814095Review.
Pancreatic Duodenal Homeobox (PDX-1) in health and disease.
Melloul D, Tsur A, Zangen D.
J Pediatr Endocrinol Metab. 2002 Nov-Dec;15(9):1461-72. doi: 10.1515/jpem.2002.15.9.1461.
PMID: 12503852Review.
See all similar articles
Cited by
Overexpression of the antioxidant enzyme catalase does not interfere with the glucose responsiveness of insulin-secreting INS-1E cells and rat islets.
Lortz S, Gurgul-Convey E, Naujok O, Lenzen S.
Diabetologia. 2013 Apr;56(4):774-82. doi: 10.1007/s00125-012-2823-7. Epub 2013 Jan 11.
PMID: 23306382
Glucose and glycogen in the diabetic kidney: Heroes or villains?
Sullivan MA, Forbes JM.
EBioMedicine. 2019 Sep;47:590-597. doi: 10.1016/j.ebiom.2019.07.067. Epub 2019 Aug 10.
PMID: 31405756Free PMC article.Review.
Delineating the role of FANCA in glucose-stimulated insulin secretion in β cells through its protein interactome.
Lagundžin D, Hu WF, Law HCH, Krieger KL, Qiao F, Clement EJ, Drincic AT, Nedić O, Naldrett MJ, Alvarez S, Woods NT.
PLoS One. 2019 Aug 28;14(8):e0220568. doi: 10.1371/journal.pone.0220568. eCollection 2019.
PMID: 31461451Free PMC article.
Oral administration of ginseng ameliorates cyclosporine-induced pancreatic injury in an experimental mouse model.
Lim SW, Doh KC, Jin L, Piao SG, Heo SB, Zheng YF, Bae SK, Chung BH, Yang CW.
PLoS One. 2013 Aug 29;8(8):e72685. doi: 10.1371/journal.pone.0072685. eCollection 2013.
PMID: 24009697Free PMC article.
Distinct Shift in Beta-Cell Glutaredoxin 5 Expression Is Mediated by Hypoxia and Lipotoxicity Both In Vivo and In Vitro.
Petry SF, Sun LM, Knapp A, Reinl S, Linn T.
Front Endocrinol (Lausanne). 2018 Mar 12;9:84. doi: 10.3389/fendo.2018.00084. eCollection 2018.
PMID: 29593651Free PMC article.
See all "Cited by" articles
Publication types
- - - - -- -- - -
--- --- - - --- ---
2025-10-13
Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection
Glucose toxicity in beta-cells： type 2 diabetes, good radicals gone bad, and the glutathione connection PY2003 IR95 教材
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/12606496/
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
Review Diabetes
. 2003 Mar;52(3):581-7. doi: 10.2337/diabetes.52.3.581.
Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection
R Paul Robertson 1, Jamie Harmon, Phuong Oanh Tran, Yoshito Tanaka, Hiroki Takahashi
Affiliations collapse
Affiliation
1Pacific Northwest Research Institute, 720 Broadway, Seattle, WA 98122, USA.
PMID: 12606496 DOI: 10.2337/diabetes.52.3.581
Abstract
Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over time, a process that is termed glucose toxicity. Our perspective about glucose toxicity as it pertains to the pancreatic beta-cell is that the characteristic decreases in insulin synthesis and secretion are caused by decreased insulin gene expression. The responsible metabolic lesion appears to involve a posttranscriptional defect in pancreas duodenum homeobox-1 (PDX-1) mRNA maturation. PDX-1 is a critically important transcription factor for the insulin promoter, is absent in glucotoxic islets, and, when transfected into glucotoxic beta-cells, improves insulin promoter activity. Because reactive oxygen species are produced via oxidative phosphorylation during anaerobic glycolysis, via the Schiff reaction during glycation, via glucose autoxidation, and via hexosamine metabolism under supraphysiological glucose concentrations, we hypothesize that chronic oxidative stress is an important mechanism for glucose toxicity. Support for this hypothesis is found in the observations that high glucose concentrations increase intraislet peroxide levels, that islets contain very low levels of antioxidant enzyme activities, and that adenoviral overexpression of antioxidant enzymes in vitro in islets, as well as exogenous treatment with antioxidants in vivo in animals, protect the islet from the toxic effects of excessive glucose levels. Clinically, consideration of antioxidants as adjunct therapy in type 2 diabetes is warranted because of the many reports of elevated markers of oxidative stress in patients with this disease, which is characterized by imperfect management of glycemia, consequent chronic hyperglycemia, and relentless deterioration of beta-cell function.
glucose toxicity
葡萄糖毒性
glucose toxicity (葡萄糖毒性)
葡萄糖毒性 (glucose toxicity)
Abstract
摘要
Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over time, a process that is termed glucose toxicity.
長期暴露於高血糖環境可導致細胞功能障礙，且此損傷可能隨時間而不可逆，這一過程被稱為葡萄糖毒性（glucose toxicity）。
Our perspective about glucose toxicity as it pertains to the pancreatic beta-cell is that the characteristic decreases in insulin synthesis and secretion are caused by decreased insulin gene expression.
我們對於葡萄糖毒性在胰臟 β 細胞中的看法是，其特徵性胰島素合成與分泌下降，主要是由胰島素基因表現降低所導致。
The responsible metabolic lesion appears to involve a posttranscriptional defect in pancreas duodenum homeobox-1 (PDX-1) mRNA maturation.
造成此現象的代謝異常似乎涉及胰臟十二指腸同源盒基因-1（pancreas duodenum homeobox-1，PDX-1）mRNA 成熟過程中的轉錄後缺陷。
PDX-1 is a critically important transcription factor for the insulin promoter, is absent in glucotoxic islets, and, when transfected into glucotoxic beta-cells, improves insulin promoter activity.
PDX-1 是調控胰島素啟動子的關鍵轉錄因子，在受到葡萄糖毒性影響的胰島中缺乏；然而，當其被轉染入葡萄糖毒性的 β 細胞中時，可恢復胰島素啟動子活性。
Because reactive oxygen species are produced via oxidative phosphorylation during anaerobic glycolysis, via the Schiff reaction during glycation, via glucose autoxidation, and via hexosamine metabolism under supraphysiological glucose concentrations, we hypothesize that chronic oxidative stress is an important mechanism for glucose toxicity.
由於在超出生理濃度的葡萄糖條件下，反應性氧化物（ROS）可經由厭氧糖解過程中的氧化磷酸化、糖化反應中的席夫反應（Schiff reaction）、葡萄糖自動氧化，以及己糖胺代謝途徑產生，因此我們推測慢性氧化壓力是葡萄糖毒性的主要機制之一。
Support for this hypothesis is found in the observations that high glucose concentrations increase intraislet peroxide levels, that islets contain very low levels of antioxidant enzyme activities, and that adenoviral overexpression of antioxidant enzymes in vitro in islets, as well as exogenous treatment with antioxidants in vivo in animals, protect the islet from the toxic effects of excessive glucose levels.
此假說的支持來自以下觀察結果：高葡萄糖濃度會提升胰島內過氧化物水平；胰島內抗氧化酵素活性極低；而在體外以腺病毒過表達抗氧化酵素的胰島模型，或在動物體內以外源性抗氧化劑處理時，皆能保護胰島免受過量葡萄糖的毒性影響。
Clinically, consideration of antioxidants as adjunct therapy in type 2 diabetes is warranted because of the many reports of elevated markers of oxidative stress in patients with this disease, which is characterized by imperfect management of glycemia, consequent chronic hyperglycemia, and relentless deterioration of beta-cell function.
在臨床上，考慮將抗氧化劑作為第二型糖尿病的輔助治療具有合理性，因為許多研究報告指出此類患者普遍存在氧化壓力標誌物升高的現象，而該疾病特徵為血糖控制不完全、慢性高血糖，以及 β 細胞功能持續惡化。
PubMed Disclaimer
Similar articles
Role of oxidative stress in pancreatic beta-cell dysfunction.
Kajimoto Y, Kaneto H.
Ann N Y Acad Sci. 2004 Apr;1011:168-76. doi: 10.1007/978-3-662-41088-2_17.
PMID: 15126294
Chronic oxidative stress as a mechanism for glucose toxicity of the beta cell in type 2 diabetes.
Robertson R, Zhou H, Zhang T, Harmon JS.
Cell Biochem Biophys. 2007;48(2-3):139-46. doi: 10.1007/s12013-007-0026-5.
PMID: 17709883
IPF1/PDX1 deficiency and beta-cell dysfunction in Psammomys obesus, an animal With type 2 diabetes.
Leibowitz G, Ferber S, Apelqvist A, Edlund H, Gross DJ, Cerasi E, Melloul D, Kaiser N.
Diabetes. 2001 Aug;50(8):1799-806. doi: 10.2337/diabetes.50.8.1799.
PMID: 11473041
Diabetes, glucose toxicity, and oxidative stress: A case of double jeopardy for the pancreatic islet beta cell.
Robertson RP, Harmon JS.
Free Radic Biol Med. 2006 Jul 15;41(2):177-84. doi: 10.1016/j.freeradbiomed.2005.04.030. Epub 2006 May 4.
PMID: 16814095Review.
Pancreatic Duodenal Homeobox (PDX-1) in health and disease.
Melloul D, Tsur A, Zangen D.
J Pediatr Endocrinol Metab. 2002 Nov-Dec;15(9):1461-72. doi: 10.1515/jpem.2002.15.9.1461.
PMID: 12503852Review.
See all similar articles
Cited by
Overexpression of the antioxidant enzyme catalase does not interfere with the glucose responsiveness of insulin-secreting INS-1E cells and rat islets.
Lortz S, Gurgul-Convey E, Naujok O, Lenzen S.
Diabetologia. 2013 Apr;56(4):774-82. doi: 10.1007/s00125-012-2823-7. Epub 2013 Jan 11.
PMID: 23306382
Glucose and glycogen in the diabetic kidney: Heroes or villains?
Sullivan MA, Forbes JM.
EBioMedicine. 2019 Sep;47:590-597. doi: 10.1016/j.ebiom.2019.07.067. Epub 2019 Aug 10.
PMID: 31405756Free PMC article.Review.
Delineating the role of FANCA in glucose-stimulated insulin secretion in β cells through its protein interactome.
Lagundžin D, Hu WF, Law HCH, Krieger KL, Qiao F, Clement EJ, Drincic AT, Nedić O, Naldrett MJ, Alvarez S, Woods NT.
PLoS One. 2019 Aug 28;14(8):e0220568. doi: 10.1371/journal.pone.0220568. eCollection 2019.
PMID: 31461451Free PMC article.
Oral administration of ginseng ameliorates cyclosporine-induced pancreatic injury in an experimental mouse model.
Lim SW, Doh KC, Jin L, Piao SG, Heo SB, Zheng YF, Bae SK, Chung BH, Yang CW.
PLoS One. 2013 Aug 29;8(8):e72685. doi: 10.1371/journal.pone.0072685. eCollection 2013.
PMID: 24009697Free PMC article.
Distinct Shift in Beta-Cell Glutaredoxin 5 Expression Is Mediated by Hypoxia and Lipotoxicity Both In Vivo and In Vitro.
Petry SF, Sun LM, Knapp A, Reinl S, Linn T.
Front Endocrinol (Lausanne). 2018 Mar 12;9:84. doi: 10.3389/fendo.2018.00084. eCollection 2018.
PMID: 29593651Free PMC article.
See all "Cited by" articles
Publication types
- - - - -- -- - -
--- --- - - --- ---
A role for glutathione peroxidase in protecting pancreatic beta cells against oxidative stress in a model of glucose toxicity PY2002教材 IR95 穀胱甘肽過氧化酶，葡萄糖毒性，胰臟β細胞，氧化壓力
A
role for glutathione peroxidase in protecting pancreatic beta cells against
oxidative stress in a model of glucose toxicity
穀胱甘肽過氧化酶在葡萄糖毒性模型中保護胰臟β細胞免受氧化壓力損傷的作用
A role for glutathione peroxidase in protecting pancreatic beta cells against oxidative stress in a model of glucose toxicity PY2002教材 IR95 穀胱甘肽過氧化酶，葡萄糖毒性，胰臟β細胞，氧化壓力
Source or References (資訊來源或是參考的資訊):
https://www.pnas.org/doi/10.1073/pnas.192445199
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/12218186/
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
穀胱甘肽過氧化酶在葡萄糖毒性模型中保護胰臟β細胞免受氧化壓力損傷的作用
A role for glutathione peroxidase in protecting pancreatic beta cells against oxidative stress in a model of glucose toxicity PY2002教材 IR95 穀胱甘肽過氧化酶，葡萄糖毒性，胰臟β細胞，氧化壓力
Source or References (資訊來源或是參考的資訊):
https://www.pnas.org/doi/10.1073/pnas.192445199
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/12218186/
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
The glutathione-dependent neuroprotective activity of the blood-CSF barrier is inducible through the Nrf2 signaling pathway during postnatal development; PY2025; France (法國);_IR95教材_
The
glutathione-dependent neuroprotective activity of the blood-CSF barrier is
inducible through the Nrf2 signaling pathway during postnatal development
在出生後的發育期間，血液－腦脊髓液屏障的穀胱甘肽依賴性神經保護活性可經由 Nrf2 訊號傳導途徑誘導產生
Source or References (資訊來源或是參考的資訊):
https://pmc.ncbi.nlm.nih.gov/articles/PMC11846383/
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
在出生後的發育期間，血液－腦脊髓液屏障的穀胱甘肽依賴性神經保護活性可經由 Nrf2 訊號傳導途徑誘導產生
Source or References (資訊來源或是參考的資訊):
https://pmc.ncbi.nlm.nih.gov/articles/PMC11846383/
Info cited on 2025-10-13-WD1 (資訊引用於 中華民國114年西元2025年10月13日) by 湯偉晉 (WeiJin Tang)
#
2025年10月4日 星期六
Advanced Age and Neurotrauma Diminish Glutathione and Impair Antioxidant Defense after Spinal Cord Injury 高齡與神經性創傷在脊髓損傷後會降低穀胱甘肽含量並削弱抗氧化防禦機制
2025-10-04
Advanced Age and Neurotrauma Diminish Glutathione and Impair Antioxidant Defense after Spinal Cord Injury; PY2022; USA (美國); IR95 Glutathione, 教材
Advanced Age and Neurotrauma Diminish Glutathione and Impair Antioxidant Defense after Spinal Cord Injury
高齡與神經性創傷在脊髓損傷後會降低穀胱甘肽含量並削弱抗氧化防禦機制
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/35373589/
Info cited on 2025-10-04-WD6 (資訊引用於 中華民國114年西元2025年10月4日) by 湯偉晉 (WeiJin Tang)
#
Advanced Age and Neurotrauma Diminish Glutathione and Impair Antioxidant Defense after Spinal Cord Injury; PY2022; USA (美國); IR95 Glutathione, 教材
Advanced Age and Neurotrauma Diminish Glutathione and Impair Antioxidant Defense after Spinal Cord Injury
高齡與神經性創傷在脊髓損傷後會降低穀胱甘肽含量並削弱抗氧化防禦機制
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/35373589/
Info cited on 2025-10-04-WD6 (資訊引用於 中華民國114年西元2025年10月4日) by 湯偉晉 (WeiJin Tang)
#
Continuous intravenous infusion of ATP in humans yields large expansions of erythrocyte ATP pools but extracellular ATP pools are elevated only at the start followed by rapid declines; PY2015; USA (美國);_IR94_
2025-10-04
Continuous intravenous infusion of ATP in humans yields large expansions of erythrocyte ATP pools but extracellular ATP pools are elevated only at the start followed by rapid declines
Source or References (資訊來源或是參考的資訊):
https://pmc.ncbi.nlm.nih.gov/articles/PMC4425716/
Info cited on 2025-10-04-WD6 (資訊引用於 中華民國114年西元2025年10月4日) by 湯偉晉 (WeiJin Tang)
#
Continuous intravenous infusion of ATP in humans yields large expansions of erythrocyte ATP pools but extracellular ATP pools are elevated only at the start followed by rapid declines
Source or References (資訊來源或是參考的資訊):
https://pmc.ncbi.nlm.nih.gov/articles/PMC4425716/
Info cited on 2025-10-04-WD6 (資訊引用於 中華民國114年西元2025年10月4日) by 湯偉晉 (WeiJin Tang)
#
Intravenous ATP infusions can be safely administered in the home setting: a study in pre-terminal cancer patients; PY2007; IR94
2025-10-04
Intravenous ATP infusions can be safely administered in the home setting: a study in pre-terminal cancer patients; PY2007; IR94
Source or References (資訊來源或是參考的資訊):
https://pmc.ncbi.nlm.nih.gov/articles/PMC2039853/
Info cited on 2025-10-04-WD6 (資訊引用於 中華民國114年西元2025年10月4日) by 湯偉晉 (WeiJin Tang)
#
Intravenous ATP infusions can be safely administered in the home setting: a study in pre-terminal cancer patients; PY2007; IR94
Source or References (資訊來源或是參考的資訊):
https://pmc.ncbi.nlm.nih.gov/articles/PMC2039853/
Info cited on 2025-10-04-WD6 (資訊引用於 中華民國114年西元2025年10月4日) by 湯偉晉 (WeiJin Tang)
#
Pharmacokinetics of intravenous ATP in cancer patients; PY2000_IR94, Glutathione
Pharmacokinetics
of intravenous ATP in cancer patients; PY2000_IR94, Glutathione
--- - - --- - - ---
2025-10-04
Pharmacokinetics of intravenous ATP in cancer patients; PY2000_IR94, Glutathione
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/10853877/
Info cited on 2025-10-04-WD6 (資訊引用於 中華民國114年西元2025年10月4日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
Clinical Trial Eur J Clin Pharmacol
. 2000 Apr;56(1):49-55. doi: 10.1007/s002280050719.
Pharmacokinetics of intravenous ATP in cancer patients
Pharmacokinetics of intravenous ATP in cancer patients
Pharmacokinetics of intravenous ATP in cancer patients
H J Agteresch 1, P C Dagnelie, T Rietveld, J W van den Berg, A H Danser, J H Wilson
Affiliations collapse
Affiliation
1Department of Internal Medicine, Erasmus University Medical Centre Rotterdam, The Netherlands.
PMID: 10853877 DOI: 10.1007/s002280050719
Abstract
Objective: To characterise the pharmacokinetics of adenosine 5'-triphosphate (ATP) in patients with lung cancer after i.v. administration of different ATP dosages.
Methods: Twenty-eight patients received a total of 176 i.v. ATP courses of 30 h. Fifty-two infusions were given as low-dose infusions of 25-40 microg kg(-1) min(-1), 47 as middle-dose infusions of 45-60 microg kg(-1) min(-1) and 77 as high-dose infusions of 65-75 microg kg(-1) min(-1) ATP. Kinetic data of ATP concentrations in erythrocytes were available from 124 ATP courses. Results are expressed as mean +/- SEM.
Results: Most ATP courses in cancer patients were without side effects (64%), and side effects occurring in the remaining courses were mild and transient, resolving within minutes after decreasing the infusion rate. Baseline ATP concentration in erythrocytes was 1,554 +/- 51 micromol l(-1). ATP plateau levels at 24 h were significantly increased by 53 +/- 3, 56 +/- 3 and 69 +/- 2% after low-dose, middle-dose and high-dose ATP infusions, respectively. At the same time, significant increases in plasma uric acid concentrations were observed: 0.06 +/- 0.01, 0.11 +/- 0.01 and 0.16 +/- 0.01 mmol l(-1), respectively. The mean half-time for disappearance of ATP from erythrocytes, measured in five patients, was 5.9 +/- 0.5 h.
Conclusions: During constant i.v. infusion of ATP in lung cancer patients, ATP is taken up by erythrocytes and reaches dose-dependent plateau levels 50-70% above basal concentrations at approximately 24 h.
PubMed Disclaimer
Similar articles
Continuous intravenous infusion of ATP in humans yields large expansions of erythrocyte ATP pools but extracellular ATP pools are elevated only at the start followed by rapid declines.
Rapaport E, Salikhova A, Abraham EH.
Purinergic Signal. 2015 Jun;11(2):251-62. doi: 10.1007/s11302-015-9450-y. Epub 2015 Apr 29.
PMID: 25917594Free PMC article.Clinical Trial.
Effects of ATP infusion on glucose turnover and gluconeogenesis in patients with advanced non-small-cell lung cancer.
Agteresch HJ, Leij-Halfwerk S, Van Den Berg JW, Hordijk-Luijk CH, Wilson JH, Dagnelie PC.
Clin Sci (Lond). 2000 Jun;98(6):689-95.
PMID: 10814606Clinical Trial.
Intravenous ATP infusions can be safely administered in the home setting: a study in pre-terminal cancer patients.
Beijer S, Gielisse EA, Hupperets PS, van den Borne BE, van den Beuken-van Everdingen M, Nijziel MR, van Henten AM, Dagnelie PC.
Invest New Drugs. 2007 Dec;25(6):571-9. doi: 10.1007/s10637-007-9076-1. Epub 2007 Sep 5.
PMID: 17786387Free PMC article.Clinical Trial.
Adenosine triphosphate infusion increases liver energy status in advanced lung cancer patients: an in vivo 31P magnetic resonance spectroscopy study.
Leij-Halfwerk S, Agteresch HJ, Sijens PE, Dagnelie PC.
Hepatology. 2002 Feb;35(2):421-4. doi: 10.1053/jhep.2002.31318.
PMID: 11826418
[Oral vinorelbine: pharmacology and treatment outcome in non-small cell bronchial carcinoma and breast carcinoma].
Bartsch V.
Onkologie. 2006 Mar;29 Suppl 1:1-28. doi: 10.1159/000091889. Epub 2006 Mar 3.
PMID: 16534241Review.German.
See all similar articles
Cited by
Intravenous administration of adenosine triphosphate combined with escitalopram in major depressive disorder: protocol for a randomised, double-blind, placebo-controlled trial.
Xin Q, Wei H, Paudel D, Hu N, Zhao Y, Feng Y, Luo X, Su M, Xue X, Huang H, Lv Z, Tang C, Zhao Y, Tan M, Luo X, Yang Y, Liu Q, Huang M, Cheng Y, Gao T, Zhang B.
BMJ Open. 2025 Aug 28;15(8):e098281. doi: 10.1136/bmjopen-2024-098281.
PMID: 40876882Free PMC article.
Intravenous administration of adenosine triphosphate and phosphocreatine combined with fluoxetine in major depressive disorder: protocol for a randomized, double-blind, placebo-controlled pilot study.
Chen Y, Cao X, Zang W, Tan S, Ou CQ, Shen X, Gao T, Zhao L.
Trials. 2019 Jan 9;20(1):34. doi: 10.1186/s13063-018-3115-4.
PMID: 30626424Free PMC article.
Application of adenosine 5'-triphosphate (ATP) infusions in palliative home care: design of a randomized clinical trial.
Beijer S, van Rossum E, Hupperets PS, Spreeuwenberg C, van den Beuken M, Winkens RA, Ars L, van den Borne BE, de Graeff A, Dagnelie PC.
BMC Public Health. 2007 Jan 8;7:4. doi: 10.1186/1471-2458-7-4.
PMID: 17210069Free PMC article.
The therapeutic potential of adenosine triphosphate as an immune modulator in the treatment of HIV/AIDS: a combination approach with HAART.
Wagner MC.
Curr HIV Res. 2011 Jun;9(4):209-22. doi: 10.2174/157016211796320289.
PMID: 21675943Free PMC article.
The pathophysiology of cancer-related fatigue: current controversies.
O'Higgins CM, Brady B, O'Connor B, Walsh D, Reilly RB.
Support Care Cancer. 2018 Oct;26(10):3353-3364. doi: 10.1007/s00520-018-4318-7. Epub 2018 Jun 30.
PMID: 29961146Review.
See all "Cited by" articles
- - - - -- -- - -
--- --- - - --- ---
--- - - --- - - ---
2025-10-04
Pharmacokinetics of intravenous ATP in cancer patients; PY2000_IR94, Glutathione
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/10853877/
Info cited on 2025-10-04-WD6 (資訊引用於 中華民國114年西元2025年10月4日) by 湯偉晉 (WeiJin Tang)
#
- - - - - - - -
Clinical Trial Eur J Clin Pharmacol
. 2000 Apr;56(1):49-55. doi: 10.1007/s002280050719.
Pharmacokinetics of intravenous ATP in cancer patients
Pharmacokinetics of intravenous ATP in cancer patients
Pharmacokinetics of intravenous ATP in cancer patients
H J Agteresch 1, P C Dagnelie, T Rietveld, J W van den Berg, A H Danser, J H Wilson
Affiliations collapse
Affiliation
1Department of Internal Medicine, Erasmus University Medical Centre Rotterdam, The Netherlands.
PMID: 10853877 DOI: 10.1007/s002280050719
Abstract
Objective: To characterise the pharmacokinetics of adenosine 5'-triphosphate (ATP) in patients with lung cancer after i.v. administration of different ATP dosages.
Methods: Twenty-eight patients received a total of 176 i.v. ATP courses of 30 h. Fifty-two infusions were given as low-dose infusions of 25-40 microg kg(-1) min(-1), 47 as middle-dose infusions of 45-60 microg kg(-1) min(-1) and 77 as high-dose infusions of 65-75 microg kg(-1) min(-1) ATP. Kinetic data of ATP concentrations in erythrocytes were available from 124 ATP courses. Results are expressed as mean +/- SEM.
Results: Most ATP courses in cancer patients were without side effects (64%), and side effects occurring in the remaining courses were mild and transient, resolving within minutes after decreasing the infusion rate. Baseline ATP concentration in erythrocytes was 1,554 +/- 51 micromol l(-1). ATP plateau levels at 24 h were significantly increased by 53 +/- 3, 56 +/- 3 and 69 +/- 2% after low-dose, middle-dose and high-dose ATP infusions, respectively. At the same time, significant increases in plasma uric acid concentrations were observed: 0.06 +/- 0.01, 0.11 +/- 0.01 and 0.16 +/- 0.01 mmol l(-1), respectively. The mean half-time for disappearance of ATP from erythrocytes, measured in five patients, was 5.9 +/- 0.5 h.
Conclusions: During constant i.v. infusion of ATP in lung cancer patients, ATP is taken up by erythrocytes and reaches dose-dependent plateau levels 50-70% above basal concentrations at approximately 24 h.
PubMed Disclaimer
Similar articles
Continuous intravenous infusion of ATP in humans yields large expansions of erythrocyte ATP pools but extracellular ATP pools are elevated only at the start followed by rapid declines.
Rapaport E, Salikhova A, Abraham EH.
Purinergic Signal. 2015 Jun;11(2):251-62. doi: 10.1007/s11302-015-9450-y. Epub 2015 Apr 29.
PMID: 25917594Free PMC article.Clinical Trial.
Effects of ATP infusion on glucose turnover and gluconeogenesis in patients with advanced non-small-cell lung cancer.
Agteresch HJ, Leij-Halfwerk S, Van Den Berg JW, Hordijk-Luijk CH, Wilson JH, Dagnelie PC.
Clin Sci (Lond). 2000 Jun;98(6):689-95.
PMID: 10814606Clinical Trial.
Intravenous ATP infusions can be safely administered in the home setting: a study in pre-terminal cancer patients.
Beijer S, Gielisse EA, Hupperets PS, van den Borne BE, van den Beuken-van Everdingen M, Nijziel MR, van Henten AM, Dagnelie PC.
Invest New Drugs. 2007 Dec;25(6):571-9. doi: 10.1007/s10637-007-9076-1. Epub 2007 Sep 5.
PMID: 17786387Free PMC article.Clinical Trial.
Adenosine triphosphate infusion increases liver energy status in advanced lung cancer patients: an in vivo 31P magnetic resonance spectroscopy study.
Leij-Halfwerk S, Agteresch HJ, Sijens PE, Dagnelie PC.
Hepatology. 2002 Feb;35(2):421-4. doi: 10.1053/jhep.2002.31318.
PMID: 11826418
[Oral vinorelbine: pharmacology and treatment outcome in non-small cell bronchial carcinoma and breast carcinoma].
Bartsch V.
Onkologie. 2006 Mar;29 Suppl 1:1-28. doi: 10.1159/000091889. Epub 2006 Mar 3.
PMID: 16534241Review.German.
See all similar articles
Cited by
Intravenous administration of adenosine triphosphate combined with escitalopram in major depressive disorder: protocol for a randomised, double-blind, placebo-controlled trial.
Xin Q, Wei H, Paudel D, Hu N, Zhao Y, Feng Y, Luo X, Su M, Xue X, Huang H, Lv Z, Tang C, Zhao Y, Tan M, Luo X, Yang Y, Liu Q, Huang M, Cheng Y, Gao T, Zhang B.
BMJ Open. 2025 Aug 28;15(8):e098281. doi: 10.1136/bmjopen-2024-098281.
PMID: 40876882Free PMC article.
Intravenous administration of adenosine triphosphate and phosphocreatine combined with fluoxetine in major depressive disorder: protocol for a randomized, double-blind, placebo-controlled pilot study.
Chen Y, Cao X, Zang W, Tan S, Ou CQ, Shen X, Gao T, Zhao L.
Trials. 2019 Jan 9;20(1):34. doi: 10.1186/s13063-018-3115-4.
PMID: 30626424Free PMC article.
Application of adenosine 5'-triphosphate (ATP) infusions in palliative home care: design of a randomized clinical trial.
Beijer S, van Rossum E, Hupperets PS, Spreeuwenberg C, van den Beuken M, Winkens RA, Ars L, van den Borne BE, de Graeff A, Dagnelie PC.
BMC Public Health. 2007 Jan 8;7:4. doi: 10.1186/1471-2458-7-4.
PMID: 17210069Free PMC article.
The therapeutic potential of adenosine triphosphate as an immune modulator in the treatment of HIV/AIDS: a combination approach with HAART.
Wagner MC.
Curr HIV Res. 2011 Jun;9(4):209-22. doi: 10.2174/157016211796320289.
PMID: 21675943Free PMC article.
The pathophysiology of cancer-related fatigue: current controversies.
O'Higgins CM, Brady B, O'Connor B, Walsh D, Reilly RB.
Support Care Cancer. 2018 Oct;26(10):3353-3364. doi: 10.1007/s00520-018-4318-7. Epub 2018 Jun 30.
PMID: 29961146Review.
See all "Cited by" articles
- - - - -- -- - -
--- --- - - --- ---
訂閱：
文章 (Atom)