Comparative Biochemistry and Metabolism; Part II - Naphthalene Lung Toxicity [1981](IR92); FNKWs{glutathione, depletion, covalent bonding};_資訊來源_dtic.mil

September 10, 2012; 08:43:17 p.m. Taipei Time

 

Comparative Biochemistry and Metabolism - Part 2 - Naphthalene Lung Toxicity [1981](IR91); FNKWs{covalent binding and glutathione depletion} (15_of_15).png

Comparative Biochemistry and Metabolism; Part II - Naphthalene Lung Toxicity [1981](IR92); FNKWs{glutathione, depletion, covalent bonding};_資訊來源_dtic.mil.png

Comparative Biochemistry and Metabolism; Part II - Naphthalene Lung Toxicity [1981](IR92); FNKWs{glutathione, depletion, covalent bonding};_資訊來源_dtic.mil_F02.png

Chronic oxidative stress compromises telomere integrity and accelerates the onset of senescence in human endothelial cells [2004](IR92) 01.png

Chronic oxidative stress compromises telomere integrity and accelerates the onset of senescence in human endothelial cells [2004](IR92) 01.png

Chronic oxidative stress compromises telomere integrity and accelerates the onset of senescence in human endothelial cells [2004](IR92) 02.png

Superoxide Dismutase in Redox Biology - The roles of superoxide and hydrogen peroxide [2011](IR93) - Ascorbate is the terminal, water-soluble, small-molecule antioxidant.png

Superoxide Dismutase in Redox Biology - The roles of superoxide and hydrogen peroxide [2011](IR93).png

Douglas Tang (湯傑堯) - 為什麼人會得癌症 [2012-05-22].jpg

May 23, 2012; 08:19:57 p.m. Taipei Time

Douglas Tang (湯傑堯) - 為什麼人會得癌症 [2012-05-22].jpg

Keywords: 

Why people get cancers?

Douglas Tang (湯傑堯) and WeiJin Tang (湯偉晉) are good partners (好夥伴, 好的合作夥伴). 

Cord blood glutathione depletion in preterm infants - correlation with maternal cysteine depletion. [2011](IR92); 在早產兒臍帶血中的 穀胱甘肽(glutathione) 之耗竭 – 與母親體內的 半胱胺酸(cysteine) 的耗竭有關

Cord blood glutathione depletion in preterm infants - correlation with maternal cysteine depletion. [2011](IR92)

在早產兒臍帶血中的 穀胱甘肽(glutathione) 之耗竭 – 與母親體內的 半胱胺酸(cysteine) 的耗竭有關

在早產兒臍帶血中的 穀胱甘肽(glutathione) 之耗竭 – 與產婦體內的 半胱胺酸(cysteine) 的耗竭有關

在早產兒臍帶血中的穀胱甘肽(glutathione)之耗竭 – 與母親體內的(產婦體內的)半胱胺酸(cysteine) 的耗竭有關

cysteine
【生物化學】半胱胺酸

Cord blood glutathione depletion in preterm infants: correlation with maternal cysteine depletion. [2011](IR92)

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Cord blood glutathione depletion in preterm infants: correlation with maternal cysteine depletion. [2011](IR92)

http://www.ncbi.nlm.nih.gov/pubmed/22110699

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0027626
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PLoS One. 2011;6(11):e27626. Epub 2011 Nov 16.
Cord blood glutathione depletion in preterm infants: correlation with maternal cysteine depletion.
Küster A, Tea I, Ferchaud-Roucher V, Le Borgne S, Plouzennec C, Winer N, Rozé JC, Robins RJ, Darmaun D.
Source
UMR Physiologie des Adaptations Nutritionnelles, INRA, Université de Nantes, Nantes, France.

Abstract
BACKGROUND:
Depletion of blood glutathione (GSH), a key antioxidant, is known to occur in preterm infants.

OBJECTIVE:
Our aim was to determine: 1) whether GSH depletion is present at the time of birth; and 2) whether it is associated with insufficient availability of cysteine (cys), the limiting GSH precursor, or a decreased capacity to synthesize GSH.

METHODOLOGY:
Sixteen mothers delivering very low birth weight infants (VLBW), and 16 mothers delivering healthy, full term neonates were enrolled. Immediately after birth, erythrocytes from umbilical vein, umbilical artery, and maternal blood were obtained to assess GSH [GSH] and cysteine [cys] concentrations, and the GSH synthesis rate was determined from the incorporation of labeled cysteine into GSH in isolated erythrocytes ex vivo, measured using gas chromatography mass spectrometry.

PRINCIPAL FINDINGS:
Compared with mothers delivering at full term, mothers delivering prematurely had markedly lower erythrocyte [GSH] and [cys] and these were significantly depressed in VLBW infants, compared with term neonates. A strong correlation was found between maternal and fetal GSH and cysteine levels. The capacity to synthesize GSH was as high in VLBW as in term infants.

CONCLUSION:
The current data demonstrate that: 1) GSH depletion is present at the time of birth in VLBW infants; 2) As VLBW neonates possess a fully active capacity to synthesize glutathione, the depletion may arise from inadequate cysteine availability, potentially due to maternal depletion. Further studies would be needed to determine whether maternal-fetal cysteine transfer is decreased in preterm infants, and, if so, whether cysteine supplementation of mothers at risk of delivering prematurely would strengthen antioxidant defense in preterm neonates.

PMID: 22110699 [PubMed - indexed for MEDLINE] PMCID: PMC3217996 Free PMC Article
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Glutathione Reductase Facilitates Host Defense by Sustaining Phagocytic Oxidative Burst and Promoting the Development of Neutrophil Extracellular Traps [2012](IR93)

May 12, 2012; 02:02:44 p.m. Taipei Time

Glutathione Reductase Facilitates Host Defense by Sustaining Phagocytic Oxidative Burst and Promoting the Development of Neutrophil Extracellular Traps [2012](IR93).png

The pivotal role of glutathione reductase in host defense against Gram-negative bacteria [2011](IR92).png

The nature of antioxidant defense mechanisms: a lesson from transgenic studies. [1998](IR91)

The nature of antioxidant defense mechanisms: a lesson from transgenic studies. [1998](IR91)

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(Memo Item created on December 17, 2011 01:41 PM)
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The nature of antioxidant defense mechanisms: a lesson from transgenic studies.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533365/
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Environ Health Perspect. 1998 October; 106(Suppl 5): 1219–1228.
PMCID: PMC1533365
Copyright notice

Research Article

The nature of antioxidant defense mechanisms: a lesson from transgenic studies.

Y S Ho, J L Magnenat, M Gargano, and J Cao
Institute of Chemical Toxicology, Wayne State University, Detroit, MI 48201, USA. yho@wayne.edu

Abstract
Reactive oxygen species (ROS) have been implicated in the pathogenesis of many clinical disorders such as adult respiratory distress syndrome, ischemia-reperfusion injury, atherosclerosis, neurodegenerative diseases, and cancer. Genetically engineered animal models have been used as a tool for understanding the function of various antioxidant enzymes in cellular defense mechanisms against various types of oxidant tissue injury. Transgenic mice overexpressing three isoforms of superoxide dismutase, catalase, and the cellular glutathione peroxidase (GSHPx-1) in various tissues show an increased tolerance to ischemia-reperfusion heart and brain injury, hyperoxia, cold-induced brain edema, adriamycin, and paraquat toxicity. These results have provided for the first time direct evidence demonstrating the importance of each of these antioxidant enzymes in protecting the animals against the injury resulting from these insults, as well as the effect of an enhanced level of antioxidant in ameliorating the oxidant tissue injury. To evaluate further the nature of these enzymes in antioxidant defense, gene knockout mice deficient in copper-zinc superoxide dismutase (CuZnSOD) and GSHPx-1 have also been generated in our laboratory. These mice developed normally and showed no marked pathologic changes under normal physiologic conditions. In addition, a deficiency in these genes had no effects on animal survival under hyperoxida. However, these knockout mice exhibited a pronounced susceptibility to paraquat toxicity and myocardial ischemia-reperfusion injury. Furthermore, female mice lacking CuZnSOD also displayed a marked increase in postimplantation embryonic lethality. These animals should provide a useful model for uncovering the identity of ROS that participate in the pathogenesis of various clinical disorders and for defining the role of each antioxidant enzyme in cellular defense against oxidant-mediated tissue injury.
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(Memo Item created on December 17, 2011 01:47 PM)
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English to Chinese translation of some medical terms relevant to this paper
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ischemia-reperfusion injury

ischemia
【醫學】局部缺血

reperfusion
再灌注

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The central role of glutathione in the pathophysiology of human diseases [2007](IR91)

The central role of glutathione in the pathophysiology of human diseases.[2007](IR91)

The central role of glutathione in the pathophysiology of human diseases.[2007](IR91)

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(Memo Item created on November 19, 2011 01:48 PM)
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The central role of glutathione in the pathophysiology of human diseases.

http://www.ncbi.nlm.nih.gov/pubmed/18158646
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Arch Physiol Biochem. 2007 Oct-Dec;113(4-5):234-58.

The central role of glutathione in the pathophysiology of human diseases.

Franco R, Schoneveld OJ, Pappa A, Panayiotidis MI.

Source
Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA.

Abstract
Reduced glutathione (L-gamma-glutamyl-L-cysteinyl-glycine, GSH) is the prevalent low-molecular-weight thiol in mammalian cells. It is formed in a two-step enzymatic process including, first, the formation of gamma-glutamylcysteine from glutamate and cysteine, by the activity of the gamma-glutamylcysteine synthetase; and second, the formation of GSH by the activity of GSH synthetase which uses gamma-glutamylcysteine and glycine as substrates. While its synthesis and metabolism occur intracellularly, its catabolism occurs extracellularly by a series of enzymatic and plasma membrane transport steps. Glutathione metabolism and transport participates in many cellular reactions including: antioxidant defense of the cell, drug detoxification and cell signaling (involved in the regulation of gene expression, apoptosis and cell proliferation). Alterations in its concentration have also been demonstrated to be a common feature of many pathological conditions including diabetes, cancer, AIDS, neurodegenerative and liver diseases. Additionally, GSH catabolism has been recently reported to modulate redox-sensitive components of signal transduction cascades. In this manuscript, we review the current state of knowledge on the role of GSH in the pathogenesis of human diseases with the aim to underscore its relevance in translational research for future therapeutic treatment design.

PMID: 18158646 [PubMed - indexed for MEDLINE]
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