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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(Memo Item created on May 4, 2012 07:36 PM)
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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