UMR Physiologie des Adaptations Nutritionnelles, INRA, Université de Nantes, Nantes, France.
PLoS One. 2011;6(11):e27626. doi: 10.1371/journal.pone.0027626. Epub 2011 Nov 16.
Depletion of blood glutathione (GSH), a key antioxidant, is known to occur in preterm infants.
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.
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.
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.
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.
已知血液谷胱甘肽（GSH）耗竭，一种关键的抗氧化剂，发生在早产儿中。
我们的目的是确定：1）出生时是否存在 GSH 耗竭；2）它是否与半胱氨酸（cys）的可用性不足有关，cys 是 GSH 的限制前体，或者与合成 GSH 的能力下降有关。
招募了 16 名分娩极低出生体重儿（VLBW）的母亲和 16 名分娩健康足月新生儿的母亲。出生后立即从脐静脉、脐动脉和母亲的血液中获得红细胞，以评估 GSH[GSH]和半胱氨酸[cys]浓度，并通过使用气相色谱-质谱法测量从标记的半胱氨酸掺入 GSH 中体外分离的红细胞中 GSH 合成率。
与足月分娩的母亲相比，早产儿分娩的母亲红细胞[GSH]和[cys]明显较低，与足月新生儿相比，VLBW 婴儿的 GSH 和 cys 明显降低。母体和胎儿 GSH 和半胱氨酸水平之间存在很强的相关性。VLBW 婴儿的 GSH 合成能力与足月婴儿一样高。
目前的数据表明：1）VLBW 婴儿出生时存在 GSH 耗竭；2）由于 VLBW 新生儿具有完全活跃的合成谷胱甘肽的能力，这种耗竭可能是由于半胱氨酸可用性不足引起的，可能是由于母体耗竭所致。需要进一步研究以确定早产儿中母体-胎儿半胱氨酸转移是否减少，如果是这样，那么是否在早产儿有风险的母亲中补充半胱氨酸会增强早产儿的抗氧化防御能力。
