Collard Keith, White Desley, Copplestone Adrian
University of Plymouth, School of Health Professions, Plymouth, United Kingdom.
Department of Haematology, Derriford Hospital, Plymouth, United Kingdom.
Blood Transfus. 2014 Apr;12(2):210-9. doi: 10.2450/2013.0142-13. Epub 2013 Nov 29.
Receipt of blood transfusions is associated with the major consequences of prematurity such as bronchopulmonary dysplasia. Transfusion-mediated (iron-induced) oxidative damage, coupled with the limited ability of the premature baby to deal with enhanced iron and oxidative load may contribute to this. Adverse effects of transfusion may be related to duration of storage. This study examined the influence of storage on iron and oxidative status in paediatric packed red blood cell units.
Paediatric packed red blood cell units were sampled 3 days post-donation, then at 7 days and weekly until day 35. The extracellular medium was separated and the following measured: total iron concentration, total iron binding capacity, non-transferrin-bound iron, haemoglobin, total and reduced ascorbate, glutathione and malondialdehyde.
Measurable total and non-transferrin bound iron were present in the extracellular fluid of paediatric packs on day 3. Both parameters rose almost linearly to maximal values at 35 days. Haemoglobin and malondialdehyde levels rose gradually from day 3 to day 21, then more steeply to day 35. Ascorbate existed mainly in the oxidised form and fell rapidly towards the end of storage. Intracellular GSH fell throughout the period of storage. Strong correlations existed between biomarkers of oxidative damage and iron parameters.
These data suggest that iron released following the initial preparation of packed red blood cell units may derive from free radical-mediated oxidative damage to the red blood cells and haemoglobin, rather than from extracellular haemoglobin. Iron continues to be released during storage as antioxidant protection declines. A cycle of free radical-mediated damage may initiate and then further exacerbate iron release during storage which, in turn, may mediate further free radical-mediated cellular damage. The potential consequences to recipients of older stored blood may be significant.
输血与早产的主要后果如支气管肺发育不良有关。输血介导的(铁诱导的)氧化损伤,加上早产婴儿处理增加的铁和氧化负荷的能力有限,可能是其原因之一。输血的不良反应可能与储存时间有关。本研究探讨了储存对儿科浓缩红细胞单位中铁和氧化状态的影响。
儿科浓缩红细胞单位在献血后3天取样,然后在第7天及之后每周取样一次,直至第35天。分离细胞外培养基并测量以下指标:总铁浓度、总铁结合能力、非转铁蛋白结合铁、血红蛋白、总抗坏血酸和还原型抗坏血酸、谷胱甘肽和丙二醛。
第3天时,儿科血袋的细胞外液中存在可测量的总铁和非转铁蛋白结合铁。两个参数几乎呈线性上升,在35天时达到最大值。血红蛋白和丙二醛水平从第3天到第21天逐渐上升,然后在第35天上升得更快。抗坏血酸主要以氧化形式存在,在储存末期迅速下降。细胞内谷胱甘肽在整个储存期间都在下降。氧化损伤生物标志物与铁参数之间存在强相关性。
这些数据表明,浓缩红细胞单位初始制备后释放的铁可能来自自由基介导的红细胞和血红蛋白氧化损伤,而非细胞外血红蛋白。随着抗氧化保护作用下降,储存期间铁持续释放。自由基介导的损伤循环可能在储存期间引发并进一步加剧铁的释放,进而可能介导进一步的自由基介导的细胞损伤。储存时间较长的血液对受血者的潜在后果可能很严重。