Strauss R G, Snyder E L
Pediatr Res. 1981 May;15(5):794-7.
The viability of neutrophils, isolated from infant blood and placed into lipid culture, was decreased when compared to that of neutrophils obtained from mothers and controls that had been stored under identical conditions (percentage viable after 20 hr of culture was 49, 75 and 78 for infant, maternal, and control neutrophils, respectively). Increased quantities of hydrogen peroxide were released into the extracellular culture media by nonphagocytic neutrophils from infants (0.25 nM/min/2.5 x 10(6) neutrophils compared to 0.14 for controls), a condition that could promote autooxidation because infant neutrophils are deficient in glutathione peroxidase and catalase (enzymes that detoxify hydrogen peroxide). Results of two studies supported the idea that cell death in culture was related to oxidative damage: (1) phagocytosis induced a loss of viability in maternal and control neutrophils of a similar degree (48 and 52% viable, respectively) to that exhibited by nonphagocytic infant cells (47% viable), a finding prevented by superoxide dismutase and catalase; (2) glucose oxidase-glucose, a hydrogen peroxide-generating system, accelerated death of nonphagocytic neutrophils in culture. It is possible that decreased viability of infant neutrophils is similarly present in vivo (e.g., in inflammatory exudates) and that this finding contributes to the impairment of host defenses.
与在相同条件下储存的母亲和对照组的中性粒细胞相比，从婴儿血液中分离并置于脂质培养基中的中性粒细胞的活力降低（培养20小时后，婴儿、母亲和对照中性粒细胞的存活百分比分别为49%、75%和78%）。婴儿非吞噬性中性粒细胞向细胞外培养基中释放的过氧化氢量增加（0.25 nM/分钟/2.5×10⁶个中性粒细胞，而对照组为0.14），由于婴儿中性粒细胞缺乏谷胱甘肽过氧化物酶和过氧化氢酶（使过氧化氢解毒的酶），这种情况可能会促进自氧化。两项研究的结果支持了培养中的细胞死亡与氧化损伤有关的观点：（1）吞噬作用导致母亲和对照中性粒细胞的活力丧失程度与非吞噬性婴儿细胞相似（分别为48%和52%存活），超氧化物歧化酶和过氧化氢酶可阻止这一发现；（2）葡萄糖氧化酶-葡萄糖，一种产生过氧化氢的系统，加速了培养中非吞噬性中性粒细胞的死亡。婴儿中性粒细胞活力降低在体内（例如在炎性渗出物中）可能同样存在，这一发现可能导致宿主防御功能受损。
