Moore L L, Humbert J R
Pediatr Res. 1984 Aug;18(8):789-94. doi: 10.1203/00006450-198408000-00027.
We developed a clear-cut nutritional iron deficiency anemia without concomittant malnutrition in rats given a low iron diet, and we restored normal iron and hemoglobin levels in these same animals with iron dextran injections. The neutrophil function studies performed during and after a period of iron deficiency showed the following: Phagocytosis of Staphylococcus aureus 502A, Streptococcus pneumoniae, and Salmonella typhimurium was not altered by iron deficiency or by the administration of iron; phagocytosis of Candida albicans was moderately abnormal during iron deficiency, and became normal with the restoration of iron sufficiency. Microbicidal activity towards Staphylococcus aureus 502A and Candida albicans, two catalase-positive microorganisms, was markedly decreased (to 50% of control values) and returned to normal when iron sufficiency was restored. Killing of a catalase-negative organism, Streptococcus pneumoniae was normal in iron-deficient rats. This pattern of differential bactericidal activities suggested an abnormality of the oxidant radical-generating machinery in neutrophils of iron-deficient animals. Indeed, iron deficiency caused a marked decrease of neutrophil nitroblue tetrazolium dye reduction, which disappeared after iron administration. Neutrophil myeloperoxidase activity was slightly decreased in iron deficient rats and returned to normal after iron administration. Microbicidal activity towards a gram-negative, catalase-positive organism, Salmonella typhimurium, was equal in iron deficient and iron sufficient animals. Our combined results suggest that a definite microbicidal defect is the consequence of nutritional iron deficiency, apart from any protein-calorie malnutrition. This defect affects the disposal in PMNs of two catalase-positive microorganisms (which require intracellular production of oxidant radicals for their destruction) but not of a catalase-negative bacterial species.(ABSTRACT TRUNCATED AT 250 WORDS)
我们通过给大鼠喂食低铁饮食,使其患上了明确的营养性缺铁性贫血且无并发营养不良的情况,并且通过右旋糖酐铁注射使这些动物恢复了正常的铁和血红蛋白水平。在缺铁期间及之后进行的中性粒细胞功能研究结果如下:缺铁或给予铁剂均未改变对金黄色葡萄球菌502A、肺炎链球菌和鼠伤寒沙门氏菌的吞噬作用;缺铁期间对白色念珠菌的吞噬作用有中度异常,铁充足后恢复正常。对两种过氧化氢酶阳性微生物金黄色葡萄球菌502A和白色念珠菌的杀菌活性显著降低(降至对照值的50%),铁充足后恢复正常。对过氧化氢酶阴性的生物体肺炎链球菌的杀灭在缺铁大鼠中正常。这种不同杀菌活性的模式表明缺铁动物中性粒细胞中产生氧化自由基的机制存在异常。事实上,缺铁导致中性粒细胞硝基蓝四氮唑染料还原显著降低,补铁后消失。缺铁大鼠中性粒细胞髓过氧化物酶活性略有降低,补铁后恢复正常。对革兰氏阴性、过氧化氢酶阳性生物体鼠伤寒沙门氏菌的杀菌活性在缺铁和铁充足的动物中相同。我们的综合结果表明,除任何蛋白质 - 热量营养不良外,明确的杀菌缺陷是营养性缺铁的后果。这种缺陷影响多形核白细胞对两种过氧化氢酶阳性微生物(其破坏需要细胞内产生氧化自由基)的清除,但不影响过氧化氢酶阴性的细菌种类。(摘要截短至250字)