OXIDANT DAMAGE MEDIATES VARIANT RED-CELL RESISTANCE TO MALARIA
OXIDANT DAMAGE MEDIATES VARIANT RED-CELL RESISTANCE TO MALARIA
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DOI：
10.1038/280245a0
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发表时间：
1979-01-01
期刊：
影响因子：
64.8
通讯作者：
FRIEDMAN, MJ
中科院分区：
文献类型：
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作者：
FRIEDMAN, MJ
据认为，地中海贫血（塔尔）和葡萄糖-6-磷酸脱氢酶缺乏症（G6 PD-）的有害特性在人群中被赋予的抗疟疾保护作用所平衡，并且变异红细胞的某些特性直接抑制疟原虫的入侵或细胞内发育。事实上，这是镰状细胞疾病的情况1，2。最近，Pasvolet al.3已经表明胎儿血红蛋白（HbF）（在胎儿和成体细胞中）抑制疟疾寄生虫的发育，已经表明HbF在具有塔尔性状的儿童中的轻微持续性是塔尔基因的选择性优势的原因。他们报告说，在成人携带者的红细胞中，寄生虫的发育没有差异。这里提出的证据表明，由于对氧化剂的敏感性，成人的α-和β-塔尔特征红细胞对寄生虫的发育都是难治的，此外，胎儿红细胞和G6 PD −细胞也是同样的原因。
IT is thought that the deleterious properties of thalassaemia (thal) and glucose-6-phosphate dehydrogenase deficiency (G6PD−) are balanced in the population by a conferred protection against malaria, and that some characteristic of the variant red cell acts directly to inhibit the invasion or intracellular development of the malaria parasite. Indeed, such is the case for sickle cell disorders1,2. Recently, Pasvolet al.3, having shown that fetal haemoglobin (HbF) (in both fetal and adult cells) inhibits malaria parasite development, have suggested that the slight persistance of HbF in children with thal trait is responsible for the selective advantage of the thal gene. They have reported no difference in parasite development in the red cells of adult carriers of thal. Evidence is presented here that bothα- andβ-thal trait red cells from adults are refractory to parasite development because of oxidant sensitivity, and, furthermore, that fetal red cells and G6PD−cells are refractory for the same reason.