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新生sla小鼠的缺铁性贫血:胎盘铁转运的遗传缺陷。

Iron deficiency anaemia in newborn sla mice: a genetic defect of placental iron transport.

作者信息

Kingston P J, Bannerman C E, Bannerman R M

出版信息

Br J Haematol. 1978 Oct;40(2):265-76. doi: 10.1111/j.1365-2141.1978.tb03663.x.

Abstract

Newborn mice with X-linked anaemia (gene symbol sla) have lower haemoglobin levels at birth than normal and carrier mice but there is considerable overlap. Serial observations showed that the haemoglobin values of segregating male mice separate into a bimodal distribution of 42 d of age, and 50 d values were used to assign genotypes retrospectively. The anaemia in newborn sla mice is attributable to iron deficiency, since their total body iron is lower than in normal newborn mice, while their birth weights are almost identical. Haemoglobin levels at birth in normal, anaemic and carrier mice are also influenced by the mother's genotype and phenotype, and the haemoglobin value was progressively lower according to the sla gene dose of the mother. Materno-fetal iron transfer was examined by labelling pregnant carrier females with radioiron in various ways. When given as single or intermittent doses by injection no clearcut differences emerged in apparent iron transfer to anaemic as compared to non-anaemic fetuses. However, when radioiron was administered continuously in food a significant reduction in iron transfer to anaemic fetuses was demonstrated. The sla gene is already known to have a major effect in reducing iron transport in the small intestine. The present studies provide evidence of an analogous defect in placental iron transport.

摘要

患有X连锁贫血(基因符号为sla)的新生小鼠出生时的血红蛋白水平低于正常小鼠和携带该基因的小鼠,但存在相当大的重叠。连续观察表明,分离的雄性小鼠的血红蛋白值在42日龄时呈双峰分布,50日龄时的值用于回顾性地确定基因型。新生sla小鼠的贫血归因于缺铁,因为它们的全身铁含量低于正常新生小鼠,而它们的出生体重几乎相同。正常、贫血和携带该基因的小鼠出生时的血红蛋白水平也受母亲的基因型和表型影响,并且根据母亲的sla基因剂量,血红蛋白值逐渐降低。通过以各种方式用放射性铁标记怀孕的携带该基因的雌性小鼠来研究母胎铁转运。当通过注射单次或间歇给药时,与非贫血胎儿相比,向贫血胎儿的明显铁转运没有出现明显差异。然而,当在食物中连续给予放射性铁时,向贫血胎儿的铁转运显著减少。已知sla基因在减少小肠铁转运方面有主要作用。目前的研究提供了胎盘铁转运存在类似缺陷的证据。

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