Clardy S L, Wang X, Zhao W, Liu W, Chase G A, Beard J L, True Felt B, Connor J R
Department of Neurosurgery, M.S. Hershey Medical Center, Hershey, USA.
J Neural Transm Suppl. 2006(71):173-96. doi: 10.1007/978-3-211-33328-0_19.
Because of the multiple biochemical pathways that require iron, iron deficiency can impact brain metabolism in many ways. The goal of this study was to identify a molecular footprint associated with ongoing versus long term consequences of iron deficiency using microarray analysis. Rats were born to iron-deficient mothers, and were analyzed at two different ages: 21 days, while weaning and iron-deficient; and six months, after a five month iron-sufficient recovery period. Overall, the data indicate that ongoing iron deficiency impacts multiple pathways, whereas the long term consequences of iron deficiency on gene expression are more limited. These data suggest that the gene array profiles obtained at postnatal day 21 reflect a brain under development in a metabolically compromised setting that given appropriate intervention is mostly correctable. There are, however, long term consequences to the developmental iron deficiency that could underlie the neurological deficits reported for iron deficiency.
由于存在多种需要铁的生化途径，缺铁会在许多方面影响脑代谢。本研究的目的是通过微阵列分析确定与缺铁的持续影响和长期后果相关的分子印记。大鼠由缺铁的母鼠所生，并在两个不同年龄进行分析：21日龄，处于断奶且缺铁状态；6月龄，经过5个月铁充足的恢复期后。总体而言，数据表明缺铁的持续影响涉及多个途径，而缺铁对基因表达的长期后果则较为有限。这些数据表明，出生后第21天获得的基因阵列图谱反映了处于代谢受损环境中正在发育的大脑，在给予适当干预后大多可以纠正。然而，发育性缺铁存在长期后果，这可能是缺铁所致神经缺陷的基础。
