Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of physical training on fasting erythrocyte and plasma zinc distributions were studied on seven previously sedentary male students. The training consisted of running over 5 km, 6 times/week for 10 weeks. Maximum aerobic capacity (VO2max) and 12 min walk-run performance increased significantly (p less than 0.01) after training. The erythrocyte concentrations of total zinc and of zinc derived from carbonic anhydrase I (CA-I) rose significantly (p less than 0.05) after training, whereas no such effects were noted in CA-II-derived zinc, Cu2Zn2 superoxide dismutase-derived zinc, and other zinc. On the other hand, no effect of training was found in total or alpha 2-macroglobulin-bound zinc in plasma, although albumin-bound zinc concentration declined significantly (p less than 0.05). Following the training period, however, the response to a VO2max test of the van Beaumont quotient (J Appl Physiol 1973;34:102-6) for total plasma zinc had decreased significantly (p less than 0.05), suggesting a relative reduction of the circulating exchangeable zinc. In addition, there were significant (p less than 0.05) decreases in plasma iron and ferritin concentrations after training, indicating latent iron deficiency anemia. These results may suggest that the changes in CA-I-derived zinc and/or albumin-bound zinc portend zinc deficiency during running training and that sports anemia precedes hypozincemia in athletes.
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PMID:Training effects on blood zinc levels in humans. 212 94

The hippocampus develops rapidly during the late fetal and early postnatal periods. Fetal/neonatal iron deficiency anemia (IDA) alters the genomic expression, neurometabolism and electrophysiology of the hippocampus during the period of IDA and, strikingly, in adulthood despite neonatal iron treatment. To determine how early IDA affects the structural development of the apical dendrite arbor in hippocampal area CA1 in the offspring, pregnant rat dams were given an iron-deficient (ID) diet between gestational day 2 and postnatal day (P) 7 followed by rescue with an iron-sufficient (IS) diet. Apical dendrite morphology in hippocampus area CA1 was assessed at P15, P30 and P70 by Scholl analysis of Golgi-Cox-stained neurons. Messenger RNA levels of nine cytoplasmic and transmembrane proteins that are critical for dendrite growth were analyzed at P7, P15, P30 and P65 by quantitative real-time polymerase chain reaction. The ID group had reduced transcript levels of proteins that modify actin and tubulin dynamics [e.g. cofilin-1 (Cfl-1), profilin-1 (Pfn-1), and profilin-2 (Pfn-2)] at P7, followed at P15 by a proximal shift in peak branching, thinner third-generation dendritic branches and smaller-diameter spine heads. At P30, iron treatment since P7 resulted in recovery of all transcripts and structural components except for a continued proximal shift in peak branching. Nevertheless, at P65-P70, the formerly ID group showed a 32% reduction in 9 mRNA transcripts, including Cfl-1 and Pfn-1 and Pfn-2, accompanied by 25% fewer branches, that were also proximally shifted. These alterations may be due to early-life programming of genes important for structural plasticity during adulthood and may contribute to the abnormal long-term electrophysiology and recognition memory behavior that follows early iron deficiency.
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PMID:Gestational and neonatal iron deficiency alters apical dendrite structure of CA1 pyramidal neurons in adult rat hippocampus. 2068 87