Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four groups of weanling male rats were fed one of three iron-deficient diets (6, 18 and 23 mg iron/kg diet) or a normal iron-containing diet (41 mg iron/kg diet) for 30 d. The effects of the diets on various iron status parameters were determined and four enzymes were assayed: cytochrome P450 (P450) and NADPH cytochrome P450 reductase (P450-RED) in liver and intestine microsomes, and glucose-6-phosphate dehydrogenase (G6P-DH) and 6-phosphogluconate dehydrogenase (6PG-DH) in liver, intestine and erythrocyte cytosol. Rats fed 6 mg iron/kg diet were severely anemic, whereas rats fed 18 or 23 mg iron/kg diet were moderately or mildly iron-deficient, as shown by their hemoglobin levels, hematocrit, red blood cell parameters, erythrocyte protoporphyrin and liver iron stores. P450 concentration and P450-RED activity in liver were unaffected by iron deficiency, but P450 concentration was markedly lower in the intestine of the three iron-deficient groups than in the controls. Activities of G6P-DH and 6PG-DH were not impaired in liver or intestine, except that liver 6PG-DH activity of severely anemic rats was less than that of control rats. However, severe and moderate iron deprivation resulted in a stimulation of G6P-DH and 6PG-DH activities per million erythrocytes. These results demonstrate that even moderate iron deficiency may alter fundamental enzymatic systems intervening in drug metabolism and in the pentose phosphate pathway.
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PMID:Effects of different degrees of iron deficiency on cytochrome P450 complex and pentose phosphate pathway dehydrogenases in the rat. 249 36

Male Wistar rats kept on the iron-deficient diet for 7-71/2 weeks showed an increase in the content of cytochromes P450 and b5 in liver microsomes that was accompanied by the elevated rate of N-demethylation of amidopyrin and dimethylalanine (type I substrates), and by that of p-hydroxylation of aniline (type II substrate). The changes described wee observed in the presence of a 20-25% reduction in the hemoglobin content in the blood of experimental animals. Administration to rats of phenobarbital (100 mg per kg mass daily for 3 days) caused an induction of the monooxygenase system of the liver endoplasmic reticulum. However under the conditions of iron deficiency in the diet the degree of cytochrome P450 induction and that of the reaction rate of N-demethylation in microsomes were slightly less than under the full-value diet.
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PMID:[Effect of dietary iron deficiency on the activity of the monooxygenase system of rat liver microsomes and its induction by phenobarbital]. 711 97

Under conditions of reduced iron availability, most frequent in calcareous soils, plants induce the "Fe Deficiency Response" to improve root Fe uptake. The transcription factor FIT is essential for such a response in strategy I plants, such as Arabidopsis thaliana. From microarray analysis of Arabidopsis roots, it is known that three different cytochrome P450 genes, CYP82C4, CYP82C3 and CYP71B5 are up-regulated under Fe deficiency through a FIT-dependent pathway. We show that, out of these three P450 genes, only CYP82C4 strongly correlates with genes involved in metal uptake/transport. The CYP82C4 promoter, unlike those of CYP82C3 and CYP71B5, contains several IDE1-like sequences (iron deficiency-responsive element) as well as an RY element. While confirming that the CYP82C4 transcript accumulates in Fe-deficient Arabidopsis seedlings, with circadian fluctuations in a light-dependent way, we also demonstrate that such accumulation is suppressed under Fe excess. Full suppression of CYP82C4 expression, as observed in the atc82c4-1 KO mutant, is associated with longer roots at the seedling stage. We propose that CYP82C4 is involved in the early Fe deficiency response, possibly through an IDE1-like mediated pathway.
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PMID:Arabidopsis CYP82C4 expression is dependent on Fe availability and circadian rhythm, and correlates with genes involved in the early Fe deficiency response. 2131 74