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

It has been reported that the mitochondrial cytochromes and citrate cycle enzymes occur in constant proportions to each other and increase or decrease roughly in parallel in response to various stimuli. The purpose of this study was to determine whether this proportionality is an obligatory consequence of the way in which mitochondria are assembled. Severe iron deficiency was used to bring about decreases of the iron-containing constituents of the mitochondrial respiratory chain in skeletal muscle. Cytochrome c concentration and cytochrome oxidase activity were decreased approximately 50%, while succinate dehydrogenase and NADH dehydrogenase activities were decreased by 78% in iron-deficient muscle. On electron microscopic examination, mitochondria in iron-deficient muscles had relatively sparse numbers of cristae. The iron deficiency had little or no effect on the levels of a range of mitochondrial matrix enzymes, including citrate synthase, isocitrate dehydrogenase, fumarase, aspartate aminotransferase, 3-hydroxyacyl-CoA dehydrogenase, 3-ketoacid-CoA transferase, and acetoacetyl-CoA thiolase. These results show that the usual constant proportions between the constituents of the mitochondrial respiratory chain and matrix enzymes are not obligatory; they provide evidence that mitochondrial matrix enzymes and respiratory chain constituents can be incorporated into mitochondria independently and that the ratios between them can vary within wide limits.
 ...
PMID:Perturbation of mitochondrial composition in muscle by iron deficiency. Implications regarding regulation of mitochondrial assembly. 302 53

Young rats maintained on an iron-deficient diet developed severe anemia and had large decreases in the levels of the iron-containing flavoproteins and cytochromes of the mitochondrial respiratory chain in skeletal muscle. In contrast, the levels of a number of mitochondrial matrix marker enzymes, including citrate synthase, isocitrate dehydrogenase, 3-hydroxyacyl-CoA dehydrogenase, 3-ketoacid-CoA transferase, and aspartate aminotransferase, increased in red skeletal muscle but not in white muscle. Phosphocreatine concentration was decreased and inorganic phosphate concentration was increased in soleus muscle frozen in situ. We hypothesize that the increase in mitochondrial matrix enzymes reflects a stimulus to mitochondrial biogenesis in posture-maintaining and weight-bearing red muscle fibers in severely iron-deficient rats. It is our working hypothesis that this stimulus to mitochondrial biogenesis arises from mild activity of the red fibers and is due to the same perturbation in cellular homeostasis that is normally caused by vigorous exercise or hypoxia. In iron deficiency, the stimulus to mitochondrial biogenesis can induce an increase in only those enzymes not prevented from increasing by iron deficiency, resulting in formation of mitochondria of grossly abnormal composition.
 ...
PMID:Induction of an increase in mitochondrial matrix enzymes in muscle of iron-deficient rats. 347 8

The effects of chronic iron deficiency anemia on brain (cortex) metabolism were estimated by 31P-nuclear magnetic resonance spectroscopy and biochemical analyses in male Wistar rats. Iron deficiency anemia was induced by supplying diet containing either approximately 2 or approximately 6 ppm Fe. Control diet was supplemented with 100 ppm Fe as ferric citrate. After 8-9 weeks, blood hemoglobin levels were approximately 13, 5, and 3 g/100 ml in the 100 ppm, 6 ppm, and 2 ppm Fe group, respectively. The blood lactate levels at rest in these groups were approximately 3, 5, and 6 mM. The blood glucose concentration also tended to be elevated in iron-deficient rats. The high-energy phosphate contents in brain were not affected by iron deficiency. The activities of succinate dehydrogenase and cytochrome oxidase per unit protein in the 2 ppm Fe group were significantly less than in the 100 ppm Fe group, but those activities were not significantly affected by feeding diet with 6 ppm Fe. The activities of lactate dehydrogenase in iron-deficient group tended to be elevated but not significantly. The activities of non-iron containing mitochondrial enzymes, citrate synthase and beta-hydroxyacyl CoA dehydrogenase, were unchanged. It is suggested that the brain has a higher tolerance to iron deficiency than skeletal muscle in terms of the metabolic characteristics, although this may be associated with a lower level of neural activity.
 ...
PMID:Effects of chronic iron deficiency anemia on brain metabolism. 756 62