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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were performed to determine the effects of iron deficiency on brain metabolism in rats. Concentrations of cytochrome pigments, oxidative phosphorylation, and catalase and monoamine oxidase activities in brain tissue were unaffected by iron deficiency. However, activities of aldehyde oxidase, a key enzyme in the pathway of serotonin degradation, were significantly reduced, and concentrations of serotonin and total 5-hydroxyindole compounds were elevated in brain tissue of iron-deficient animals. Aldehyde oxidase activities and concentrations of 5-hydroxyindole compounds in brain tissues returned to approximately normal values one week after treatment of iron deficient animals with iron dextran.
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PMID:Iron deficiency in the rat: biochemical studies of brain metabolism. 64 92

Platelet and plasma amine oxidase activity was determined in a group of 99 healthy male (active duty military) alcoholics referred for hospital treatment who had been abstinent from alcohol for 2-10 days, and compared with that of a control military group. Platelet MAO activity was slightly but significantly lower in the alcoholic group. Both groups were significantly lower in MAO activity compared to a group of 42 non-military controls. In the alcoholic group there was no correlation between platelet MAO and severity or chronicity of drinking, nor was there evidence of iron deficiency to account for the lowered MAO activity. When the alcoholic and military control groups were split at the median, the first degree relatives of both the 'low' MAO alcoholics and the 'low' MAO military controls had a higher incidence of alcoholism than did the relatives of both 'high' MAO subgroups. No personal or family history data of alcohol-related problems were available on the non-military control group.
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PMID:Platelet and plasma amine oxidase activity in alcoholic individuals. 65 22

Platelet monoamine oxidase (MAO) activity was found to be significantly reduced in human alcoholics as compared to matched controls. A probable transitory increase in activity was observed during the abstinence phase. The low platelet MAO activity was not due to iron deficiency or to the presence of acetaldehyde. Since we have previously found a lowered MAO activity in the brains of suicide victims, especially in those with a previous history of alcohol abuse, we suggest that low platelet MAO activity reflects a primarily "weak" monoaminergic system in the CNS which causes an increased vulnerability to alcohol abuse and suicidal behaviour.
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PMID:Low platelet monoamine oxidase activity in human alcoholics. 89 16

Daily intraperitoneal administration of manganese chloride (15 mg/kg) to rats, maintained on an irondeficient diet, produced marked alterations in the activity of succinic dehydrogenase, monoamine oxidase, and in the morphology of the liver. Manganese accumulation was also significantly increased in such rats than after similar treatment to normally fed rats. Iron deficiency leads to increased absorption of manganese which is responsible for increased susceptibility to manganese toxicity in these animals.
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PMID:Role of iron deficiency in inducing susceptibility to manganese toxicity. 98 99

Chronic iron deficiency in rats resulted in decreased MAO activity both in vitro and in vivo. Since MAO is an important enzyme in inactivation of catecholamines, urinary excretion of DA, NE, E, MN-NMN, and VMA was measured in 24-hour samples from 11 iron-deficient children before and after treatment with intramuscular iron. Pretreatment NE excretion was abnormally high and returned to normal (P=0.001) within one week of therapy. VMA excretion also was higher before than after treatment (P greater than 0.05), but most values were within the normal range for healthy children of comparable size. There was no significant difference between DA, E, and MN-NMN excretion before and after iron therapy. Anemic, non-iron-deficient children had normal urinary NE, E, and VMA excretion before and after transfusion. These findings suggest that the irritability, lack of attentiveness, and low performance scores of iron-deficient children may be related to alterations in catecholamine metabolic pathways secondary to dependence of MAO on adequate iron stores.
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PMID:Iron deficiency anemia and increased urinary norepinephrine excretion. 112

To assess the effects of iron therapy on platelet monoamine oxidase (MAO) activity and urinary excretion of total metanephrines (MN) in infants and young children with iron deficiency anemia, 24 subjects were tested before and after one month of oral iron treatment. Thirteen healthy children comprised the control group. In the control group, platelet MAO level was 0.21 +/- 0.02 U/mg protein (mean +/- SE), urinary total metanephrine was 2.51 +/- 0.47 micrograms/mg creatinine. In cases with iron deficiency, mean platelet MAO level was 47.6% lower (p less than 0.005) whereas mean urinary metanephrine plus normetanephrine (MN-NMN) was only 20.7% lower (p greater than 0.05) than the control values. After one month, the anemic patients receiving oral iron therapy showed a significant increase in hemoglobin concentration, per cent transferrin saturation and platelet MAO activity (p less than 0.05). However, urinary metanephrine excretion was found to be lower in this group when compared to the metanephrine levels in iron deficiency before the medication (p less than 0.05). Although hemoglobin and transferrin saturation did not return to normal levels, these findings suggested that platelet MAO activity increased and urinary excretion of metanephrines decreased after iron medication.
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PMID:Iron deficiency anemia and catecholamine metabolism. 205 11

Eight weeks of latent iron deficiency in weaned rats maintained on an experimental low iron content diet (18-20 mg/kg) did not significantly alter the packed cell volume and hemoglobin concentration; however, the hepatic and brain nonheme iron contents decreased by 66% and 21% (p less than 0.001), respectively. The tryptophan concentration decreased by 31% and 34% in liver and brain, respectively, in rats on experimental diet (p less than 0.01). The brain 5-hydroxytryptamine and 5-hydroxyindoleacetic acid contents were reduced by 21% and 23% (p less than 0.01 and p less than 0.02), respectively. However, in the brain, weight, protein, DNA, and the activities of monoamine oxidase, aldehyde dehydrogenase, and liver tryptophan oxygenase were found to remain unaltered. When rehabilitated with a diet containing 390 mg/kg iron, rats previously maintained on the experimental diet for 2 weeks showed partial recovery in tryptophan levels both in liver and brain. However, brain 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels remained unaltered. The hepatic iron content improved without any change in brain iron content. The latent iron deficiency produced significant alterations in the metabolism of 5-hydroxytryptamine and brain iron content that could not be recovered 2 weeks after the iron rehabilitation.
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PMID:Effect of latent iron deficiency on 5-hydroxytryptamine metabolism in rat brain. 279 24

n-Pentylamine enters into intermediary metabolism by the action of monoamine oxidase. [1-(14)C] Pentylamine injected into rats is rapidly converted to (14)CO(2). The rate of catabolism decreases progressively in the course of nutritional iron deficiency, reaching about 60 percent of control values in 3 weeks. Feeding with iron yields control levels within 6 days. The catabolism of amyl alcohol, which shares a common pathway with n-pentylamine by way of valeric aldehyde, is not significantly affected by the deficiency. The results demonstrate that the maintenance of normal monoamine oxidase activity in vivo depends upon an adequate supply of dietary iron.
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PMID:Iron- and riboflavin-dependent metabolism of a monamine in the rat in vivo. 511 26

In a group of 7- to 12-year-old children without manifest clinical iron deficiency, urinary excretion of free norepinephrine was found to have substantial positive correlation with measure of total iron-binding capacity and negative correlation with serum ferritin. Results support earlier reports of an inverse contingency between iron status and urinary norepinephrine level as observed with severe iron lack, findings consistent with speculation that monoamine oxidase activity may be modified by iron availability.
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PMID:Relationship of iron status to urinary norepinephrine excretion in children 7-12 years of age. 718 33

An iron deficiency nonanemic rat model was established by feeding with low-iron diet (11.9 mg/kg) to study if there exists biochemical abnormality in brain tissues. Iron contents of the brain, activities of monoamine oxidase (MAO) in the corpus striatum, and the contents of monoamine neurotransmitter and its metabolite in the cerebral cortex and hippocampus were determined by DCP-AES technique, enzyme histochemical method, and high performance liquid chromatography with electrochemical detection (HPLC-ECD), respectively. Results showed that iron contents and activities of MAO in brain tissues of iron deficiency nonanemic rats reduced significantly, and contents of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in cerebral cortex were significantly higher than those of controls, while 5-hydroxydroxytryptamine acid (5-HIAA) metabolite of 5-HT in the hippocampus was lower than that of controls. It indicated that there existed metabolic abnormality of monoamine neurotransmitter in the brain tissues of iron deficiency nonanemic rats. Also, this study laid a biochemical basis for abnormal mental and behavioral development caused by iron deficiency.
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PMID:[Changes in brain monoamine neurotransmitter in iron deficiency nonanemic rats]. 938 11


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