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

Recent recommendations on nutrition, such as the Surgeon General's Report on Nutrition and Health, have emphasized the relationship between diet and disease. In the Surgeon General's report, Americans have been advised to limit their consumption of fat, cholesterol, sodium, and alcoholic beverages, and to increase their consumption of complex carbohydrates and fiber. Two of the recommendations in this report related to the consumption of iron and calcium are particularly important to women's health. Women are advised to increase their consumption of food high in calcium and to include foods containing iron, such as lean meats, fish, certain beans, iron-enriched cereals, and whole grain products. Iron is essential as a constituent of hemoglobin, myoglobin, and certain enzymes. Iron losses during menstruation and the increased need for iron during pregnancy place women at risk for iron deficiency. Bone mass continues to increase until the late twenties, and one method to prevent osteoporosis may be adequate calcium intake during these years of early adulthood. Food guides that list amounts and types of foods to be eaten are helpful for the individual or as an educational tool for the nurse or educator. A Daily Food Guide was recently designed to meet the nutritional needs of women throughout the life cycle, and the government has very recently released a Food Guide Pyramid. Although it is important for women to learn how to control certain dietary components, they should also be aware of the protective nature of certain nutrients, such as iron and calcium.
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PMID:Nutrition in women across the life span. 144 70

The influence of chronic iron deficiency anaemia on myoglobin content, maximal enzyme activities and capillarization in the human skeletal muscle was investigated. Muscle samples from musculus vastus lateralis were screened in an Indonesian population. The causes of iron deficiency were chronic intestinal bleeding or repeated pregnancy combined with low iron intake. The maximal activities of iron-dependent and non-iron-dependent glycolytic and oxidative enzymes as well as myoglobin showed similar values in the iron-deficient group and the matched control group. The activities of the oxidative enzymes in both the iron-deficient group and the controls were lower, however, compared even to untrained Swedish subjects. The capillary density was essentially within a normal range in both groups. It is concluded that chronic iron deficiency anaemia of a moderate or severe degree, with Hb concentrations of about 80-100 g.1(-1), does not cause an impaired biochemical function of the human skeletal muscle.
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PMID:Effects of chronic iron deficiency anaemia on myoglobin content, enzyme activity, and capillary density in the human skeletal muscle. 337 73

An adult man contains roughly 4-5 g of iron. Nearly 70% of this amount is present in hemoglobin and myoglobin. About 11% is accounted for by iron enzymes, e.g., heme enzymes that play a decisive role in cellular metabolism. Almost 19% of the body iron are deposed in iron stores. The distribution of iron in the body to the tissues and organs is handled by transferrin, a protein that binds iron so tightly that scarcely any free, i.e., ionized and hence toxic iron can exist. Since iron can only be excreted to an insignificant extent either in the urine or bile, the metabolism of iron is balanced almost exclusively by the absorption of this metal from food. This is especially true in the case of iron deficiency, e.g., in the young and growing organism, in pregnant females, or after iron loss.
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PMID:[Iron and the supply of iron in warm-blooded animals]. 360 Aug 12

In sports, vitamins along with minerals, particularly iron, and the energy nutrients such as carbohydrates, are considered especially important. Frequently single or multiple vitamins in combination with other active substances such as iron, other minerals or carbohydrates are administered. In sports, vitamins are added to carbohydrate mixtures or electrolytes enriched with vitamins are offered and frequently used. There is no doubt that due to the numerous effects of vitamins, a connection must exist between the vitamin status and athletic performance capability. It can be concluded that vitamin deficiencies have a negative effect on physical and mental performance. The release of energy can only attain its maximum output when the organism has the required substances at its disposal. Iron is of central importance among these active substances, since its presence in haemoglobin is essential for the transport of oxygen and carbon dioxide, makes it possible for myoglobin to function as an oxygen supply depot and guarantees the functioning of internal respiration in the respiratory chain and various key enzymes. Muscle training increases not only the respiratory chain but also several other iron-rich enzymes. This makes even more astonishing the fact that a variety of recently published articles report on iron deficiency among athletes. The effect of the iron deficiency with anaemia (sports anaemia) is manifest in a reduction of aerobic capacity with an increase in lactate acidosis, greater fatigue, loss of appetite, muscular cramps and vasomotor disturbances.
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PMID:[Effect of vitamins and iron on performance and recovery in humans and in sports anemia]. 360 97

Hemoglobin and myoglobin are a major source of dietary iron in man. Heme, separated from these hemoproteins by intraluminal proteolysis, is absorbed intact by the intestinal mucosa. The absorbed heme is cleaved in the mucosal cell releasing inorganic iron. Although this mucosal heme-splitting activity initially was ascribed to xanthine oxidase, we investigated the possibility that it is catalyzed by microsomal heme oxygenase, an enzyme which converts heme to bilirubin, CO, and inorganic iron. Microsomes prepared from rat intestinal mucosa contain enzymatic activity similar to that of heme oxygenase in liver and spleen. The intestinal enzyme requires NADPH; is completely inhibited by 50% CO; and produces bilirubin IX-alpha, identified spectrophotometrically and chromatographically. Moreover, duodenal heme oxygenase was shown to release inorganic (55)Fe from (55)Fe-heme. Along the intestinal tract, enzyme activity was found to be highest in the duodenum where hemoglobin iron absorption is reported to be most active. Furthermore, when rats were made iron deficient, duodenal heme oxygenase activity and hemoglobin-iron absorption rose to a comparable extent. Upon iron repletion of iron-deficient animals, duodenal enzyme activity returned towards control values. In contrast to heme oxygenase, duodenal xanthine oxidase activity fell sharply in iron deficiency and rose towards base line upon iron repletion. Our findings suggest that mucosal heme oxygenase catalyzes the cleavage of heme absorbed in the intestinal mucosa and thus plays an important role in the absorption of hemoglobin iron. The mechanisms controlling this intestinal enzyme activity and the enzyme's role in the overall regulation of hemoglobin-iron absorption remain to be defined.
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PMID:Intestinal absorption of hemoglobin iron-heme cleavage by mucosal heme oxygenase. 443 36

The purpose of this study was to determine the interrelationships between iron stores, serum iron, hemoglobin, myoglobin, and cytochrome c under conditions of iron deficiency that did not interfere with normal growth. Rats were given diets containing from 7 to 500 mg iron per kilogram of diet during a period of 3 weeks of rapid growth between weaning at 21 days and approaching sexual maturity at 42 days. We found that the level of iron intake required for a maximum concentration of hemoglobin was similar to that which results in a maximum level of tissue cytochrome c. The severity of iron deficiency anemia was proportionally similar to the degree of depletion of muscle cytochrome c at all levels of iron intake below 25 mg/kg diet. The results indicate that even the mildest degree of nutritional iron deficiency anemia also affected tissue cytochrome c and could impair cytochrome-dependent mitochondrial function.
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PMID:Manifestation of iron deficiency at various levels of dietary iron intake. 624 52

Male weanling rats were fed a control diet (46 ppm iron) or an iron-deficient diet (11 ppm iron) for 7 wk to determine the influence of iron deficiency on heme proteins and skeletal muscle mitochondrial respiration. At the end of 7 wk, the hemoglobin in the blood of the iron deficient rats was 35% less and skeletal muscle myoglobin was 20 to 37% less than in the control animals. The concentration of myoglobin in the heart was not appreciably diminished by iron deficiency. Cytochrome c concentration was 20% less in the heart and 35% less in the mixed-fiber gastrocnemius in the iron-deficient animals. Iron deficiency did not influence the activity of metmyoglobin reductase in either heart or skeletal muscle. There was about 30% more methemoglobin reductase activity in the red blood cells of the iron-deficient animals, which resulted in methemoglobin levels that were so low as to be virtually unmeasurable. In the iron-deficient rats, skeletal muscle mitochondrial respiration with either pyruvate-malate or palmitylcarnitine as substrate was 17 to 20% less than in the control animals. This study demonstrates that dietary iron deficiency of sufficient severity to reduce blood Hb and skeletal muscle myoglobin or cytochrome c also results in an impaired skeletal muscle oxidative capacity. The study also illustrates the preferential utilization of iron, not only between tissues, but within tissues, and tissue specific adaptive responses to iron deficiency.
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PMID:Influence of dietary iron deficiency on hemoglobin, myoglobin, their respective reductases, and skeletal muscle mitochondrial respiration. 627 Oct 3

This study was designed to determine the interrelationships among storage iron, transport iron, and iron compounds that serve known physiological functions (Hb, myoglobin, and cytochrome c) during the gradual progression of dietary iron deficiency. These three categories of iron compounds are generally considered to become depleted in three corresponding, sequential stages. However, there is scattered evidence of substantial overlap between these stages in man. The presence of such overlap may prove pertinent to the interpretation of laboratory tests used in the diagnosis of iron deficiency. The rat was used as an experimental model to allow more complete evaluation of the interrelationships between the stages of iron deficiency than would be possible in man. Rats were given diets containing 2, 6 and 50 mg iron/kg diet during early adult development, between 36 and 90 days of age. The iron-deficient diets (2 and 6 mg iron/kg diet) resulted in decreases in hematocrit and in muscle and intestinal cytochrome c well before storage iron in the liver and spleen was exhausted. The results in the rat model may help to explain why there is not a consistent pattern of laboratory abnormalities in individuals with chronic, mild dietary iron deficiency.
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PMID:Sequence of development of iron deficiency in the rat. 628 Apr 87

The effects of iron deficiency in rat and/or man on iron-containing enzymes of different tissues is reviewed. Iron deficiency results in a decrease of skeletal muscle iron containing proteins e.g. myoglobin, cytochromes c, a + a3, and alpha-glycerophosphate oxidase. Iron deficiency produces a reduction in the activity of several respiratory enzymes in the mitochondrial fraction of cardiac muscle, particularly: NADH cytochrome c reductase, succinic cytochrome c reductase, succinic dehydrogenase and NADH ferricyanide oxidoreductase. The effects of iron deficiency on brain tissue is emphasized with respect to cytochromes, monoaminoxidase and amino acids metabolism. Host defence to infection (controversial data), decrease in body temperature, alteration of DNA synthesis, collagen and lipid metabolism, liver and gastrointestinal mucous cytochromes activity perturbations are discussed.
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PMID:The activity of tissue enzymes in iron-deficient rat and man: an overview. 637 45

The effects of iron deficiency and endurance training on muscle myoglobin (Mb), body weights, and blood lactic acid concentration were studied in rats. Fifty animals were divided into four groups: anemic trained (AT), normal trained (NT), anemic sedentary (AS), and normal sedentary (NS). Following 5 weeks of dietary control, the mean hemoglobin values for the AT and AS rats were 0.013 +/- 0.002 mmol X l-1 (8.7 +/- 1.4 g X dl-1) and 0.014 +/- 0.003 mmol X l-1 (9.2 +/- 1.7 g X dl-1) respectively, and did not significantly change throughout the study. AT and NT rats were run on a motor driven treadmill 4 days/week for 6 weeks up to a pre-established time of 90 min. Following the training, body weights of the AT (157 +/- 13 g) and NT (153 +/- 13 g) rats were lower than their respective sedentary groups AS (172 +/- 9 g) and NS (176 +/- 15 g). Resting blood lactic acid concentration following training was lower in both trained groups, AT (3.3 +/- 2.0 mM) and NT (2.3 +/- 1.9 mM) compared to AS (8.2 +/- 2.6 mM) and NS (3.8 +/- 1.6 mM). Training increased Mb concentration in hearts of both the anemic and normal trained groups (AT, 0.66 +/- 0.13 mg X g-1; NT, 0.95 +/- 0.08 mg X g-1) compared to the sedentary groups (AS, 0.44 +/- 0.08 mg X g-1; NS, 0.70 +/- 0.13 mg X g-1). Only the AT rats showed an increase in skeletal muscle Mb. This study provides evidence that myoglobin may limit aerobic metabolism.
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PMID:Effects of iron deficiency and exercise on myoglobin in rats. 654 Jun 69


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