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Biomedical subjects

C A Finch

Publications and source records attributed to C A Finch.

At least 73 records · Page 4Linked to original sources
PubMed1984

Iron deficiency in the rat: effects on oxidative metabolism in distinct types of skeletal muscle.

Studies performed on iron-deficient and control rats demonstrated that oxidative energy production (phosphorylation) by mitochondria from iron-deficient red and intermediate skeletal muscles was greatly reduced with pyruvate-malate, succinate, and alpha-glycerophosphate as substrates. Although phosphorylation was also decreased in iron-deficient white skeletal muscle with succinate and pyruvate-malate as substrates, no change was found with alpha-glycerophosphate as substrate.

Anemia, Hypochromic↗
PubMed1984

Iron deficiency in the rat: effects on neutrophil activation and metabolism.

Studies were performed to determine the effects of iron deficiency in the rat on neutrophil activation and on levels of neutrophil myeloperoxidase and cytochrome b. The period of time required for neutrophil activation was not significantly affected by iron deficiency, but the maximum rates of respiration attained after activation were markedly lower (60% decrease) in iron-deficient neutrophils than in control cells. The myeloperoxidase activity of neutrophils from iron-deficient rats was also markedly decreased (approximately 75%) compared with the activity of control cells; however, the concentration of cytochrome b in the neutrophils was unaffected by iron deficiency.

Anemia, Hypochromic↗
PubMed1984

Transferrin: physiologic behavior and clinical implications.

The transferrin iron transport system, along with its procurement sites and delivery receptors, provides a highly effective means of satisfying internal iron requirements. Iron uptake by individual tissues is determined by their receptor number, by the relative amounts of monoferric and diferric transferrin in circulation, and by the amount of available iron in donor tissues. Although the modus operandi of this system under basal conditions has been characterized, its exquisite regulation remains an enigma. In some manner, the procurement of iron is determined by iron requirements. What seems to be an inappropriate behavior of the absorptive mechanism in thalassemia and certain other erythroid overload states may actually be life-saving in the absence of transfusion, since it results in higher levels of plasma iron and thereby higher levels of erythropoiesis. The definition of the regulatory mechanism in such conditions may well lead to an understanding of the molecular defect in idiopathic hemochromatosis.

Anemia, Hemolytic↗
PubMed1984

A mono-sited transferrin from a representative deuterostome: the ascidian Pyura stolonifera (subphylum Urochordata).

An iron-binding protein has been found in the plasma of Pyura stolonifera. This protein has a molecular weight of about 41,000 +/- 2,000 and binds 1 mol iron/mol protein. The absorption maxima are lambda = 280 and lambda = 429 nm (E429/E280 = 0.044). Bicarbonate is bound concomitantly with high affinity and is necessary for optimal color formation at lambda = 429 nm. The protein showed a negligible exchange of iron with human apotransferrin under physiologic conditions over two hours. Upon incubation with rat reticulocytes, the protein reacts with membrane receptors for transferrins, and the protein, with its iron, is transported intracellularly where the iron is incorporated into heme. The 59Fe protein, after intravenous injection, disappears rapidly from the plasma and is excreted largely in the urine, with a substantial fraction present in the kidney and another large fraction present in the gut. These findings established the protein as a "transferrin" and support the concept that the larger transferrin molecule in vertebrates, with two iron-binding sites, resulted from a gene duplication.

Animals↗
PubMed1983

Iron deficiency in the rat: biochemical studies of fetal metabolism.

The effects of dietary-induced iron deficiency on fetal and maternal metabolism were studied in the rat. Concentrations of phenylalanine, but not tyrosine, were significantly elevated in plasma from iron-deficient maternal and fetal rats at day 20 of gestation with individual fetal plasma levels of phenylalanine as high as 10 mg per 100 ml. Concentrations of total 5-hydroxyindole compounds were significantly decreased in brain tissue from iron-deficient fetuses (day 20 of gestation), suggesting that synthesis of the compounds may be inhibited by iron deficiency. Mitochondrial NADH oxidase activity was markedly decreased (60%) in homogenates of fetuses at day 14 of gestation and may account for the high fetal resorption rate and small fetal size observed in the rat in iron deficiency.

Animals↗
PubMed1983

Competitive advantage of diferric transferrin in delivering iron to reticulocytes.

Radioiron- and radioiodine-labeled forms of human diferric and monoferric transferrin and apotransferrin, isolated by preparative isoelectric focusing, were used to define transferrin-iron uptake by human reticulocytes. In mixtures of human diferric and monoferric transferrin, the diferric molecule had a constant 7-fold advantage in delivering iron to reticulocytes, as compared with the 2-fold advantage when single solutions of mono- and diferric transferrins were compared. This was shown to be due to competitive interaction in iron delivery, probably at a common membrane-receptor binding site for transferrin. Apotransferrin did not interfere with the iron-donating process and its limited cellular uptake was inhibited in noncompetitive fashion by diferric transferrin.

Apoproteins↗
PubMed1983

Fetal iron balance in the rat.

Maternal and fetal iron balance through pregnancy was examined in the rat. The 20th day was selected for detailed study because of the peak iron requirements at that time. The standard diet provided a borderline iron supply to the fetus due to the limited availability of its iron for absorption. When a more available form of iron was used, normal fetal development occurred over a range of dietary iron content from 16 to 2500 mg/kg. At a level of 5 to 8 mg/kg, there was attrition of placental tissues with frequent fetal death and resorption. When the iron-deficient pregnancy was sustained, both maternal and fetal iron deficiency were present. At progressively higher levels of dietary iron, feto-placental iron content was constant despite a progressive increase in maternal iron stores. Fetal iron supply appeared to be determined primarily by plasma iron concentration, and, at normal levels, about 25% of transferrin iron passing through the uterine vasculature, was removed by the intact placentas. Low levels of plasma iron resulted in damage to fetal tissues and reduced the capacity of placental tissues to take up iron. At high levels of plasma iron, plasma iron turnover initially increased 5-fold over basal levels in nonpregnant animals due to increased placental uptake. However, with continued hyperferremia, uptake was regulated so as to maintain fetal iron at a normal level. A comparison of these data with human iron requirements explained the occurrence of both maternal and fetal iron deficiency in the rat, but only maternal iron deficiency in the human.

Animals↗
PubMed1983

The significance of transferrin for intestinal iron absorption.

A mechanism is proposed by which apotransferrin is secreted from mucosal cells, loaded with iron in the intestinal lumen, and then the intact complex is taken into the cell. Within the cell, iron is released and transferred to the blood stream, whereas iron-free transferrin returns to the brush border to be recycled. We have investigated this hypothesis by measuring intestinal absorption of radioiron and 125I-labeled plasma transferrin using tied-off gut segments in normal and iron-deficient rats. There was no absorption of diferric transferrin from the ileum, but high absorption from the duodenum and jejunum segments. Jejunal absorption occurred as a function of the dose offered and showed saturation kinetics. In normal animals, 4 micrograms of the 50 micrograms of transferrin iron was absorbed over 1 hr. In iron-deficient animals, mean values as high as 13 micrograms were observed. Radioiron content of the jejunal mucosa bore a linear relationship to the dose administered and was inversely proportional to the amount of iron entering the plasma. Recycling of transferrin was indicated by the presence of labeled apotransferrin in the lumen, first observed between 15 and 60 min after the injection of diferric transferrin. A high resistance of diferric and apotransferrin to proteolytic degradation within the gut lumen was demonstrated. Comparative studies with lactoferrin and ferritin disclosed poor availability of their iron for absorption. The small amount that was absorbed did not relate to the iron status of the recipient animal. These studies support the role of mucosal transferrin as a shuttle protein for iron absorption.

Anemia, Hypochromic↗
PubMed1982

Iron status of elderly Americans.

Studies of iron nutriture in the elderly are limited and very few include observations on individuals over the age of 75. The two Health and Nutrition Examination Surveys carried out by the United States Department of Health, Education and Welfare demonstrate that the mean iron intake of Americans is adequate until the age of 75. However, with changes in the major food sources there is a decrease in iron derived from meat and a concomitant rise in the proportion supplied by breakfast cereals. Alterations in dietary iron bioavailability++ that may result from this have not been studied. Physiological data suggest that the elderly do not represent a target population for iron deficiency since iron requirements are no greater than those of adult men and lower than those of children and menstruating women. Furthermore, there is little direct evidence of a high prevalence of iron deficiency in the elderly, but the laboratory measurements that have proved useful in defining iron status in younger people have not been standardized for or extensively used in older people. Anemia is still the most important known consequence of significant iron deficiency. However, the application of Hb or hematocrit standards used in younger people to the elderly as well as the assumption that anemia can be equated with iron deficiency invalidates the conclusions of many surveys. Hb and hematocrit measurements are not suitable screening tests for iron deficiency in the elderly and there is an urgent need for a clearer understanding of the physiological and nutritional factors responsible for lower Hb values in older people, particularly older Blacks.

Adolescent↗
PubMed1982

Hepatocyte iron kinetics in the rat explored with an iron chelator.

The hepatocyte metabolism of 59Fe-labelled ferritin, haemoglobin-haptoglobin and transferrin has been examined in rats. All three forms of 59Fe became transiently available to desferrioxamine (DF) at the time they would otherwise have entered storage or alternative pathways of iron metabolism. However, differences in both the patterns of spontaneous 59Fe reutilization by normal and iron deficient rats and the partition of chelate iron excretion between bile and urine, suggested that iron in transit within hepatocytes did not behave as a single common pool. Ferritin 59Fe, entering a pool of non-radioactive iron the size of which is determined by liver iron stores, was chelated predominantly into the bile. Transferrin 59Fe was distinguished by a greater reflux to the erythron in iron deficient rats, and by excretion of a larger proportion of 59Fe chelated by DF in the urine. Haemoglobin-haptoglobin 59Fe followed a metabolic pathway which was relatively independent of both the iron stores and DF. If the heterogeneous behaviour of rat hepatocyte transit iron has a parallel in man, alterations in the size of similar chelatable iron pools could explain the dependence of DF-induced urine and faecal iron excretion on both liver iron stores and the level of erythropoiesis.

Animals↗
PubMed1982

Effect of incubation temperature on human red cell survival.

The effect of in vitro response of normal human erythrocytes to temperatures between 41 degrees C and 43 degrees C for two hours was determined. In vivo survival was measured employing 51Cr and 14C-cyanate as red cell tags. No significant difference was observed between cells exposed to these temperatures and erythrocytes incubated at 37 degrees C. The results of this study are of value in various types of extracorporeal blood treatment where an elevated temperature is desired.

Adult↗
PubMed1982

Effect of transfused reticulocytes on iron exchange.

A animal model was developed whereby reticulocyte-rich blood was introduced into normal rats by exchange transfusion. Measurements of plasma iron turnover was made at similar plasma iron concentrations before and after exchange transfusions. High reticulocyte blood obtained from animals rendered iron deficient by diet or by treatment with phenylhydrazine resulted in a mean increase of 86% in internal iron exchange, while the plasma iron turnover was unaffected by exchange with normal red cells. Since iron input from reticuloendothelial cells could have increased due to breakdown of transfused cells, iron absorption was also measured. Within 1 hr and for a least 6 hr after exchange with high reticulocyte blood, mean absorption in six groups of animals was increased over control animals by 50%-130%. The increased plasma iron turnover and absorption was not mediated by a decrease in plasma iron or an increase in unsaturated iron-binding capacity. Indeed, a higher plasma iron and transferrin saturation augmented the movement of iron into the plasma from iron-donating tissues. It is proposed that the donation of iron by transferrin in some way immediately facilitates the procurement of more iron by transferrin.

Animals↗
PubMed1982

Continuous RBC transfusions in a patient with sickle cell disease.

A patient with severe sickle cell anemia received approximately 600 RBC transfusions during a period of 30 years. Continuous prophylactic transfusions were administered for 13 years. During the 13-year period, except for tissue damage already inflicted by sickle cell disease, she was free of symptoms. When a hemoglobin concentration of 12 g/dL was maintained, she was shown to have ineffective erythropoiesis postulated to be due to the inability of her reticulocytes to cross the sinusoidal barrier from marrow to blood. Up to the time of her death at the age of 47 years, there was no evidence that her massive iron overload produced clinical symptoms other than unexplained, although her massive iron overload remains suspect.

Anemia, Sickle Cell↗