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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We tested the hypothesis that hypoxia decreases PPARalpha-regulated gene expression in heart muscle in vivo. In two rat models of systemic hypoxia (cobalt chloride treatment and iso-volemic hemodilution), transcript levels of PPARalpha and PPARalpha-regulated genes (pyruvate dehydrogenase kinase 4 (PDK4), muscle carnitine palmitoyltransferase-I (mCPT-I), and malonyl-CoA decarboxylase (MCD)) were measured using real-time quantitative RT-PCR. Data were normalized to the housekeeping gene beta-actin. Atrial natriuretic factor (ANF) and pyruvate dehydrogenase kinase 2 (PDK2), which are not regulated by PPARalpha, served as controls. CoCl(2) treatment decreased PPARalpha, PDK4, mCPT-I, and MCD mRNA levels. Iso-volemic anemia also caused a significant decrease in PPARalpha, PDK4, and MCD mRNA levels. Transcript levels of mCPT-I showed a slight, but not significant decrease (P = 0.08). Gene expression of beta-actin, ANF, and PDK2 did not change with either CoCl(2) treatment nor with anemia. Myocardial PPARalpha-regulated gene expression is decreased in two models of hypoxia in vivo. These results suggest a transcriptional mechanism for decreased fatty oxidation and increased reliance of the heart for glucose during hypoxia.
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PMID:Hypoxia in vivo decreases peroxisome proliferator-activated receptor alpha-regulated gene expression in rat heart. 1154 45

This discussion of nutritional anemia reviews definitions and epidemiology before focusing on the following: iron deficiency anemia (review of iron metabolism, iron requirements and recommended intake, and consequences, causes, treatment, and prevention of iron deficient anemia); folic acid deficiency anemia (review of folic acid metabolism, requirements, and recommended intake, and consequences, causes, and treatment of folic acid deficiency anemia); vitamin B12 deficiency anemia (review of vitamin B12 metabolism, requirements, and recommended intake, and consequences, causes, treatment, and prevention of vitamin B12 deficiency anemia); other possible causes of nutritional anemia; and the contribution of nutritional factors to causes of anemia. Nutritional anemia, the most widespread nutritional disorder in the world, affects mainly developing countries and to a lesser extent developed nations. It is estimated that 500 million to 1 billion individuals in the world are affected by nutritional anemia. In a healthy person, a state of nutritional balance exists: the amount of food eaten is equal to the amount of nutrients utilized in order to ensure the effective functioning of the body and maintain sufficient reserves. This balance may be upset under various circumstances: decrease in nutrition, increase in losses, increased needs, decreased absorption, and decreased utilization. When this balance is upset for 1 or more of the identified reasons, a nutrient deficiency arises. The body dips into its reserves to meet its needs. When these are exhausted, all the bodily functions in which this nutrient plays a part are affected. In the case of hematopoietic nutrients, the production of red corpuscles hemoglobin ceases. This is anemia. Among the elements which contribute to the formation and development of red corpuscles and to the synthesis of hemoglobin, the following should be noted: iron; other minerals, i.e., copper, zinc, magnesium, cobalt, molybdenum; vitamins, especially folic acid and vitamin B12; and amino acids. Nutritional anemia can only be overcome if its prevalence, and the respective prevalences of iron, folic acid, and/or vitamin B12 deficiencies, are accurately determined for various population groups through reliable epidemiological studies. Many factors contribute to the development of nutritional anemia including lack of food, certain customs and habits, and parasitoses. An increase in available foodstuffs, better utilization of resources, and better living conditions lead to more balanced nutrition.
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PMID:Nutritional anaemia. 1226 81

Investigation of new stable iron (II) compounds is still an actual problem of today. Therefore we synthesized ferrous oxalate and prepared a stable antianaemic powder Ferosol-1 including copper, zinc and cobalt. We used colour tests, precipitation reactions and paper chromatography for identification of components of this powder. Quantitative analysis of iron and other elements was performed using atomic absorption spectroscopy. We used Lichfield and Wilkinson method modificated by Roth to detect acute Ferosol-1 toxicity. To estimate a local action of this powder we used guinea pigs which were grouped into control and trial ones. We determined bioavailability of Ferosol-1 by giving it to rabbits with experimental posthemorrhagic anemia. Iron resorption was tested on 20-25 days old piglets. We also tried this drug on newborn piglets while atching their weight gain and calculation daily weight gain. This data was used to estimate indirect impact of Ferosol-1 on metabolism of piglets. According to our data Ferosol-1 is of low toxicity (LD50 = 2.25 g/kg), it does not irritate mucosa of duodenum and ventriculus and could be used orally. Iron from Ferosol-1 was found to be well assimilated and to take place in hemopoetic processes of rabbit. After administration of Ferosol-1 to piglets iron concentration in their serum increased from 35.03 +/- 0.66 to 54.88 +/- 6.63 mumol/l, hemoglobin concentration increased to 96.4 +/- 2.5 g/l, erythrocyte number increased to 4.4 +/- 0.14 x 10(12)/l. The same data of control piglets were respectively 83.7 +/- 3.1 g/l and 3.52 +/- 0.3 x 10(12)/l. According to our results Ferosol-1 is an effective drug for prevention of iron-deficiency anemia and causes slight weight gain of piglets.
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PMID:[Preparation, analysis and anti-anemic action of peroral powders with ferrous oxalate. Ferosol-1]. 1247 20

Quinolinic acid (QA) is a potent endogenous excitotoxin; elevation of its concentration in an organism has been implicated in the pathogenesis of various disorders. The purpose of this study was the assessment of QA impact on the process of erythropoiesis. Marked increase of QA concentration was observed in plasma and peripheral tissues of uremic rats. These changes were proportional to the amount of the removed renal tissue and positively correlated with the concentration of creatinine but negatively correlated with hematological parameters, i.e., hematocrit and Hb red blood cells count. The changes were accompanied by a slight decrease in the concentration of endogenic erythropoietin (EPO) in the plasma of animals with uremia. Chronic treatment with QA diminished the increase in EPO concentration after introduction of cobalt in rats. These changes were associated with the decrease in all hematological parameters after QA administration. The in vitro study in the conditions of hypoxia showed that QA inhibited the EPO release from HepG2 cells to the culture base. Additionally, in HepG2 cells QA had a dose-dependent inhibitory effect on hypoxia- and cobalt-induced EPO gene expression without any cell toxicity. In conclusion, the erythropoiesis in chronic renal failure could be attributed to the influence of QA on EPO synthesis. Thus we propose that QA can be a uremic toxin responsible for anemia in animals or patients with renal failure.
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PMID:Contribution of quinolinic acid in the development of anemia in renal insufficiency. 1262 Sep 22

During active blood regeneration in anemia in dogs an increase occurs in the stroma protein of the red cells. When vitamin B(12) with radioactive cobalt is given at the start of this blood regeneration one finds concentration of labeledB(12)in the stroma protein but not in the hemoglobin. After the acute phase of red cell regeneration is ended the concentration of B(12) in stroma protein falls rapidly to very low levels within 2 weeks. Subsequent episodes of red blood cell regeneration seems not to cause remobilization of radioactive cobalt into red cells from other body stores. It appears that the vitamin B(12) is a factor of importance in the first steps of stroma protein formation in the first few days of the life of the red cell in the dog. This response in dogs and the response in pernicious anemia to vitamin B(12) may have some points in common. Distribution of the B(12)-radioactive cobalt in the organs and tissues at autopsy has been recorded. Some very suggestive localizations were noted and some variation 1 week and 7 weeks after B(12) injections. Radioactive cobalt escapes in the urine during the weeks following B(12) injections.
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PMID:Red cell stroma protein rich in vitamin B12 during active regeneration; anemia studies using radioactive cobalt B12 in dogs. 1327 85

We observed transient excretion of dark-brown urine after acute exposure to cobalt in rats and investigated the mechanism of it. We injected cobalt into rats s.c. at a dose of 15 mg/kg and collected urine, peripheral blood, and organ samples at the indicated times after injection. Biochemical and histopathological examinations of these samples were conducted. Obvious macroscopic and biochemical methemoglobinuria was observed just after injection of cobalt, but the level of urinary methemoglobin decreased gradually, almost disappearing by 24 h. The levels of cobalt in peripheral blood and urine showed a very similar pattern to that of methemoglobinuria. Neither anemia nor bilirubinemia was observed, indicating no extrarenal intravascular hemolysis. Pathological examination of the kidneys revealed that the glomerular capillaries were filled with red blood cells at 1 h after injection. Electron microscopy showed deformed red blood cells in the glomerular capillaries and condensed hemoglobin in Bowman's capsule that passed through the basement membrane. There were no trends toward increases in plasma levels of creatinine or blood urea nitrogen. These results indicate that exposure to cobalt induces transient methemoglobinuria through the lysis of red blood cells and oxidation of iron in hemoglobin at the glomerular capillaries without causing renal dysfunction.
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PMID:Acute exposure to cobalt induces transient methemoglobinuria in rats. 1526 90

The role of essential nutrient metal ions (Mg, Fe, Cu, Zn, Mn and Co) often deficient in our foodstuffs, although vitally essential in the function of the human organism as well as the different reasons for these deficiencies both in foods and in the human body have been studied. The most frequent nutritional disease is iron deficient anaemia. Inorganic salts, artificial synthetic monomer organic metal complexes of high stability or organic polymer complexes of high molecular mass are unsatisfactory for supplementation to the human body, owing to poor absorption, low availability and/or harmful side effects. In contrast, we have recently found that mixed metal complexes of oligo/polygalacturonic acids with medium molecular weight prepared from natural pectin of plant origin are efficient for oral supplementation. Sufficient absorption of essential metal ions from metal oligo/polygalacturonate mixed complexes with polynuclear innersphere structure is due to the high ionselectivity and medium stability values. Metal oligo/polygalacturonate mixed complexes contain all deficient essential metal ions in adequate amounts and ratios for higher bioavailability of metal ions and optimal vital function. Therefore, by oral administration of these complexes, metal ion homeostasis and optimal interactions with vitamins and hormones can be ensured. Prelatent or latent macroelement Mg deficiency can often be observed among clinical or ambulance patients. Latent or manifest mesoelement iron deficiency is the most common, however, the occurrence of microelement copper, zinc, manganese and cobalt latent deficiencies is not seldom either. Supplementation studies utilizing essential metal oligo/polygalacturonate complexes led to satisfactory outcome without harmful side effects.
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PMID:[The role of essential metal ions in the human organism and their oral supplementation to the human body in deficiency states]. 1528 49

Cobalt has been widely used in the treatment of anemia and as a hypoxia mimic in cell culture and it is known to activate hypoxic signaling by stabilizing the hypoxia inducible transcription factor 1alpha (HIF1alpha). However, cobalt exposure can lead to tissue and cellular toxicity. These studies were conducted to determine the role of HIF1alpha in mediating cobalt-induced toxicity. Mouse embryonic fibroblasts (MEFs) that were null for the HIF1alpha protein were used to show that HIF1alpha protein plays a major role in mediating cobalt-induced cytotoxicity. Previous work from our lab and others has shown that two BH3 domain containing cell death genes, BNip3 and NIX, are targets of hypoxia signaling. These experiments document that BNip3 and NIX expression is HIF1alpha-dependent, and cobalt induces their expression in a time and dose dependent manner. In addition, their expression is correlated with an increase in BNIP3 and NIX protein. Characteristically, the elevated level of BNIP3 was correlated with an increased presence of chromatin condensation, one marker for cell injury. Interestingly, this increased chromosomal condensation was not coupled to caspase-3 activation as usually seen in a typical apoptotic response. These results show that HIF1alpha is playing a major role in mediating cobalt-induced toxicity in mouse embryonic fibroblasts and may offer a possible mechanism for the underlying pathology of injuries seen in workers exposed to environmental contaminants that can influence the hypoxia signaling system, such as cobalt.
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PMID:The role of hypoxia inducible factor 1alpha in cobalt chloride induced cell death in mouse embryonic fibroblasts. 1537 94

A protocol of induction chemotherapy followed by half-body radiation therapy for treatment of lymphoma was used in 94 dogs. Seventy-three (78%) dogs achieved complete remission. Substage (P = .011) and phenotype (P = .015) were identified as predictors of complete remission rate. Of these, 52 dogs received half-body irradiation. Cranial and caudal halves received a total dose of 8.0 Gy, given in 2 fractions of 4.0 Gy on consecutive days with cobalt-60 photons and a 3-week interval between halves. Median 1st remission for these dogs was 311 days. Anemia was identified as the only predictor for length of 1st remission (P = .024). Toxicoses after half-body irradiation generally were mild and infrequent and included myelosuppression and gastrointestinal signs. Thirty-one dogs relapsed and 20 resumed treatment with induction followed by maintenance chemotherapy. Seventeen (85%) dogs achieved a 2nd complete remission. Median overall remission for all 52 dogs was 486 days. Results of this study suggest that half-body radiation therapy after induction chemotherapy is well tolerated and might increase remission duration compared with conventional protocols that use chemotherapy alone, but this increase might not be long enough to be clinically relevant or to justify application of the method described herein.
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PMID:Chemotherapy followed by half-body radiation therapy for canine lymphoma. 1551 88

Pregnant women often develop anemia concomitant with the increase in serum erythropoietin levels, which are actually lower than those of nonpregnant anemic women due to the possible suppressive effect of endogenous estradiol on erythropoietin induction. The anemia, derived from hemodilution, does not act as a drive for erythropoietin induction, but iron deficiency, often observed during pregnancy, might. In order to demonstrate this, we investigated the effects of iron deficiency on estradiol-induced suppression of erythropoietin induction in rats. Single doses of estradiol suppressed hypoxia-, cobalt-, and bleeding-stimulated elevation of plasma erythropoietin levels and renal erythropoietin mRNA expression. Repeated administration of estradiol at 0.1 and 1 mg/kg for 2 months induced a slight anemic trend without elevation of plasma erythropoietin. Feeding an iron-deficient diet for 2 months induced plasma erythropoietin elevation without obvious anemia, but the simultaneous repeated administration of estradiol suppressed it and reversed the iron deficiency. Plasma erythropoietin levels had distinct negative correlations with plasma iron, plasma ferritin, and iron concentrations in the organs, but not with plasma hemoglobin level. These results suggest that iron deficiency would significantly stimulate erythropoietin induction during pregnancy, although estradiol might suppress it through iron restoration.
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PMID:The effects of iron deficiency on estradiol-induced suppression of erythropoietin induction in rats: implications of pregnancy-related anemia. 1578 34


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