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

Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism. Selenium deficiency and disturbed thyroid hormone economy may develop under conditions of special dietary regimens such as long-term total parenteral nutrition, phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced nutrition in children, elderly people, or sick patients.
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PMID:The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health. 1248 69

Iron-deficiency anemia has been shown to alter body mineral concentrations and activities of iron- and non-iron-containing enzymes, especially those with antioxidant functions. These effects, however, have been less studied in nonanemic iron-depleted individuals. Thus, this study assessed indices of selenium status in 12 college-aged females with adequate iron stores and 15 college-aged females with low iron stores before and after iron therapy. Blood samples were drawn at baseline for both groups and following iron supplementation in the low-iron-stores group. Hematocrit, hemoglobin, and serum ferritin concentrations of the low iron- stores group were significantly lower than those of the control group. The serum transferrin receptor-to-serum ferritin ratio in the low-iron stores group was significantly greater than that of the control group. Serum selenium and glutathione peroxidase concentrations of the low-iron-stores group were not significantly different from those of the controls. Iron supplementation significantly increased hemoglobin, hematocrit, and serum ferritin concentrations and significantly decreased the serum transferrin receptor concentration and serum transferrin receptor:serum ferritin ratio in the low-iron-stores group posttreatment compared to pretreatment. Serum selenium and glutathione peroxidase concentrations did not differ significantly from pretreatment to posttreatment in the low-iron-stores group. Results of this study indicate that low iron stores without anemia are not associated with impaired selenium status in college-aged females.
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PMID:Iron depletion without anemia is not associated with impaired selenium status in college-aged women. 1271 7

This study was designed to measure the effect of iron supplementation on antioxidant status in iron-deficient anemia, including the time for hemoglobin normalization and at the time of filling of iron body stores. The extent of plasma lipid peroxidation was evaluated by measuring the levels of malondialdehyde and glutathione peroxidase (GSH-Px), and the activities of superoxide dismutase (SOD) and catalase in 63 patients with iron-deficiency anemia before and after 6 wk of iron supplementation and at the time when body iron stores are saturated. After 6 wk of iron supplementation, a significant decrease of oxidative stress was observed in the treated subjects relative to controls (p<0.05). No significant differences existed between treated patients at 6 wk and at the end of the study. The erythrocyte levels of catalase, SOD, and GSH-Px were significantly lower in treated patients relative to controls (p<0.05). These levels increased after 6 wk of supplementation (p<0.05) and showed no significant differences with those at the end of the study.
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PMID:Effect of iron supplementation on oxidative stress and antioxidant status in iron-deficiency anemia. 1471 90

Anemia occurs in more than 30% of patients with epithelial ovarian cancer before any surgery. High levels of proinflammatory cytokines and increased oxidative stress may contribute to the development of cancer-related anemia. We assessed a population of previously untreated patients with advanced epithelial ovarian cancer to evaluate whether there was a correlation between hemoglobin (Hb) and parameters of inflammation and oxidative stress, stage of disease, and performance status (PS). In 91 patients with epithelial ovarian cancer and 95 healthy women matched for age, weight, and height, levels of Hb, C-reactive protein (CRP), fibrinogen (Fbg), proinflammatory cytokines, leptin, reactive oxygen species (ROS), and antioxidant enzymes were assessed at diagnosis before treatment. The correlations between Hb, parameters of inflammation and oxidative stress, stage, and PS were evaluated. Hb levels were lower in patients with advanced epithelial ovarian cancer than in control subjects and inversely related to stage and PS. Hb negatively correlated with CRP, Fbg, interleukin 1beta (IL-1beta), IL-6, tumor necrosis factor alpha (TNFalpha), and ROS, and positively correlated with leptin and glutathione peroxidase (GPx). Multivariate regression analysis showed that stage and IL-6 were independent factors determining Hb values. This evidence suggests that anemia in epithelial ovarian cancer is common and its presence is related to stage of disease and markers of inflammation.
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PMID:Hemoglobin levels correlate with interleukin-6 levels in patients with advanced untreated epithelial ovarian cancer: role of inflammation in cancer-related anemia. 1577 16

Haematological and biochemical features of sixteen cases of post-parturient haemoglobinuria (PPH) from 15 farms in the Waikato and Bay of Plenty regions are described. Characteristically there was a marked regenerative anaemia as well as spherocytosis and haemoglobinaemia. Heinz body formation occurred in 140% of erythrocytes depending on the case. Nine of 11 cases examined had subnormal serum inorganic phosphorus concentrations. On two of eight farms there was widespread anaemia in clinically healthy herd mates and in one of these the anaemia was associated with large numbers of Heinz bodies. Hypophosphataemia was widespread in four of ten herds and individual cows were hypophosphataemic in all ten. Six of eight herds had a low selenium status as determined by glutathione peroxidase activity in whole blood. Hypocupraemia and hypomagnesaemia were not consistent findings. It is concluded that there are two distinct entities of PPH in the region. On one farm the disease was typical of that seen in Northland, New Zealand. The clinical case was a young cow and there was widespread subclinical Heinz body anaemia in herd mates. All but one of the cows sampled in that herd had normal serum inorganic phosphorus levels. On most other farms PPH closely resembled that described from North America. Affected cases were miltiparous, high producing and had low serum inorganic phosphorus levels. The possible pathogenesis of these two entities is discussed.
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PMID:Bovine post-parturient haemoglobinuria: two distinct entities in New Zealand. 1603 Dec 10

The erythrocytes of patients suffering from chronic renal failure (CRF) are exposed to an increased activity of free radicals. These compounds are generated by uremic toxins and hemodialysis itself. They cause the peroxidation of lipids and proteins in red blood cell membrane. It leads to a decrease of erythrocytes' stability and a lower resistance to hemolysis. The advanced oxidation protein products and advanced glycation end products (AOPP and AGE) also contribute to these changes. The described processes deepen the anemia in CRF and make difficulties in its treatment. In addition, the quoted references present a lot of disturbances in activities of the enzymes and metabolic pathways, which provide antioxidant reactions. This group consists of: superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), glutathione reductase (GSSG-R) end the enzymes of the pentose-phosphate shunt (PPS). The intensity of changes is according to the stage of the disease and the efficiency of treatment. Its most appropriate form is renal transplantation.
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PMID:[Oxidative stress as a reason of treatment difficulties in chronic renal failure]. 1649 15

Since the discovery of hydrogen peroxide in 1819 it was known as a toxic agent for human organs. Due to the recent findings its role should be reevaluated. This review discusses the toxic and physiological roles of hydrogen peroxide and functions of enzyme catalase which is the main regulator of hydrogen peroxide metabolism. The concentration of hydrogen peroxide changes between 0,05 micromol/l and 117 micromol/l in exhaled breath condensate and in human fluids. Hydrogen peroxide is generated by physiological processes such as glycation, phagocytosis, cell metabolism and by pathological changes such as different tumors and side effects of some drugs. The main regulator of toxic concentration of hydrogen peroxide is the enzyme catalase while glutathione peroxidase and hemoglobin has a limited role in this process. Low concentration of hydrogen peroxide plays a role in degradation of some proteins, as a messenger in cell signaling and could contribute to apoptosis. The enzyme catalase, due to its structure and function, is very effective in destroying the toxic concentration of hydrogen peroxide without changing its low, physiologic concentration. Decrease in catalase due to anemia, decreased synthesis and especially to its inherited deficiency may be a risk factor in diabetes, cell damage due to ischemia, in uricase and ascorbic acid treatment as well as in sterilization with hydrogen peroxide. The hydrogen peroxide paradox means that its low concentration is vital for some physiological processes while its high concentration is toxic for human cells. The main regulator of hydrogen peroxide concentration is the enzyme catalase and its deficiency may be a risk factor for some pathological changes.
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PMID:[The hydrogen peroxide paradox]. 1678 44

Anemia is one of the main complications seen in patients with end stage renal disease (ESRD) treated with hemodialysis. We hypothesized that oxidative stress and decrease of antioxidant defense enzyme activity may be major causes underlying functional insufficiency of erythrocytes. Blood samples of 16 patients with ESRD undergoing hemodialysis were investigated. All patients received Recormon for treatment of anemia. In spite of effective hemodialysis procedures cleared patient blood the erythrocyte activities of superoxide dismutase (SOD), glutathione peroxidase (GP) were lower than in healthy controls and hemodialysis procedure insignificantly influenced enzyme activities. After 6 months repeated study of the erythrocyte enzymes revealed further decrease of SOD and GP activities.
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PMID:[Diagnostic and prognostic value of antioxidant enzyme assay in erythrocytes of patients with end stage renal disease treated with hemodialysis]. 1680 95

Free radicals and associated oxidative stress induced by alloxan are implicated in eliciting pathological changes in diabetes mellitus. Terminalia arjuna bark, an indigenous plant used in ayurvedic medicine in India, primarily as a cardiotonic is also used in treating diabetes, anemia, tumors and hypertension. The present study examined the effect of ethanolic extract (250 and 500 mg/kg body weight) of Terminalia arjuna stem bark in alloxan induced diabetic rats and its lipid peroxidation, enzymatic and nonenzymatic activity was investigated in the liver and kidney tissues. The extract produced significant (P<0.05) reduction in lipid peroxidation (LPO). The effect of oral T. arjuna at the dose of 500 mg/kg body weight was more than the 250 mg/kg body weight. The extract also causes a significant (P<0.05) increase in superoxide dismutase, catalase, glutathione peroxidase, glutathione-s-transferase glutathione reductase and glucose-6-phosphate dehydrogenase, reduced glutathione, vitamin A, vitamin C, vitamin E, total sulfhydryl groups (TSH) and non protein sulfhydryl groups (NPSH) in liver and kidney of alloxan induced diabetic rats, which clearly shows, the antioxidant property of T. arjuna bark. The result indicates that the extract exhibit the antioxidant activity through correction of oxidative stress and validates the traditional use of this plant in diabetic animals.
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PMID:Effect of Terminalia arjuna stem bark on antioxidant status in liver and kidney of alloxan diabetic rats. 1705 32

The antioxidant status of rats experimentally infected with Trypanosoma evansi isolated from a camel was studied using established parasitological, haematological and biochemical methods. The results indicated that infections in all rats resulted in a fulminating parasitaemia. Changes in blood parameters in T. evansi-infected rats indicated leukocytosis and a macrocytic hypochromic anaemia. A degree of anisocytosis was also observed. The activities of plasma glucose-6-phosphate dehydrogenase and glutathione peroxidase in whole blood of infected rats were significantly higher (p<0.05 and p<0.001, respectively) compared with control. No statistically significant difference was observed in the activity of superoxide dismutase in infected and control rats. Results obtained indicated that trypanosomosis caused oxidative stress and induced antioxidant enzymes.
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PMID:Study on the antioxidant status of rats experimentally infected with Trypanosoma evansi. 1716 91


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