Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new procedure utilizing dried blood spots was developed for detecting glutathione peroxidase deficiency. Samples from a known patient with a partial defect and from rats with an induced deficiency were distinguished from respective control groups by their longer defluorescence endpoints. Samples from 100 patients with anemia and 2 phenyl-ketonuric infants on low-protein diets contained glutathione peroxidase activity similar to that in 82 controls, when screened for the enzyme defect by the new procedure.
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PMID:Glutathione peroxidase in dried blood spots. 3 67

The activities of 2Cu,2Zn-superoxide dismutase, ferroxidase (ceruloplasmin), catalase and glutathione peroxidase were measured in the blood of rats during copper depletion. Two control groups of animals were used; one received the regular diet containing all essential components including copper and the other group was maintained on a diet, containing 1% the amount of copper in normal diet, copper being supplied as Cu(Leu)2 in the drinking water. Both groups showed no detectable differences, either in the copper content of blood or in the measured four enzymic activities. Excessive copper (injected intraperitoneally) caused only an insignificant rise in the enzymic activities (0-10%) compared to either control. After starting copper depletion ferroxidase activity decreases to 15% on the 15th day, while the 2Cu,2Zn-superoxide dismutase activity decreases to 40% on the 45th day. Ferroxidase activity shows rapid but transient changes immediately after perturbation in plasma copper levels. By contrast, the 2Cu,2Zn-superoxide dismutase activity more closely parallels the overall copper deficiency. Dietary repletion with copper raises the 2Cu,2Zn-superoxide dismutase activity to 94% and the ferroxidase activity to 80% of the control values within 36 h. Apart from the copper-dependent anemia catalase activity was decreased. However, 15 days after the start of the copper depletion catalase activity rises again and reaches the control value on the 40th day and a 30% stimulation was even seen on the 58th day. Upon copper repletion catalase activity reaches 166% of the control within 14 days. No copper-dependent differences of glutathione peroxidase activity were seen regardless whatever copper level was present in the rats.
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PMID:Copper deficiency and erythrocuprein (2Cu, 2Zn-superoxide dismutase). 97 14

Cobalt deficiency was produced in goats by feeding them rhode grass hay. The deficient animals excreted increased amounts of methyl malonic acid in their urine, indicating a lack of vitamin B12. Erythrocyte reduced glutathione levels increased with the onset of anemia. There was a concomitant increase in the levels of erythrocyte glutathione reductase (GSSG NADPH Reductase) and glutathione peroxidase (GSH:H2O2 peroxidase)during deficiency. These results are compared with similar observations reported for vitamin B12 deficiency in humans.
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PMID:Erythrocyte glutathione metabolism in cobalt-deficient goats. 103 28

The extent of reduced glutathione, activity of glutathione peroxidase, amount of membrane lipid peroxidation products, and the extent of hemoglobin release from host erythrocytes during in vitro Plasmodium falciparum growth was studied. Highly synchronized parasite cultures were studied to examine the alterations caused by different growth stages of the parasite. There was a moderate increase in the reduced glutathione content as the parasite matured, which was significant only in schizont-rich erythrocyte lysates (p < 0.05) whereas the activity of glutathione peroxidase was significantly low in all the parasitized red blood cells (ring-infected RBC, p < 0.005; trophozoite- and schizont-infected RBC, p < 0.001). The lipid peroxidation product, malonyldialdehyde, of the host red cells increased gradually to more than fourfold in schizont-rich cells as compared with normal erythrocytes (p < 0.001). The hemoglobin release from cultured cells was significantly higher in all parasitized red cell cultures as well as in uninfected cells kept in in vitro, as compared with normal erythrocytes. The consequence of such changes induced by the malarial parasites in the host red cells in the pathogenesis of erythrocyte destruction and anemia of P. falciparum malaria is discussed.
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PMID:Oxidative damage of erythrocytes infected with Plasmodium falciparum. An in vitro study. 139 Nov 22

Erythrocyte antioxidants catalase, superoxide dismutase, reduced glutathione and glutathione peroxidase were studied in cells harbouring different growth stages of Plasmodium falciparum. Catalase and superoxide dismutase showed significant decrease during parasite maturation indicating hampered metabolism of hydrogen peroxide and superoxide anions. Glutathione peroxidase also exhibited a downward trend during the growth of P. falciparum, while there was a moderate accumulation of reduced glutathione. These findings suggest decreased utilization of the reduction potential in detoxification of reactive oxygen species. The fall in all three antioxidant enzymes studied was highly significant (P less than 0.001) in erythrocytes with mature stages of the parasite (trophozoites, schizonts). The increased vulnerability of erythrocytes to damage, which parallels the growth phases of the parasite emphasizes the need for early treatment of P. falciparum malaria to minimise red cell destruction and the resulting anaemia.
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PMID:Plasmodium falciparum induced perturbations of the erythrocyte antioxidant system. 139 36

This study tests the hypothesis that Cu and Se deficiencies enhance doxorubicin-induced cardiotoxicity and anemia. Male Sprague-Dawley rats (n = 48) were fed Cu and Se-adequate (+Cu+Se), Cu-deficient (-Cu), Se-deficient (-Se) or Cu and Se-deficient (-Cu-Se) diets for 5.5 wk. Doxorubicin (4 mg/kg body wt) or saline was administered once weekly for the last 4 wk of the study. Copper deficiency was confirmed by 79% lower liver Cu, 67% lower liver Cu,Zn superoxide dismutase (Cu,Zn SOD) activity and 76% lower erythrocyte Cu,Zn SOD activity. Selenium deficiency was confirmed by 90% lower liver glutathione peroxidase activity. Rats fed the -Cu diet had greater reductions in hematocrit than did those fed the +Cu diet after administration of doxorubicin. Doxorubicin, Cu deficiency and Se deficiency all produced electrocardiographic abnormalities and ultrastructural anatomical lesions. However, the dietary deficiencies did not enhance doxorubicin-induced cardiotoxicity. Doxorubicin, but not Cu or Se deficiency, raised lipid peroxidation 16% in liver (P < 0.01) and 18% in heart (not significant). These data suggest that the cardiomyopathies caused by doxorubicin and Cu and Se deficiencies have some similarities, but cardiac changes may be related to mechanisms other than lipid peroxidation.
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PMID:Copper and selenium deficiencies do not enhance the cardiotoxicity in rats due to chronic doxorubicin treatment. 143 53

Ten patients with chronic renal failure (CRF) treated by hemodialysis (HD) were examined. All the patients demonstrated remarkable anemia. The red blood cell count was (2.7 +/- 0.2) x 10(12)/I the concentration of hemoglobin 79.5 +/- 5.6 g/l, on the average, hematocrit 23.2 +/- 1.8%. The content of malonic dialdehyde in the patients' red blood cells was far greater than in controls, amounting to 132% (per 1 ml of hemolysate), 134% (per 1 mg of protein) (p < 0.05). Catalase and glutathione peroxidase activity in the patients' red blood cells did not differ from that in controls. Superoxide dismutase activity reduced by 43% as compared to that in donors (p < 0.001). The authors review possible mechanisms of lipid peroxidation (LPO) and a decrease of antioxidant defense in red blood cells of CRF patients on hemodialysis. It is concluded that activation of LPO processes and the decrease of antioxidant defense produce a noticeable destructive effect on the integrity of the red blood cell membrane. They also influence the development of hemolysis.
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PMID:[Lipid peroxidation as a possible mechanism of erythrocyte damage in patients with chronic kidney failure on hemodialysis]. 144 Mar 43

The effect of selenium status on the development of Heinz body anaemia was studied in 16 three months old Saanen goats which received a diet with a low selenium content. The control group (Se-, n = 8) received no supplementary selenium while the treated group (Se+, n = 8) received selenium by injection. Erythrocyte glutathione peroxidase concentration was significantly higher in the Se+ group than in the control group (105 vs 36 U/g Hgb). The animals were drenched once per day with 30 mg of dimethyl disulphide (DMDS) per kg of body weight for 14 days and with 50 mg per kg during the following 11 days. Erythrocytes with Heinz bodies appeared within one week after increasing the DMDS dose to 50 mg/kg/day and reached a peak one week later (30% and 37% of erythrocytes with Heinz bodies in group Se+ and Se- respectively). Within the next three weeks haemoglobin levels dropped from 135 g/l to 123 g/l and 114 g/l in the Se+ and the Se- group respectively. Differences between the two groups were statistically significant for the percentage of erythrocytes with Heinz bodies and for haemoglobin values (p less than 0.05). The data support the hypothesis that selenium status influences the resistance of ruminants to brassica-induced Heinz body anaemia.
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PMID:[The effect of the selenium status of goats on the resistance of erythrocytes to oxidative damage]. 187 69

We investigated the effects of ethylene glycol (EG) on the hepatic drug metabolizing enzymes. The exposed group was given 1% EG solution and the control group was provided with distilled water for 2 weeks ad libitum. The body weight of the exposed group was the same as that of the control group. The liver and kidney weight per body weight did not change. The daily drinking volume for the exposed group on the average showed an increase of 13.5% over that of the control group. Hematologically and biochemically, anemia, liver and renal dysfunction were not seen. The content of the hepatic microsomal cytochrome P-450 in the exposed group showed an increase of 17% over that of the control group, but the contents of cytochrome b5, protoheme and the activities of NADPH-cytochrome c reductase, NADH-ferricyanide reductase did not change. The activities of the hepatic cytosolic alcohol dehydrogenase and glutathione reductase, glutathione peroxidase, glutathione-S-transferase also did not change. These results indicate that the hepatic microsomal cytochrome P-450 takes part in the metabolism of EG.
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PMID:[Effects of ethylene glycol on drug metabolizing enzymes in rat liver]. 202 9

When Wistar male rats were exposed to ethylene oxide (EtO) at a concentration of about 500 ppm, 6 hr a day, 3 days a week for 2, 6, or 13 weeks, hematological examination showed macrocytic, normochromic anemia with a high reticulocyte count. This result raised the possibility that the hemolytic process was responsible for the anemia. Thus, the following possible causes of hemolysis were investigated with erythrocytes obtained from control and EtO-exposed rats. (1) Metabolism in erythrocytes; (a) Hexose monophosphate cycle: The activity of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, or glutathione peroxidase was not affected, but the activity of glutathione reductase (GR) significantly decreased and did not recover by the addition of flavin adenine dinucleotide. Reduced glutathione content also decreased and the glutathione stability test was positive. (b) Embden-Meyerhof pathway: Adenosine triphosphate content did not decrease. (c) Lapoport-Luebering cycle: 2,3-Diphosphoglycerate content was not affected. (2) Membrane alterations: Osmotic fragility was not affected and the activity of acetylcholine esterase in the ghost membranes of the exposed group increased. (3) Hemoglobin stability: The heat test and the isopropanol test were negative. GR has an important function in maintaining the reducing power in erythrocytes, and the decrease in the activity caused by EtO induced an alteration of the glutathione stability. Although the mechanism of EtO-induced anemia could not be clearly explained, the inhibition of GR activity might be related to the anemia.
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PMID:Biochemical changes in rat erythrocytes caused by ethylene oxide exposure. 225 9


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