UMLS:C0002871 - FACTA Search

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

Intravenous iron (Fe) and recombinant human erythropoietin (rHuEPO) are routine treatments in the management of anemia in patients with chronic renal failure. We investigated the oxidative stress acutely induced by these therapies and whether pretreatment with oral melatonin (MEL) would have a beneficial effect. Nine patients (four women) were studied within 1 month of entering a chronic hemodialysis program in the interdialytic period. Plasma malondialdehyde (MDA), red blood cell glutathione (GSH), and catalase (CAT) activity were measured in blood samples obtained before (baseline) and 1, 3, and 24 hours after the administration of Fe (100 mg of Fe saccharate intravenously over 1 hour) or rHuEPO (4,000 U intravenously). One hour before these treatments, patients were administered a single oral dose of MEL (0.3 mg/kg) or placebo. Each patient was studied on four occasions, corresponding to studies performed using either placebo or MEL in association with intravenous Fe and rHuEPO administration. Baseline data showed increased oxidative stress in patients with end-stage renal failure. Increments in oxidative stress induced by Fe were more pronounced at the end of the administration: MDA, baseline, 0.74 +/- 0.09 nmol/mL; 1 hour, 1.50 +/- 0.28 nmol/mL (P: < 0.001); GSH, baseline, 2.51 +/- 0.34 nmol/mg of hemoglobin (Hb); 1 hour, 1.66 +/- 0.01 nmol/mg Hb (P: < 0.001); and CAT activity, baseline, 27.0 +/- 5.7 kappa/mg Hb; 1 hour, 23.3 +/- 4.2 kappa/mg Hb (P: < 0.001). rHuEPO-induced increments in oxidative stress were more pronounced (P: < 0.001) at 3 hours (MDA, 1.24 +/- 0.34 nmol/mL; GSH, 1.52 +/- 0.23 nmol/mg Hb; CAT activity, 18.0 +/- 3.1 kappa/mg Hb). MEL administration prevented the changes induced by Fe and rHuEPO and had no adverse side effects. These studies show that intravenous Fe and rHuEPO in doses commonly used to treat anemia in chronic hemodialysis patients acutely generate significant oxidative stress. Oral MEL prevents such oxidative stress and may be of clinical use.
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PMID:Melatonin prevents oxidative stress resulting from iron and erythropoietin administration. 1127 75

This retrospective study has been performed with radiation victims who were accidentally exposed to a 60Co source and its release into the environment. The aim of the study was to assess the effects of elevated radiation exposures on plasma level, on erythrocyte thio barbituric acid reactive substance (TBARS) level and on erythrocyte glutathione (GSH) levels. Patients were treated in different hospitals with different symptoms such as nausea, vomiting, dizziness, along with severe anemia in some patients. Blood samples were collected 3-5 days following the radiation accident. Increases in plasma (6.25 +/- 0.90 nmol ml(-1)) and erythrocyte TBARS levels (330.5 +/- 30.5 micromol gHb(-1)) were found in comparison to a healthy group (3.72 +/- 0.68 nmol ml(-1) and 150.7 +/- 20.5 micromol gHb(-1), respectively) at a significant level (p<0.001). Erythrocyte GSH levels (5.2 +/- 0.30 micromol gHb(-1)) were found to be decreased among the victims (healthy group: 10.2 +/- 0.7 micromol gHb(-1)) at the same significance level (p<0.001). These observations confirm a significant change induced by radiation in the oxidant/antioxidant status among the victims. It is suggested here that antioxidant supplementation therapy might be effective in preventing the harmful effects of 60Co radiation among radiation victims.
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PMID:The effects of exposure of 60Co on the oxidant/antioxidant status among radiation victims. 1246 68

The unknown biochemical basis for neurologic dysfunction in cobalamin deficiency and the frequent divergence between neurologic and hematologic manifestations led us to study homocysteine metabolism in 22 patients with pernicious anemia. Serum levels of total homocysteine (tHcy), methionine, S-adenosylmethionine (AdoMet), cysteine, cysteinylglycine (cys-gly), and glutathione (GSH) were measured. Only levels of tHcy and cysteine were increased and only GSH was decreased in cobalamin deficiency as a whole, compared with 17 control subjects. AdoMet correlated only with methionine levels (P =.015) and cysteine only with cys-gly (P =.007) in healthy subjects, but in cobalamin-deficient patients AdoMet correlated instead with cysteine, cys-gly, and folate levels only (P =.008, P =.03, and P =.03, respectively). Significant differences appeared in clinically subgrouped cobalamin-deficient patients. The 11 patients with neurologic defects had higher mean levels of folate (27.9 versus 15.4 nM), AdoMet (117.2 versus 78.6 nM), cysteine (462 versus 325 microM), and cys-gly (85.0 versus 54.7 microM) than the 11 neurologically unaffected patients. Cobalamin therapy restored all metabolic changes to normal. The results indicate that changes in several metabolic pathways differ in patients with and without neurologic dysfunction. Cysteine levels were the most significant predictors of neurologic dysfunction, but it is unclear if they are direct or indirect indicators of neurotoxicity. The higher AdoMet levels in neurologically affected patients may result from inhibition of glycine N-methyltransferase by those patients' higher folate levels. The origin of the folate differences is unclear and possibly varied. Low AdoMet and GSH levels were independent predictors of anemia.
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PMID:Cobalamin deficiency with and without neurologic abnormalities: differences in homocysteine and methionine metabolism. 1251 17

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

Oral iron-supplementation is a general practice to correct iron deficiency anemia. Exposure of iron-deficient intestine to large doses of iron is known to induce oxidative damage, leading to loss of functional integrity, and reduced mucosal cell turnover. Conditioning of intestine with anti-oxidants during iron administration was shown to suppress iron-induced oxidative damage. Zinc is known to protect cells from peroxidative damage by inducing metallothionein and maintaining the sulfhydryl group stability. Nevertheless, co-administration of iron and zinc may antagonize each other with respect to absorption. In the present study, we show that combined supplementation of iron and zinc though marginally inhibits iron uptake significantly attenuates the oxidative stress by induction of metallothionein and elevating the levels of GSH. Further, presence of zinc in situ reduced the iron-induced hydroxyl radical production in the intestinal mucosa, as assessed by EPR spectroscopy. These results strongly suggest a protective role for zinc on iron-induced oxidative stress, which might have implications in anemia control programs.
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PMID:A protective role for zinc on intestinal peroxidative damage during oral iron repletion. 1514 71

Some selected oxidative stress parameters were measured in 56 Fanconi anaemia (FA) patients (42 untransplanted and 14 transplanted), 54 FA heterozygotes (parents) and 173 controls. Untransplanted FA patients showed a highly significant increase in leukocyte 8-hydroxy-2'-deoxyguanosine (8-OHdG) (P = 0.00003) and a borderline increase (P = 0.076) in urinary levels of 8-OHdG versus child controls. These increases were more pronounced in female FA patients (P = 0.00005 for leukocyte 8-OHdG and P = 0.021 for urinary 8-OHdG). Female FA patients also displayed a highly significant excess of spontaneous chromosomal breaks versus male patients (P = 0.00026), in the same female:male ratio ( approximately 1.4) as detected for both leukocyte and urine 8-OHdG levels. Plasma methylglyoxal (MGlx) levels were increased in untransplanted FA patients versus child controls (P = 0.032). The increases in leukocyte and urinary 8-OHdG and in MGlx levels were detected in young FA patients (< or =15 years), whereas patients aged 16-29 years failed to display any differences versus controls in the same age group. A significant increase in oxidized:reduced glutathione (GSSG:GSH) ratio was observed (P = 0.046) in the FA patients aged < or =15 years, whereas those aged 16-29 years, both untransplanted and transplanted, displayed a decrease (P = 0.06) in the GSSG:GSH ratio versus the controls of the respective age groups. No significant changes were detected in plasma levels of vitamin C, vitamin E or uric acid. Transplanted FA patients showed lesser alterations in leukocyte 8-OHdG and in GSSG:GSH ratio versus untransplanted patients. The parents of FA patients displayed a significant increase in plasma MGlx levels (P = 0.0014) versus adult controls. The results suggest a gender- and age-related modulation of oxidative stress in FA patients. The observed increase in urinary 8-OHdG in untransplanted FA patients suggests a proficient removal of oxidized DNA bases.
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PMID:Gender- and age-related distinctions for the in vivo prooxidant state in Fanconi anaemia patients. 1519 13

Intravenous Fe is widely used to treat anemia in renal disease patients. However, concerns of potential Fe toxicity exist. To more fully define its spectrum, this study tested Fe's impact on systemic inflammation following either endotoxemia or the induction of direct tissue damage (glycerol-mediated rhabdomyolysis). The inflammatory response was gauged by tissue TNF-alpha message expression and plasma TNF-alpha levels. CD-1 mice received either intravenous Fe sucrose, -gluconate, or -dextran (FeS, FeG, or FeD, respectively; 2 mg), followed by either endotoxin (LPS) or glycerol injection 0-48 h later. Plasma TNF-alpha was assessed by ELISA 2-3 h after the LPS or glycerol challenge. TNF-alpha mRNA expression (RT-PCR) was measured in the kidney, heart, liver, lung, and spleen with Fe +/- LPS treatment. Finally, the relative impacts of intramuscular vs. intravenous Fe and of glutathione (GSH) on Fe/LPS- induced TNF-alpha generation were assessed. Each Fe preparation significantly enhanced LPS- or muscle injury-mediated TNF-alpha generation. This effect was observed for at least 48 h post-Fe injection, a time at which plasma iron levels were increased by levels insufficient to fully saturate transferrin. Fe did not independently increase plasma TNF-alpha or tissue mRNA. However, it potentiated postinjury-induced TNF-alpha mRNA increments and did so in an organ-specific fashion (kidney, heart, and lung; but not in liver or spleen). Intramuscular administration, but not GSH treatment, negated Fe's ability to synergize LPS-mediated TNF-alpha release. We conclude 1) intravenous Fe can enhance TNF-alpha generation during LPS- or glycerol-induced tissue damage; 2) increased TNF-alpha gene transcription in the kidney, heart, and lung may contribute to this result; and 3) intramuscular administration, but not GSH, might potentially mitigate some of Fe's systemic toxic effects.
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PMID:Parenteral iron compounds sensitize mice to injury-initiated TNF-alpha mRNA production and TNF-alpha release. 1549 44

An increased oxidative stress is now considered one of the major risk factors in chronic renal failure (CRF) patients that may be exacerbated by dialysis. It has been postulated that this increased oxidative stress might cause an augmented red blood cell (RBC) membrane lipid peroxidation with the consequent alteration in membrane deformability. The aim of this study was to evaluate RBC susceptibility to an in vitro induced oxidative stress and RBC antioxidant potential in different groups of CRF patients undergoing different substitutive treatment modalities. Fifteen end-stage CRF patients were evaluated in conservative treatment, 23 hemodialysis (HD) patients, 15 continuous ambulatory peritoneal dialysis (CAPD) patients, 15 kidney transplanted patients, and 16 controls. Their RBCs were incubated with the oxidative stress-inducing agent tert-butylhydroperoxide both in the presence and in the absence of the catalase inhibitor sodium azide, and the level of malondialdehyde (MDA) (a product of lipid peroxidation), was measured at 0, 5, 10, 15, and 30 min of incubation. In addition, the RBC content of reduced glutathione (GSH) was measured by HPLC. As opposed to the controls, RBCs from end-stage CRF patients exhibited an increased sensitivity to oxidative stress induced in vitro, both in the absence and presence of a catalase inhibitor, as demonstrated by a significantly higher level of MDA production at all the incubation times (P < 0.05). Different substitutive treatments had different impacts on this phenomenon; CAPD and kidney transplantation were able to normalize this alteration while HD was not. GSH appeared to be related to the increase in RBC susceptibility to oxidative stress; its content being significantly elevated in end-stage CRF and HD patients as compared with CAPD and transplanted patients and controls (P < 0.05). No significant changes were observed in the RBC glutathione content during the HD session. The increase of GSH in RBCs of end-stage CRF and HD patients seems to indicate the existence of an adaptive mechanism under increased oxidative stress occurring in vivo. Unlike HD, the beneficial effect of CAPD on the anemia of dialysis patients might partly be due to a condition of lower oxidative stress that might in addition counterbalance the cardiovascular negative effects of dislipidemia of CAPD patients.
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PMID:Erythrocyte susceptibility to oxidative stress in chronic renal failure patients under different substitutive treatments. 1564 86

Side effects of treatment with chlorpromazine include anaemia which could result from decreased formation or accelerated clearance of circulating erythrocytes. Recently, a novel mechanism leading to erythrocyte clearance has been disclosed. Osmotic shock, oxidative stress and glucose deprivation lead to activation of cation channels, Ca(2+) entry, activation of a Ca(2+)-sensitive erythrocyte scramblase and subsequent exposure of phosphatidylserine at the erythrocyte surface. As macrophages are equipped with phosphatidylserine receptors, they bind, engulf and degrade phosphatidylserine exposing cells. The present experiments have been performed to explore whether chlorpromazine triggers phosphatidylserine exposure of erythrocytes. The phosphatidylserine exposure was estimated from annexin binding as determined in fluorescence activated cell sort (FACS) analysis. A 24 h exposure to glucose-free medium decreased cytosolic ATP levels, decreased cellular levels of reduced glutathione (GSH) and increased annexin binding. The effect on annexin binding and ATP but not on GSH was significantly enhanced in the presence of chlorpromazine (10 microM). Higher concentrations of chlorpromazine (40 microM) increased cytosolic Ca(2+) activity. Osmotic shock and Cl(-) removal similarly increased annexin binding, effects again being enhanced in the presence of chlorpromazine. In conclusion, the present observations point to a novel side effect of chlorpromazine, i.e. increased sensitivity of erythrocytes to glucose deprivation. The effect could well contribute to the known anaemia observed in the treatment with this antipsychotic drug.
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PMID:Stimulation of erythrocyte phosphatidylserine exposure by chlorpromazine. 1647 2

To assess the antioxidant status and oxidative stress in bovine theileriosis due to Theileria annulata blood samples were collected from 35 clinically affected cattle referred to Veterinary Teaching Hospital, School of Veterinary Medicine, Urmia University, Urmia, Iran. Complete blood count, piroplasm parasitemia percentage, erythrocyte glutathione peroxidase, superoxide dismutase, catalase and glucose-6-phosphate dehydrogenase activities, malondialdehyde concentration, osmotic fragility test and median corpuscular fragility were determined and the results were compared with those of 50 healthy controls. Of 35 affected cattle, 12 (34.28%) had severe anemia and 23 had mild to moderate anemia and parasitemia varied from 5 to 40%. The activities of erythrocyte glutathione peroxidase, superoxide dismutase and glucose-6-phosphate dehydrogenase were significantly lower (P<0.0001) and the activity of catalase was significantly higher in the affected cattle than in healthy ones (P<0.001). Malondialdehyde concentration in erythrocytes of affected cattle was significantly more than those of healthy cattle (P<0.001). The affected cattle showed increased fragility of erythrocytes, so that median corpuscular fragility (MCF) in affected group was significantly lower than those of healthy group (P<0.0001). Median corpuscular fragility showed a positive correlation with the severity of parasitemia (r=0.81, P<0.0005) and a negative correlation with the activities of GSH-Px (r=-0.78, P<0.0001), SOD (r=-0.71, P<0.0005), catalase (r=-0.53, P<0.018) and G6PD (r=-0.58, P<0.0005). The results of this study suggest that oxidative damage to RBCs may contribute to the pathogenesis of anemia in bovine theileriosis.
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PMID:Evaluation of antioxidant status and oxidative stress in cattle naturally infected with Theileria annulata. 1690 49

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