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)

Male and female rats were used to investigate the effects of type of dietary carbohydrate (CHO), copper, and ethanol consumption on lung antioxidant enzyme activities and levels of phosphorylated compounds in whole blood. Copper-deficient female rats exhibited a greater degree of copper deficiency than males, as assessed by hepatic copper concentration and hepatic copper superoxide dismutase (CuSOD) activity. However, copper-deficient male rats fed fructose-containing diets exhibited greater growth retardation, anemia, and heart hypertrophy than females consuming the same diets and males fed starch. In addition, one of 10 copper-deficient male rats that ate a fructose-based diet and drank water and one of 10 copper-deficient male rats that ate a starch-based diet and drank ethanol died. Copper-deficient, starch-fed males exhibited the highest activities of glutathione peroxidase (GSH-Px) and catalase as compared with fructose-fed rats. Ethanol consumption elevated the activities of GSH-Px and catalase. Copper-deficient female rats exhibited higher catalase but lower GSH-Px activities than males. It is suggested that in copper deficiency, the ability to increase antioxidant enzyme activities in rats consuming starch is greater than in rats consuming fructose. Rats fed starch are provided with a greater degree of protection against oxidative damage than rats fed fructose. In addition, polyphosphorylated compounds in blood were reduced in copper-deficient male rats that consumed fructose-based diets. This may impair supply of oxygen to tissues.
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PMID:Antioxidant defense system in lung of male and female rats: interactions with alcohol, copper, and type of dietary carbohydrate. 854 77

In 4 chronic hemodialysis patients we have tested whether the administration of reduced glutathione (GSH; Glutamed, Boehringer Mannheim Italia; 1,200 mg i.v.) at the end of each hemodialytic session during 90 days could minimize oxidative damage to the red blood cells (RBC) and reduce the recombinant human erythropoietin requirements. Treatment with GSH was followed by an increase in RBC GSH content (n = 3), a normalization of the ascorbine cyanide test (n = 4), an increase in RBC survival (n = 3), and a reduction in 2 patients of the erythropoietin need (41 and 26%, respectively, after 3 months of therapy). When the GSH supplements were terminated, we noticed after 3 months a re-establishment of the baseline values. On the other hand, malonyldialdehyde, RBC deformability, and RBC splenic pool were abnormal before and remain abnormal during the test period. Since no adverse reactions were noticed, these findings seem to indicate the GSH could ameliorate the intraerythrocytic oxidative defense and could be as useful drug in the treatment of anemia in patients affected by chronic renal failure.
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PMID:Reduced glutathione for the treatment of anemia during hemodialysis: a preliminary communication. 856 84

A previous study revealed that DQ-2511, a new gastroprokinetic drug, induced hemolytic anemia together with increased Heinz body formation, preceded by a marked decrease in erythrocyte reduced glutathione (GSH) content, after 2 weeks of dosing onward in dogs. In this study, the effect of DQ-2511 on erythrocytes in the early period of dosing, in comparison with that of beta-acetylphenylhydrazine (APHZ), was investigated to confirm the difference between this drug and APHZ in the mechanism of increased Heinz body formation. DQ-2511 and APHZ were administered orally to beagle dogs for 1 week at dose levels of 600 and 4 mg/ kg, respectively. Dogs receiving APHZ showed anemia after dosing for 7 days, together with an increase in methemoglobin and Heinz body formation after 3 days of dosing. In contrast, blood GSH, glutathione reductase, and gamma-glutamylcysteine synthetase were only slightly decreased after dosing for 7 days. In dogs treated with DQ-2511, erythrocyte GSH began to decrease after 1 day of treatment and was about 25% of the control value after 7 days; however, no changes were seen in blood glutathione reductase, GSH peroxidase, or gamma-glutamylcysteine synthetase level. Hepatic GSH was decreased slightly. In another experiment, SD rats were administered DQ-2511 and APHZ orally for 1 week at dose levels of 1600 and 15 mg/kg, respectively. Rats receiving DQ-2511 showed no anemia or any changes in erythrocyte GSH and Heinz body formation. In contrast, rats treated with APHZ showed a marked anemia and increases in Heinz body formation and erythrocyte GSH. These results demonstrate that DQ-2511 causes a marked decrease in GSH in dogs, resulting in Heinz body anemia, whereas APHZ induces Heinz body formation after a significant increase in methemoglobin, and suggest that impairment of the GSH redox cycle and synthetases of GSH are not involved in the decreased GSH after DQ-2511 treatment. This difference in effects on GSH content may indicate the existence of a species difference in the anemia induced by DQ-2511.
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PMID:A possible mechanism of heinz body hemolytic anemia induced by DQ-2511, a new gastroprokinetic drug, in dogs. 892 30

During acute Trypanosoma vivax infection of calves, produced by intravenous inoculation, the mean packed cell volume and red blood cell counts of the infected animals decreased significantly (P < 0.05) between Days 6 and 13 post-infection (pi). The moderately severe normocytic anaemia started to develop during the first wave of parasitaemia which occurred from Day 2 pi and peaked between Days 4 and 5 pi. The mean erythrocyte glutathione (GSH) concentration of the infected calves decreased significantly (P < 0.05) from 58.4 +/- 11.4 mg 100ml-1 red blood cells (RBC) on Day 0 pi to 44.5 +/- 12.8 mg 100ml-1 RBC on Day 5 pi. As the GSH values recovered on Day 6 pi and increased thereafter, another slight decrease (P > 0.05) in GSH concentration occurred on Day 12 pi at the second peak of parasitaemia followed by a significant (P < 0.05) increase to 79.1 +/- 14.6 mg 100ml-1 RBC on Day 13 pi. In the uninfected calves, the mean GSH values ranged from 47.7 +/- 7.0 to 60.8 +/- 6.8 mg 100ml-1 RBC. When washed, erythrocytes of the infected and uninfected calves were separately challenged with hydrogen peroxide. They produced comparable amounts of thiobarbituric acid reactive substances as a measure of by-products of lipid peroxidation. This suggested that the ability of the erythrocytes to prevent peroxidative injury was not reduced, because GSH regeneration was probably enhanced and the antioxidant capacity of the erythrocytes was maintained.
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PMID:Effect of acute Trypanosoma vivax infection on cattle erythrocyte glutathione and susceptibility to in vitro peroxidation. 896 88

Endogenous oxygen radical scavengers such as glutathione peroxidase (GSH-Px), catalase (CAT), glutathione and vitamin E are powerful regulatory systems against free radical toxicity. These oxidative injuries are increased in patients with chronic renal failure leading to various abnormalities including anemia. In this study, activities of GSH-Px, CAT, glutathione and vitamin E were measured in the erythrocytes of 54 chronic renal failure patients compared with 32 healthy controls. GSH-Px activities were lower significantly from controls (20.5 +/- 6.79 vs 28.3 +/- 9.0 u/gHb, p < 0.001). Erythrocytes CAT (6.52 +/- 2.3 vs 7.54 +/- 1.9 u/gHb, p < 0.05), glutathione (63.59 +/- 20.2 vs 75.1 +/- 6.3 mg/dl, p < 0.05) vit. E (2.23 +/- 0.53 vs 3.38 +/- 0.44 g/ml RBC, p < 0.001) were also lower in the patients group. Plasma malondialdehyde (MDA) known as lipid peroxidation product was higher significantly than controls (p < 0.001). Abnormal erythrocyte osmotic fragility test, expressed by glycerol lysis time (GLT50) was found in the patients group (p < 0.001) and correlated significantly with RBC vitamin E. Results demonstrated defects in erythrocytes enzymatic antioxidant defense mechanism in chronic renal failure patients. To improve antioxidant systems seems to be promising in preventing hemolysis and anemia in these patients.
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PMID:Reduced free radical scavengers and chronic renal failure. 907 94

Blood and erythrocytes of 50 healthy volunteers and 105 patients with different forms of hemoblastoses were investigated. 54 patients had acute phase, 51 patients--remission stage of disease. Essential differences in the activity of antioxidant enzymes (SOD, CAT, GSH-Px) were detected and compared with content of MDA and degree of anaemia. Acute phase had more significantly alteration of antioxidant defence: diverse changes of the activity of SOD and CAT, significantly inhibition of GSH-Px, the high level of MDA and increased degree of anaemia.
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PMID:[Possible use of erythrocyte antioxidant enzymes as markers of the course of disease in patients with hemoblastoses]. 914 1

The given report deals with investigation of the level of spontaneous lipid peroxidation (LPO) (as judged by the accumulation of MDA) and activity of antioxidative enzymes (GSH-peroxidase, GSH-reductase) in red blood cells of pregnant women (24-26 weeks) suffering from minor (blood Hb is 95 g/l) and medium (blood Hb is 85-90 g/l) anemias. We have found that as the anemia becomes deeper, the red blood cells of pregnant women demonstrate a linear increase in the level of spontaneous LPO, which rises by 54% during anemia of moderate severity (p < 0.02) as compared with control. At the same time, simultaneously with LPO, the activity of the above glutathione-containing enzymes increases as the anemia progresses, which, apparently, is of the compensatory nature, aimed at the maintenance of the reduced glutathione pool, the latter being an important component of the cell antioxidative system during LPO activation. The authors think the increased activity of the physiological antioxidative system and intensification of the LPO processes to be a natural adaptive process, since lipid hydroperoxides are the activators of synthesis of prostaglandins, which are required in delivery.
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PMID:[Intensity of lipid peroxidation processes and activity of antioxidant enzymes in erythrocytes during anemia in pregnancy]. 927 21

Reduced glutathione (GSH) is an important scavenger of free radicals in the red blood cell (RBC) membrane, and its deficiency may be a partial cause of increased hemolysis and shortened RBC survival in uremics. In this study we employed exogenous GSH (1200 mg i.v. at the end of each dialysis session for at least nine months) to treat anemia in a group of 28 hemodialyzed patients, 14 of whom were also receiving erythropoietin. RBC survival (51Cr T/2) was calculated before (26 patients) and at the end (15 pts) of GSH therapy. After the first three months anemia (RBC, hemoglobin, hematocrit, reticulocytes) improved significantly in 17 patients (60%), for as long as they were under therapy, but rapidly dropped to pre-treatment values when GSH was discontinued. The 51Cr T/2 increased significantly in responders, but not in those who did not respond. No significant differences were found between responders and non-responders as regards urea KT/V, PTH, serum iron, ferritin, dialysis membrane, dose of erythropoietin and basal 51Cr T/2. These results suggest that exogenous GSH may be a promising drug for the treatment of anemia in most hemodialyzed patients, particularly considering its low cost.
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PMID:Effect of exogenous reduced glutathione on the survival of red blood cells in hemodialyzed patients. 936 18

A study to investigate the association between blood glutathione (GSH) levels and biliary excretory status was conducted in apparently healthy Ghanaian subjects without frank biliary disease and anaemia. The results showed that, in adults (mean age: 38.5 years) and children (mean age: 13.0 years), plasma conjugated bilirubin is inversely correlated with blood GS (respective site r = -0.524, p < 0.011 and -0.395, p < 0.005). Persons with elevated plasma conjugated bilirubin compared to controls (mean: 6.0 versus 2.5 umol/L, p < 0.001) also exhibited low blood GSH values (3.5 versus 4.2 umol/gHb, p < 0.029). Malaria parasites with counts up to 2,453 parasites/ul blood had no effect on the obtained data. The results suggest that low blood GSH levels may be relevant to delays in biliary excretion of conjugated toxins from the liver, as exemplified by the rise in conjugated bilirubin levels in the plasma, and predispose liver cells to increased oxidant state and damage.
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PMID:Biliary excretion in persons with low blood glutathione levels. 974 34

This study examined whether lead-induced alterations in selected parameters that are indicative of oxidative stress accompany the toxic effects of lead in red blood cells (RBCs) in vivo. It also explored the possibility that treatment with N-acetylcysteine (NAC) or succimer (meso-2,3-dimercaptosuccinic acid) was capable of reversing parameters indicative of lead-induced oxidative stress. Fisher 344 rats were given 2000 ppm lead acetate in their drinking water for 5 weeks. The lead was then removed and the animals were given NAC (800 mg/kg/day) or succimer (90 mg/kg/day) in their drinking water for 1 week, after which the RBCs were harvested. Animals not given lead and those given lead, but not NAC or succimer, served as negative and positive controls, respectively. At the end of the experiment, blood-lead levels were 35 +/- 4 microg/dl in lead-treated animals, which were reduced to 2.5 +/- 1 microg/dl by treatment with succimer and to 25 +/- 3 microg/dl by treatment with NAC. Lead-exposed animals demonstrated signs of anemia as evidenced by anisocytosis, poikilocytosis, and alterations in hemoglobin, hematocrit, and mean corpuscular volume. Lipid peroxidation, as evidenced by increased malondialdehyde (MDA) content, as well as decreases in reduced glutathione (GSH) and increases in catalase and glucose 6-phosphate dehydrogenase (G6PD) activity were noted in RBCs from lead-treated rats, suggesting that the lead induced oxidative stress. In addition, a significant reduction in blood delta-aminolevulinic acid dehydratase (ALAD) activity suggested that accumulation and autooxidation of delta-aminolevulinic acid might contribute to lead-induced oxidative stress. Treatment with either NAC or succimer reversed lead-induced alterations in MDA and GSH content, but only succimer appeared to partially restore ALAD activity. These results provide in vivo evidence supporting the hypothesis that lead induces oxidative stress in RBCs, which is reversible by treatment with a thiol antioxidant (NAC), as well as a chelating agent (succimer).
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PMID:Antioxidant effects of N-acetylcysteine and succimer in red blood cells from lead-exposed rats. 975 41


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