Malonyldialdehyde Content Research Articles

Disappearance of oxidative damage to red blood cell membranes in uremic patients following renal transplant.

Hemodialysis patients display increased oxidative damage to red blood cell (RBC) membranes, characterized by elevated levels of malonyldialdehyde (MDA), a short chain aldehyde produced by the oxidation of the polyunsaturated fatty acids (PUFA) in the RBC membranes. This is the result of a metabolic blockage of the pentose-phosphate shunt in uremic patients, which causes reduced detoxification of highly oxidative free radicals. The oxidative damage induces increased RBC rigidity and decreased RBC deformability, therefore favoring hemolysis. The aim of this work was to determine if a functioning renal graft would restore normal erythrocyte metabolism, reducing the oxidative damage. To this end, we have determined RBC MDA concentrations in 20 hemodialysis (HD) patients (RBC MDA 18.22 +/- 4.36 micrograms/ml packed RBC), 20 renal transplant (T) patients with well functioning grafts (serum creatinine less than 2 mg%) (RBC MDA 1.2 +/- 0.4 micrograms/ml packed RBC) (T vs. HD P less than 0.005) and 20 healthy controls (HC) (RBC MDA 1.44 +/- 0.6 micrograms/ml packed RBC) (HC vs. HD P less than 0.005; HC vs. T NS). Our findings show that a well-functioning renal graft restores normal RBC metabolism and eliminates the oxidative damage induced by uremia.

Disappearance of Oxidative Damage to Red Blood Cell Membranes in Uremic Patients Following Renal Transplant

Hemodialysis patients display increased oxidative damage to red blood cell (RBC) membranes, characterized by elevated levels of malonyldialdehyde (MDA), a short chain aldehyde produced by the oxidation of the polyunsaturated fatty acids (PUFA) in the RBC membranes. This is the result of a metabolic blockage of the pentose-phosphate shunt in uremic patients, which causes reduced detoxification of highly oxidative free radicals. The oxidative damage induces increased RBC rigidity and decreased RBC deformability, therefore favoring hemolysis. The aim of this work was to determine if a functioning renal graft would restore normal erythrocyte metabolism, reducing the oxidative damage. To this end, we have determined RBC MDA concentrations in 20 hemodialysis (HD) patients (RBC MDA 18.22 ± 4.36 μg/ml packed RBC), 20 renal transplant (T) patients with well functioning grafts (serum creatinine < 2 mg%) (RBC MDA 1.2 ± 0.4 μg/ml packed RBC) (T vs. HD P< 0.005) and 20 healthy controls (HC) (RBC MDA 1.44 ± 0.6 μg/ml packed RBC) (HC vs. HD P < 0.005; HC vs. T NS). Our findings show that a well-functioning renal graft restores normal RBC metabolism and eliminates the oxidative damage induced by uremia.

Superoxide anion generation, erythrocytes superoxide dismutase activity, and lipid peroxidation during hemoperfusion and hemodialysis in chronic uremic patients

In 11 chronic uremic patients superoxide anion generation in whole blood, both without and with opsonized zymosan stimulation, was lower than that in 11 healthy controls, while erythrocyte superoxide dismutase (SOD-1) activity and erythrocyte and plasma malonyldialdehyde (MDA) concentrations were elevated. During hemoperfusion (HP) and hemodialysis (HD) superoxide anion generation transiently significantly increased. Changes in the erythrocyte SOD-1 activity and plasma and erythrocyte MDA concentrations during HP suggested that this procedure exerted beneficial effects on lipid peroxidation. On the other hand, during HD erythrocyte membrane lipid peroxidation seemed to be enhanced even further; this phenomenon took place mainly within the dialyzer and a decrease in the erythrocyte SOD-1 activity seemed to be one of the contributing factors. Results of in vitro experiments with cross-incubation of erythrocytes and blood plasma and incubation of whole blood with cuprophan membrane suggest existence of an SOD-1 activator in the uremic blood plasma, which is possibly eliminated during HD.

Platelet Lipid Peroxidation in Haemodialysis Patients: Effects of Vitamin E Supplementation

In haemodialysis patients, increased concentrations of malonyldialdehyde and decreased vitamin E content indicate lipid peroxidation in the platelets from oxidative damage. The same process has been described in red blood cells and in mononuclear cells in peripheral blood. However, platelet aggregation is within normal limits and does not change after treatment with vitamin E. On the other hand vitamin E supplementation reverts completely the biochemical abnormality of the platelets.

Red blood cell membrane lipid peroxidation in continuous ambulatory peritoneal dialysis patients.

We have recently described that in the erythrocytes from uremic patients on chronic hemodialysis, the pentose-phosphate shunt is defective, the membrane concentrations of malonyldialdehyde, resulting from peroxidation of polyunsaturated fatty acids in the membranes themselves, are increased, and the concentrations of vitamin E, an antioxidizing agent, are reduced. In the present study we have analyzed these same metabolic aspects in a group of uremic patients in continuous ambulatory peritoneal dialysis. We have found normal function of the pentose-phosphate shunt, slightly elevated concentrations of malonyldialdehyde compared to controls, but definitely lower than in chronic hemodialysis patients, and higher tocopherol concentrations than in both controls and chronic hemodialysis patients.

Phospholipid and malonyl dialdehyde content in rat cerebral cortex during incomplete ischemia and in the postischemic period

Phospholipid and malonyl dialdehyde content in rat cerebral cortex during incomplete ischemia and in the postischemic period

Neutrophils mediate lipid peroxidation in human red cells

Activated neutrophils (ANs) are known to release reactive oxygen species that may cause oxidative damage to surrounding tissues. We determined if ANs could induce lipid peroxidation (LP) in human red cells and investigated the mechanism involved in this interaction. We studied neonatal glucose-6-phosphate dehydrogenase (G6PD) deficient, and sickle red cells, since each of these are known to be susceptible to oxidant injury. Neutrophils were isolated from whole blood and activated by incubation with opsonized zymosan. Mixtures of such neutrophils and red cells at a ratio of 1:100 were incubated for two hours at 37 degrees C, after which the malonyldialdehyde content in red cells was measured as an index of LP. All red cells underwent LP after AN treatment, and the degree of LP was proportional to the amount of AN in the mixture. Superoxide dismutase and catalase partially inhibited LP. When compared to normal red cells, only sickle cells demonstrated a significant increase in AN-mediated LP. Conversion of hemoglobin to carboxy-hemoglobin increased AN-mediated LP, whereas conversion to met-hemoglobin decreased AN-mediated LP. The protective effect of met-hemoglobin on LP was less in sickle cells than in normal cells. We conclude that AN can induce LP in red cells in vitro and that sickle cells are more susceptible to this process than normal cells. Hemoglobin can serve as an electron trap and protect the cell against peroxidative damage, but this mechanism is impaired in sickle cells. We speculate that the pathogenesis of hemolysis associated with infectious disease may include AN-induced red cell LP.

Neutrophils Mediate Lipid Peroxidation in Human Red Cells

Abstract Activated neutrophils (ANs) are known to release reactive oxygen species that may cause oxidative damage to surrounding tissues. We determined if ANs could induce lipid peroxidation (LP) in human red cells and investigated the mechanism involved in this interaction. We studied neonatal glucose-6-phosphate dehydrogenase (G6PD) deficient, and sickle red cells, since each of these are known to be susceptible to oxidant injury. Neutrophils were isolated from whole blood and activated by incubation with opsonized zymosan. Mixtures of such neutrophils and red cells at a ratio of 1:100 were incubated for two hours at 37 degrees C, after which the malonyldialdehyde content in red cells was measured as an index of LP. All red cells underwent LP after AN treatment, and the degree of LP was proportional to the amount of AN in the mixture. Superoxide dismutase and catalase partially inhibited LP. When compared to normal red cells, only sickle cells demonstrated a significant increase in AN-mediated LP. Conversion of hemoglobin to carboxy-hemoglobin increased AN-mediated LP, whereas conversion to met- hemoglobin decreased AN-mediated LP. The protective effect of met- hemoglobin on LP was less in sickle cells than in normal cells. We conclude that AN can induce LP in red cells in vitro and that sickle cells are more susceptible to this process than normal cells. Hemoglobin can serve as an electron trap and protect the cell against peroxidative damage, but this mechanism is impaired in sickle cells. We speculate that the pathogenesis of hemolysis associated with infectious disease may include AN-induced red cell LP.

Platelet derived malonyldialdehyde production in patients with thalassaemia major.

Malonyldialdehyde, a product of membrane lipid peroxidation, was measured in the platelets of 16 normal subjects after stimulation with a variety of aggregating and stimulating agents. Nethylmaleimide and hydrogen peroxide generated the largest amounts of malonyldialdehyde. These agents were used to stimulate platelets from 11 patients with thalassaemia major suffering from iron overload due to repeated transfusion. Mean malonyldialdehyde concentrations were the same in normal subjects as in thalassaemic patients, but high concentrations were recorded in patients with severe iron overload. There was a highly significant correlation between malonyldialdehyde and serum ferritin concentrations in all thalassaemic patients. Platelet derived malonyldialdehyde may be a useful test of continuing membrane damage in patients with iron overload.

The accumulation of malonyldialdehyde, a product of fatty acid peroxidation, can disturb aminophospholipid organization in the membrane bilayer of human erythrocytes.

The distribution of phospholipids across erythrocyte membrane bilayer is asymmetrical. The present study reports the effect of malonyldialdehyde (MDA), a product of fatty acid peroxidation, on the organization of phosphatidylserine (PS) and phosphatidylethanolamine (PE) in human erythrocytes using a nonpermeable bee venom phospholipase A2 and trinitrobenzene-sulfonilic acid. MDA accumulation in the erythrocytes was accomplished both by its increased endogenous generation after exposure of cells to H2O2, as well as by the treatment of erythrocytes with exogenous authentic MDA. The above treatments resulted in a significantly increased movement of PS and PE from inner bilayer to outer bilayer, which had a highly positive correlation with the concentration of MDA in the erythrocyte membranes. Antioxidants vitamin E, butylated hydroxytoluene, and butylated hydroxyanisole inhibited the effect of H2O2 treatment on erythrocyte membrane lipid organization by scavenging fatty acid peroxidation and formation of MDA. Thus, lipid peroxidation and MDA accumulation can disturb organization of PS and PE in the human erythrocyte membrane bilayer.

1444 DIMINISHED ANTIOXIDANT ACTIVITY (AOA) OF NEWBORN PLASMA

Newborn infants appear to be unusually susceptible to oxidative damage. In order to determine if the overall antioxidant potential of one biological fluid, plasma, is demonstrably different in newborns, cord blood plasma from healthy term infants was compared with adult control specimens using the thiobarbituric acid (TBA)-malonyldialdehyde (MDA) reaction as a measure of polyunsaturated lipid autoxidation in a homogenate of brain tissue. In this assay, a 5.0 ml homogenate of calf brain is permitted to incubate with 50 μ1 plasma at 37°c for 1 hour. MDA concentrations in the 1 hour and a zero time aliquot are measured by the TBA reaction following trichloracetic acid precipation of protein. AOA of plasma is defined as percentage inhibition of spontaneous autoxidation as measured in an untreated control homogenate. The AOA of cord plasma and adult plasma are as follows: No correlation was observed between plasma alpha tocopherol levels and the AOA of either cord plasma or adult plasma. AOA of cord plasma is probably dependent on a wide variety of substances including metal complexes such as ceruloplasm, acids such as ascorbic acid and unsaturated lipid materials such as alpha tocopherol. The exact role of each of these and the relationship of plasma AOA to disease states remains unknown.

Variability of the Lipid Peroxidation Potential in the Erythrocytes of the Domestic Fowl

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