Erythrocyte SOD Activity Research Articles

Enhanced blood activity of selenic glutathione peroxidase in patients with coronary heart disease after treatment with selenium-containing antioxidant preparation adrusen zinco

This study analyzed the effects of nutriceutic Adrusen Zinco containing vitamin E and prosthetic groups of antioxidant enzymes (selenium, copper, zinc) on the parameters of free radical oxidation of blood lipids in patients with coronary heart disease and hypercholesterolemia. Adrusen Zinco considerably increased activity of erythrocyte and serum selenic glutathione peroxidase as soon as after 1-month treatment, while erythrocyte SOD activity significantly increased only after 2 months.

Glutathione peroxidase (EC 1.11.1.9) and superoxide dismutase (EC 1.15.1.1) activities in riboflavin-deficient rats infected with Plasmodium berghei malaria.

Riboflavin deficiency interferes with the growth and multiplication of malaria parasites as well as the host response to malaria. The objective of the present work was to determine the effects of riboflavin deficiency on erythrocyte glutathione peroxidase (EC 1.11.1.9; GPx) and superoxide dismutase (EC 1.15.1.1; SOD) in rats infected with Plasmodium berghei malaria. Riboflavin in its co-enzyme form, FAD, is required by glutathione reductase (EC 1.6.4.1) to regenerate GSH and GSH is an important cellular antioxidant both in its own right and also as a substrate for the enzyme GPx. Weanling rats were deprived of riboflavin for 8 weeks before intraperitoneal injection of 1 x 10(6) P. berghei parasites. Control animals were weight-matched to the respective riboflavin-deficient group. At 10 d post-infection, parasite counts were higher in the weight-matched control group than the riboflavin-deficient group (P = 0.004). GPx activity was higher in erythrocytes of rats parasitized with P. berghei than comparable non-infected rats regardless of riboflavin status (P < 0.05). As mature erythrocytes do not synthesize new protein, the higher GPx activities were probably due to the presence of the parasite protein. In erythrocytes from riboflavin-deficient rats, GPx activity tended to be lower than in those rats fed on diets adequate in riboflavin (weight-matched controls) whether parasitized or not, but the difference was not significant. Neither riboflavin deficiency nor malaria had any effect on erythrocyte SOD activity. It was concluded that riboflavin deficiency has no marked effect on erythrocyte GPx or SOD activity in the rat.

Cadmium-Induced Lipid Peroxidation and the Antioxidant System in Rat Erythrocytes : the Role of Antioxidants

Cadmium (Cd)-induced oxidative damage in erythrocytes causes loss of membrane function by enhancing lipid peroxidation (LPO) and altering the erythrocyte antioxidant system. Vitamin E and/or selenium (Se) was administered to rats, prior to Cd intoxication, in order to prepare the animals to withstand oxidative assault. The treatment with Cd increased LPO in erythrocytes while animals pretreated with vitamin E and/or Se prior to Cd treatment showed decreased LPO as compared with animals given Cd alone. The erythrocyte SOD and CAT activities decreased significantly with Cd treatment. The pretreatment with vitamin E and/or Se prior to Cd administration partially reversed such changes. The erythrocytes showed a marked depletion in glutathione (GSH) content with Cd treatment. The antioxidant treatments before Cd administration helped to maintain the erythrocyte GSH content. The erythrocyte glutathione reductase (GSH-R) activity increased markedly when treatments with vitamin E and Se were applied. The GSH-R activity was not observed to decrease in animals treated with antioxidant prior to Cd intoxication, which may mean that the replenishment of erythrocyte GSH content is via GSH-R. The glutathione-S-transferase (GST) activity increased significantly with Cd intoxication; however, treatment with antioxidants prior to Cd treatment decreased erythrocyte GST activity. The results show that Cd-induced LPO decreased the antioxidant capability of the erythrocytes, causing erythrocyte membrane damage.

The role of erythrocytes in the deperoxidative processes in people on hemodialysis.

The defenses against the production of free radicals and reactive oxygen species (ROS) are to be found in plasma (ascorbate, urate, alpha tocopherol) and in erythrocytes (superoxide dismutase or SOD; catalase or CAT; glutathione peroxidase or GPx). In chronic renal failure, an increased lipid peroxidation and a reduced antioxidant activity seem to be present, but previous reports are conflicting. To clarify the peroxidative status and the defense mechanisms taking place in patients on dialysis, in 30 patients on dialysis (15 men, 15 women) and in 20 control subjects (10 men, 10 women), the following parameters were measured: plasma 4-hydroxinonenal (4-HNE) and erythrocyte reduced glutathione (GSH), SOD, GPx, and glucose-6-phosphate dehydrogenase (G-6-PD). Patients on dialysis, in comparison with control subjects, had 1) increased levels of 4-HNE (p < 0.001); 2) a significant increase in erythrocyte-GSH (p < 0.05); and 3) significant decreases in erythrocyte-SOD (p < 0.001), erythrocyte-G-6-PD (p < 0.005), and the erythrocyte-SOD/GPx ratio (p < 0.001). The dialysis procedure induced a certain reduction in plasma 4-HNE, an increase in erythrocyte-SOD activity, and an important consumption of erythrocyte-GSH, while the erythrocyte-SOD/GPx ratio changed. The current study supports the view that 1) erythrocytes act as small detoxifying packets; 2) in chronic renal failure, the antioxidant system is largely inadequate; and 3) in patients on dialysis, the antioxidant mechanism of erythrocytes in scavenging ROS is effectively exerted during dialysis but remains largely inadequate, as signs of lipid peroxidation persist with time.

Study on the effects of "foshousan" plus danshen in preventing IUGR rats with passive smoking from peroxidation in erythrocyte lipid.

The pregnant rats with cigarette smoking exposure were used as the animal model for studying the pathogenesis of IUGR. The mechanism of preventing intrauterine growth retardation with "Foshousan" plus Danshen by protecting erythrocytes against lipid peroxidation damage was also preliminarily discussed. The erythrocyte membrane lipid peroxide content, erythrocyte SOD activities were detected by ultraviolet split-beam spectrophotometry and chemiluminescence technique. The results showed that the erythrocyte MDA levels and ratio of abnormal erythrocyte in model group were significantly higher than those in control group and treated group, and the fetal mean birth weight, erythrocyte SOD levels were all statistically significantly lower than those in control group and treated group. The fetal birth weight showed a significant positive correlation with SOD levels and a significant negative correlation with MDA level. The results suggest "Foshousan" plus Danshen can protect erythrocytes against lipid peroxidation damage, thus conserving the normal form, structure and function of erythrocytes, improving the uteroplacental blood flow and thereby increasing the fetal mean birth weight.

Amyotrophic lateral sclerosis: human challenge for neuroscience.

Amyotrophic lateral sclerosis: human challenge for neuroscience.

Superoxide anion generation and lipid peroxidation processes during hemodialysis with reused cuprophan dialyzers

In 11 chronic uremic patients superoxide anion (O 2 ▪ ) generation and lipid peroxidation processes were determined during hemodialyses with cuprophan dialyzers used three times. Intradialytic changes observed during the first 20 min of hemodialysis, that is the period of the most marked alterations, with consecutive uses of the same dialyzer included: decreased whole blood O 2 ▪ generation at rest and following stimulation with opsonized zymosan, decreased reductions in the erythrocyte superoxide dismutase (SOD-1) activity, increased reductions in the plasma malonydialdehyde (MDA) concentrations, and unchanged erythrocyte MDA concentrations. However, immediately before hemodialysis with third-used dialyzer whole blodd O 2 ▪ generation at rest and following opsonized-zymosan stimulation, and erythrocyte SOD-1 activity were slightly, but statistically significantly, lower ( p < 0.05), while plasma MDA concentrations were higher ( p < 0.05) than those before hemodialysis with first-used dialyzer; erythrocyte MDA concentrations remained unchanged. The results seem to indicate that dialyzer reuse may exert beneficial effects on whole blood O 2 ▪ generation and protect erythrocyte membrane lipids from peroxidation, but, however, it leads to slightly increasing predialysis plasma lipid peroxidation.

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.

ERYTHROCYTE SUPEROXIDE DISMUTASE ACTIVITY AND ZINC COPPER CONCENTRATIONS IN LOW BIRTHWEIGHT (LBW) AND FULL TERM INFANTS DURING THE FIRST SIX MONTHS

During a longitudinal study erythrocyte superoxide dismutase activity (SOD) was sptctrophotometrically measured in 65 full ters AGA (mean birthweight 3080±235 g. and mean gestational age 39.0±0.9 weeks) and 65 LBW AGA (mean birthweight 1585±247 g. and mean gistational a 34.1±1.7 weeks) infants at different postnatal age Red cells zinc and copper concentrations were also measured by atomic absorption in order to explore their relations to SOD activity. The results are reported in table I. Erythrocyte SOD activity and Zn, Cu concentrations were lower in LBW than in full term infants (P<0.05). This difference was not present <200 days of postnatal age. A significant correlation between SOD activity seems to be particularly influenced by Cu concentration. A different role of these two trace elements in activity of this enzyme is suggested.

The effects of cobalt on superoxide dismutase activity, methemoglobin formation and lipid peroxide in rabbit erythrocytes.

Daily administrations of 25mg/kg cobalt chloride to rabbits for three days evoked a significant increase of lipid peroxides in erythrocytes and plasma accompanied by an increase in the reticulocyte count.The proportion of blue cells that is an overall blue coloration after the supravital staining with crystal violet, did not correlate with the increase of lipid peroxides in erythrocytes of cobalt-treated rabbits. Cobalt induced a slight but nevertheless significant increase in the percentage of methemoglobin but caused a decrease in SOD activity in erythrocytes.

Erythrocyte superoxide dismutase deficiency in Fanconi's anaemia established by two independent methods of assay

Erythrocyte superoxide dismutase (SOD; E.C.1.15.1.1) levels were quantitated in human haemolysates, both by an immunological technique and by an activity assay. The erythrocyte SOD activity level in a group of seven Fanconi's anaemia patients was significantly decreased (27%, on the average) compared to a control group of nineteen healthy individuals. The fact that both the activity per antigenic unit and the electrophoretic mobility of the erythrocyte SOD was normal indicates that the deficiency in these Fanconi's anaemia patients is most probably not due to a mutation in the structural gene for the enzyme but more likely due to a disturbed mechanism regulating the SOD level in the erythrocyte.