Erythrocyte CuZn Superoxide Dismutase Activity Research Articles

Erythrocyte CuZn Superoxide Dismutase Activity Is Decreased in Iron-Deficiency Anemia

Iron and copper are essential microminerals that are intimately related. The present study was performed to determine the effect of iron-deficiency anemia (IDA) and treatment with iron on laboratory indicators of copper status. Hemoglobin, mean corpuscular volume erythrocyte Zn protoporphyrin, serum ferritin, serum copper, serum ceruloplasmin, and erythrocyte CuZn-superoxide dismutase (SOD) activity were studied in 12 adult women with IDA before and after iron treatment for 60-90 d (100 mg/d Fe, as ferric polymaltose) and in 27 women with normal iron status. Prior to treatment with iron, serum copper and ceruloplasmin were not different between the groups and treatment with iron did not affect these measures. IDA women, before and after treatment with iron, presented a 2.9- and 2-fold decrease in erythrocyte CuZn-SOD activity compared to women with normal iron status (p < 0.001). Treatment with iron increased erythrocyte CuZn-SOD activity of the IDA group; however, this change was not statistically significant. In conclusion, CuZn-SOD activity is decreased in IDA. Measurement of this enzyme activity is not useful for evaluating copper nutrition in iron-deficient subjects.

Plasma Lipid Peroxidation Zinc And Erythrocyte Cu-Zn Superoxide Dismutase Enzyme Activity In Patients With Type 2 Diabetes Mellitus In Gorgan City (South East Of The Caspian Sea)

The aim of this study was to determine the changes of plasma lipid peroxidation, zinc and erythrocyte Cu-Zn superoxide dismutase activity in patients with type 2 diabetes mellitus and healthy control in Gorgan city. Fifty type 2 patients with diabetes mellitus and 50 people without diabetes were included in this randomized study. None of patients studied had any diabetic complications. The levels of plasma malondialdehyde and zinc from type 2 diabetes mellitus patients (6.24±0.85 nmol mL-1 and 116.78±5.51 μ dL-1) and control groups (3.63±0.97 nmol mL-1 and 146.86±9.06 μg dL-1) were determined. Erythrocyte Cu-Zn superoxide dismutase activity from patients with diabetes (675.34±60.89 U g-1 Hb) and control groups (1052.70± 52.76 U g-1 Hb) were determined. The increased plasma lipid peroxidation and decreased plasma zinc and erythrocyte Cu-Zn superoxide dismutase activity that we observed in patients with type 2 diabetes mellitus may predispose to the development of cardiovascular complications. We propose that diabetic patients may have elevated requirement for antioxidants. Supplementation with zinc and vitamin or dietary free radical scavengers such as vitamins E and C or tomato, orange and etc. have a potential role in boosting antioxidant-related defences and maybe important in patients with diabetes.

Plasma and erythrocyte levels of trace elements and related antioxidant enzyme activities in low-birthweight infants during the early postnatal period.

To discover the relationship between antioxidant enzyme activities and trace elements in low-birthweight infants during the early postnatal period, we analysed catalase (CAT), CuZn-superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px) activities in erythrocytes. and compared them with Fe, Cu. Zn and Se levels in plasma, and Cu, Zn and Se levels in erythrocytes until 16 wk after birth. Thirteen low-birthweight infants whose mean birthweight and gestation were 1520 +/- 293 g and 32.0 +/- 2.8 wk were enrolled in this study. All infants were without chronic complications, well nourished, and predominantly fed standard formula or preterm formula based on cow's milk, commercially available in Japan. Cu and Zn levels in erythrocytes did not decline after birth, in contrast to a temporal decrease in plasma Zn. Erythrocyte CAT activity was significantly higher at 16 wk than that at birth or 4 wk of age. Erythrocyte CuZn-SOD activity did not change throughout the study period. Only Se in plasma and erythrocytes decreased remarkably after birth, which resulted in a significant decline in erythrocyte GSH-Px activity at 8 and 16 wk (11.2 +/- 2.0 and 11.0 +/- 1.1 U/g Hb) compared to that at birth (12.4 +/- 2.1 U/g Hb). During the early postnatal period. erythrocyte CAT and CuZn-SOD activities did not decrease in formula-fed, low-birthweight infants. Japanese commercial formula not supplemented with Se, however, caused postnatal plasma and erythrocyte Se deficiency and a concomitant decline in erythrocyte GSH-Px activity in the same subjects.

Plasma and erythrocyte levels of trace elements and related antioxidant enzyme activities in low‐birthweight infants during the early postnatal period

To discover the relationship between antioxidant enzyme activities and trace elements in low‐birthweight infants during the early postnatal period, we analysed catalase (CAT), CuZn‐superoxide dismutase (CuZn‐SOD) and glutathione peroxidase (GSH‐Px) activities in erythrocytes, and compared them with Fe, Cu, Zn and Se levels in plasma, and Cu, Zn and Se levels in erythrocytes until 16 wk after birth. Thirteen low‐birthweight infants whose mean birthweight and gestation were 1520 ± 293 g and 32.0 ± 2.8 wk were enrolled in this study. All infants were without chronic complications, well nourished, and predominantly fed standard formula or preterm formula based on cow's milk, commercially available in Japan. Cu and Zn levels in erythrocytes did not decline after birth, in contrast to a temporal decrease in plasma Zn. Erythrocyte CAT activity was significantly higher at 16 wk than that at birth or 4 wk of age. Erythrocyte CuZn‐SOD activity did not change throughout the study period. Only Se in plasma and erythrocytes decreased remarkably after birth, which resulted in a significant decline in erythrocyte GSH‐Px activity at 8 and 16 wk (11.2 ± 2.0 and 11.0 ± 1.1 U/g Hb) compared to that at birth (12.4 ± 2.1 U/g Hb). Conclusion: During the early postnatal period, erythrocyte CAT and CuZn‐SOD activities did not decrease in formula‐fed, low‐birthweight infants. Japanese commercial formula not supplemented with Se, however, caused postnatal plasma and erythrocyte Se deficiency and a concomitant decline in erythrocyte GSH‐Px activity in the same subjects.

CuZn-superoxide dismutase, extracellular superoxide dismutase, and glutathione peroxidase in blood from individuals homozygous for Asp90Ala CuZu-superoxide dismutase mutation.

The Asp90Ala CuZn-superoxide dismutase mutation is associated with amyotrophic lateral sclerosis (ALS) in both homo- and heterozygous form. We analyzed antioxidant enzymes in blood from 44 individuals homozygous and 114 individuals heterozygous for the Asp90Ala mutation as well as 66 blood relatives carrying the wild-type allele only. Erythrocyte CuZn-superoxide dismutase activity was reduced by 9% in the homozygous individuals, confirming previous findings on a smaller cohort. The specific activity of Asp90Ala mutant CuZn-superoxide dismutase in erythrocytes was equal to that of isolated mutant enzyme and slightly higher than that of isolated wild-type enzyme. There was no evidence for the presence of inactive mutant molecules in erythrocytes, and the lower activity is due to the occurrence of fewer active molecules. There were no significant differences between the groups in plasma extracellular superoxide dismutase content, and the erythrocyte glutathione peroxidase activities were virtually identical. Also, there were no differences in these parameters between homozygous individuals with or without ALS. There was no evidence for any association with ALS of a polymorphic extracellular superoxide dismutase mutation, Arg213Gly. The absence of response of the blood antioxidant enzymes to the Asp90Ala CuZn-superoxide dismutase mutation does not support the theory that the ALS-linked CuZn-superoxide dismutase mutations cause disease by increased oxidant stress.

Amyotrophic lateral sclerosis associated with homozygosity for an Asp90Ala mutation in CuZn-superoxide dismutase

Recent reports have shown heterozygosity for some twenty different mutations in the CuZn-superoxide dismutase (CuZn-SOD) gene in familial amyotrophic lateral sclerosis (FALS), and analysed samples from patients have shown decreased enzymic activity. Here we report homozygosity for an exon 4 mutation, Asp90Ala in fourteen patients among four unrelated ALS families and four apparently sporadic ALS patients from Sweden and Finland. The erythrocyte CuZn-SOD activity is essentially normal. Our findings suggest that this CuZn-SOD mutation causes ALS by a gain of function rather than by loss, and that the Asp90Ala mutation is less detrimental than previously reported mutations.

Copper Status of Very Low Birth Weight Infants during the First 12 Months of Infancy

The Cu intake and status of 106 very low birth weight (VLBW) infants (birth weight 1152 +/- 251 g, gestational age 29 +/- 3 wk, mean +/- SD) were determined approximately 1 mo before hospital discharge, at discharge (time 0), and at 3, 6, 9, and 12 mo +/- 3 wk corrected for gestational age. Infants were fed either formula plus supplemental Zn/Cu (SUPPL, n = 29); formula plus placebo (PLAC, n = 26); or a low birth weight formula (LBWF, n = 26) or were breast-fed (BRMLK, n = 25). Plasma Cu levels in the formula-fed infants increased significantly at each time period with no significant differences between feeding groups. Hair Cu was significantly higher in the SUPPL group compared to the PLAC, LBWF, and BRMLK groups at 3 and 6 mo. Erythrocyte Cu,Zn-superoxide dismutase (CuZnSOD) activity was lowest in the PLAC group. Cu intake was positively correlated with both hair Cu (r = 0.291, p less than 0.0001) and erythrocyte CuZnSOD activity (r = 0.281, p less than 0.001) but not with plasma Cu. An increasing number of formula-fed infants had very low CuZnSOD activity (less than 2 SD below mean) with increasing age (n = 1, 2, 8, 11, and 13 infants at times 0, 3, 6, 9, and 12 mo, respectively). At 12 mo, approximately one third of the formula-fed VLBW infants in this study had low Cu status as assessed by CuZnSOD activity. Infants with the lowest CuZnSOD activity were those with the largest weight gains from 0 to 6 mo and were observed in all formula-fed groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Semi-automated assay of erythrocyte Cu-Zn superoxide dismutase activity

A semi-automated enzymatic colorimetric method for determining Cu-Zn superoxide dismutase (SOD) in erythrocytes using an FP9 parallel analyzer is described. The method is based on the reaction described by McCord and Fridovich (xanthine/xanthine oxidase, ferricytochrome C), which permits kinetic measurements to be determined colorimetrically for the assay of enzyme activity. The coefficients of variation for within- and between-run analyses were less than 6%. The limit of linearity is 3.5-times the mean value of the normal range while recovery of added SOD ranged from 91 to 120%. The method, which is both reliable and simple, allows rapid, simultaneous measurements of multiple samples.

Effects of Inflammation and Copper Intake on Rat Liver and Erythrocyte Cu-Zn Superoxide Dismutase Activity Levels

Stress such as inflammation produces an acute phase response that includes elevated levels of ceruloplasmin, the main copper component of plasma. Inflammatory effects on cellular copper enzyme activity levels are largely unknown. Cu-Zn superoxide dismutase (SOD) activities in liver, the main site of ceruloplasmin secretion, decreased with turpentine-induced inflammation (0.1 mL, intramuscular, leg) in rats fed any of three copper levels (adequate = 6 mg/kg, marginal = 2.5 mg/kg and deficient less than 0.5 mg/kg). Ceruloplasmin activities rose significantly with inflammation in the adequate and marginal groups but not in the deficient animals. Hepatic Cu-Zn SOD immunoreactive protein levels were unaffected by copper status or inflammatory state. Erythrocyte Cu-Zn SOD activities were influenced by dietary copper but not inflammation. An additional group of rats fed 15 mg copper/kg did not show a turpentine-induced decrease in liver Cu-Zn activity levels. Inflammatory effects on other copper enzyme activities did occur as evidenced by increases in ceruloplasmin and decreases in serum extracellular SOD. In conclusion, an acute phase response in rats increased the amount of dietary copper required to maintain hepatic Cu-Zn SOD activity at levels equal to those of nonstressed, copper-adequate rats. Rat erythrocyte Cu-Zn SOD activities provided a blood measurement reflective of copper intake with or without stress, but these values did not reflect decreases in liver Cu-Zn SOD activities after 3 d of inflammation.

Effect of long-term penicillamine therapy on erythrocyte CuZn superoxide dismutase activity.

The effect of long-term penicillamine therapy on erythrocyte CuZn superoxide dismutase activity was investigated. For comparison the serum ceruloplasmin and serum copper contents were also analysed. Seven of the 11 penicillamine-treated patients had CuZn superoxide dismutase activities below the reference interval of the parameter. Levels down to about 50% of the mean of controls were observed in several cases. In five and in four of the 11 patients respectively decreases in serum ceruloplasmin and serum copper were found. Whereas among the penicillamine-treated patients there was a good correlation between serum ceruloplasmin and serum copper, the correlation between these parameters and erythrocyte CuZn superoxide dismutase was only fair. Erythrocyte CuZn superoxide dismutase is probably a suitable parameter for monitoring intracellular copper availability during penicillamine therapy.