Red Cell Glutathione Peroxidase Activity Research Articles

A Case–Control Study Examining the Effects of Active Versus Sedentary Lifestyles on Measures of Body Iron Burden and Oxidative Stress in Postmenopausal Women

Approximately half of the Canadian adults have sedentary lifestyles that increase their risk of developing cardiovascular disease (CVD). Women are 10 times more likely to die from CVD than from any other disease. Their risk almost doubles with the onset of menopause, which may result in increased body iron burden and oxidative stress in sedentary women. Body iron burden may catalyze the production of cytotoxic oxygen species in vivo. We hypothesized that postmenopausal women who engage in moderate forms of aerobic exercise for at least 30 min three or more times per week would have significantly (i) lower levels of body iron burden, (ii) increased glutathione peroxidase (GPx) activity, and (iii) decreased oxidative stress in comparison to sedentary controls. An age-matched, case-control study was employed to examine the effects of active (N = 25) versus sedentary (N = 25) lifestyles in women aged 55-65 years on measures of body iron burden as quantified by total serum iron, transferrin saturation, and serum ferritin levels; GPx activity; and oxidative stress as quantified by 4-hydroxynonenal, malondialdehyde, and hexanal. Measures of body iron burden were significantly elevated in sedentary women in comparison to active women (p < .001). Red cell GPx activity was higher in active women compared to sedentary women (p < .001). Measures of oxidative stress were significantly higher in sedentary versus active women (p < .001). These findings suggest that aerobic forms of exercise may mitigate the risk of developing CVD in postmenopausal women by improving antioxidant capacity and decreasing body iron burden.

Selenium, glutathione and glutathione peroxidases in blood of patients with chronic liver diseases.

Disturbances in the antioxidant system could play a role in pathogenesis of chronic liver disease. The aim of our study was to evaluate the levels/activities of antioxidants in blood of patients with chronic liver disease. We estimated selenium and glutathione concentrations and glutathione peroxidase activities in blood of 59 patients with chronic hepatitis B or C virus infection (group 1) and 64 patients with alcoholic, autoimmune or cryptogenic chronic liver disease (group 2). The results were compared with 50 healthy controls. Whole blood and plasma selenium and red cell glutathione concentrations were significantly lower in the patients compared with the controls. Red cell glutathione peroxidase activity was slightly reduced in both subgroups of group 1 and in group 2 with normal alanine aminotransferase values. Plasma glutathione peroxidase activity was slightly but significantly higher in patients with elevated aminotransferase values. The findings suggest that disturbances in antioxidant parameters in blood of patients with chronic liver disease may be the cause of the peroxidative damage of cells.

Selenium, glutathione and glutathione peroxidases in blood of patients with chronic liver diseases.

Disturbances in the antioxidant system could play a role in pathogenesis of chronic liver disease. The aim of our study was to evaluate the levels/activities of antioxidants in blood of patients with chronic liver disease. We estimated selenium and glutathione concentrations and glutathione peroxidase activities in blood of 59 patients with chronic hepatitis B or C virus infection (group 1) and 64 patients with alcoholic, autoimmune or cryptogenic chronic liver disease (group 2). The results were compared with 50 healthy controls. Whole blood and plasma selenium and red cell glutathione concentrations were significantly lower in the patients compared with the controls. Red cell glutathione peroxidase activity was slightly reduced in both subgroups of group 1 and in group 2 with normal alanine aminotransferase values. Plasma glutathione peroxidase activity was slightly but significantly higher in patients with elevated aminotransferase values. The findings suggest that disturbances in antioxidant parameters in blood of patients with chronic liver disease may be the cause of the peroxidative damage of cells.

Asthma and oxidant stress: nutritional, environmental, and genetic risk factors.

A considerable body of evidence suggests that oxidant stress results in inflammation and tissue damage in the respiratory system, and later in immune damage, and that individuals with lowered cellular reducing capacity are at increased risk to develop asthma. Reducing capacity in the erythrocyte is generated through the pentose phosphate pathway and this pathway also generates a major portion of the reducing capacity in all cells of the body. Therefore, dietary, environmental, and genetic factors which diminish cellular reducing capacity will increase tissue vulnerability to oxidant stress and are likely to increase asthma risk. Dietary selenium deficiency lowers red cell glutathione peroxidase activity and is associated with an increased risk for asthma, and low dietary intakes of vitamins C and E also appear to increase asthma risk. High body iron stores increase free radical production and may also elevate asthma risk. Environmental lead exposure depresses the activities of a several enzyme systems that influence cellular reducing capacity (glucose-6-phosphate dehydrogenase, NAD synthetase, glutathione peroxidase, superoxide dismutase, catalase) and consequently may increase asthma risk. Genetically-determined low activity of glucose-6-phosphate dehydrogenase lowers cellular reducing capacity and may also heighten asthma risk. Simple dietary and environmental interventions may significantly reduce oxidant stress and prevent or minimize the development of asthmatic symptoms and should prove to be a cost effective approach to asthma management in addition to current pharmacological strategies.

The relationship between micronutrient depletion and oral health in geriatrics

Changes in the oral microbial flora, some of which are related to mucosal disease, have been detected in the elderly, but the causes are not fully understood. This study has examined the possible role of micronutrient depletions in the reduced colonisation resistance and oral infection exhibited by some elderly subjects. The oral health, oral microbiology and micronutrient status of 37 geriatric patients aged 65-91 years (mean 81 years) were examined. Ten of the patients had no oral mucosal disease. Mucosal pathology in the remainder included erythema (27%), denture stomatitis (24%), angular cheilitis (16%) and atrophic glossitis (41%). Those with mucosal pathology had significantly lower serum iron concentrations (P = 0.02). Serum or plasma concentrations of zinc, copper, selenium, C-reactive protein, transferrin, caeruloplasmin, albumin, vitamin A and vitamin E were not significantly different between those with oral disease and those with healthy mouths. Similarly, activity of the selenium-containing enzyme, red cell glutathione peroxidase, did not differ significantly between the two groups. In both groups, plasma selenium concentrations (82%), red cell glutathione peroxidase activity (47%), plasma zinc concentrations (58%) and albumin concentrations (44%) tended to be below the lower limit of the reference interval. The influence of subclinical infection on these values is discussed.

Influence of selenium status in merino weaners on resistance to trichostrongylid infection

Weaned merino lambs, grazing pastures low in selenium, were used to investigate the effect of selenium status on immunity to trichostrongylids. Six weeks following selenium supplementation to 14 of the 27 sheep using intraruminal selenium pellets, 5000 Ostertagia circumcincta and 5000 Trichostrongylus colubriformis larvae were administered orally to all sheep. At four weeks after infection, the mean total worm burden in the selenium supplemented sheep (5537 +/- 343, n = 14) was not significantly different (P greater than 0.05) from that in the unsupplemented sheep (5614 +/- 374, n = 12) and faecal worm egg concentrations were also similar in the two treatment groups. At this time, mean red cell glutathione peroxidase activities in the supplemented and unsupplemented groups were 430 and 11 U g-1 haemoglobin, respectively, and clinical white muscle disease had been observed in the latter group. These results suggest that increasing selenium status of selenium deficient sheep by the use of intraruminal selenium supplementation, has a negligible effect on resistance to an artificial challenge infection of O circumcincta and T colubriformis.

Selenium repletion and glutathione peroxidase— differential effects on plasma and red blood cell enzyme activity

We studied three children with chronic gastrointestinal disease who had been on intravenous hyperalimentation for periods of time ranging from 4 to 23 months. Each child was found to have low plasma and red blood cell glutathione peroxidase activity. This was associated, in the two children tested, with a marked deficiency of serum selenium. Their plasma glutathione peroxidase levels ranged between 4 and 24% of normal and their red blood cell levels ranged between 4 and 14% of normal. The intravenous alimentation was then supplemented with sodium selenite (240 micrograms Se/d). Within 4-5 weeks, the plasma glutathione peroxidase activity returned to normal. Red cell glutathione peroxidase activity remained essentially unchanged for 4-6 weeks, after which it increased over the following 3-4 months. Red cells were separated by density on a continuous Percoll-diatrizoate gradient. In normal individuals, the specific activity of glutathione peroxidase did not differ across the gradient despite a 2.5-fold difference in the specific activity of pyruvate kinase. When studied initially, glutathione peroxidase activity from the deficient patients did not change across the gradient. As the red cell enzyme activity increased with selenium repletion, the highest specific activity was initially found at the top of the gradient (youngest cells). After 3-4 months of supplementation, the specific activity became equal across the gradient. Thus, with selenium repletion, there is a rapid increase in plasma glutathione peroxidase activity, a 4-6 week lag prior to an increase in red cell enzyme activity, and the increase in red cell activity is due to newly synthesized red cells made in the presence of selenium.

Ethnic variation in red cell glutathione peroxidase activity

Glutathione peroxidase activity was measured in blood and cultured fibroblasts from healthy persons of several different population groups. Individuals of Jewish ancestry and others of Mediterranean origin were found to manifest a decrease of red cell but not of leukocyte or fibroblast enzyme activity. Oriental populations differed in that the scatter in red cell enzyme activity was significantly lower than in Occidental populations. The erythrocyte enzyme of individuals with low activity was found to be less stable to heating than was the enzyme from persons with high activity. As a possible explanation for these data, a provisional genetic model is presented: a low GSH Px allele with a frequency of 0.556 in the Jewish population and of only 0.181 in the United States-Northern European population. Our results suggest that an association between GSH Px deficiency and hemolytic anemia need not represent a cause-and-effect relationship.

Hemozygous Erythrocyte Glutathione-Peroxidase Deficiency: Clinical and Biochemical Studies

Abstract An adult Puerto Rican male is described who developed an acute hemolytic episode following the infusion of three units of stored autologous red cells. The acute episode was associated with the presence of numerous red cells containing Heinz bodies. Investigation of his red cells revealed a markedly decreased level of the enzyme glutathione peroxidase. Examination of family members revealed moderately decreased levels of red cell glutathione peroxidase activity in both parents and in a sibling suggesting an autosomal recessive mode of inheritance. Metabolic studies on the erythrocytes from this patient revealed a normal level of hexose monophosphate shunt activity under basal conditions but a lack of normal activation of this pathway in the presence of hydrogen peroxide. The results of these studies support the concept that this enzyme, glutathione peroxidase, plays a major role in mediating the normal red cell response to the presence of peroxides.