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C K Chow

Publications and source records attributed to C K Chow.

At least 91 records · Page 5Linked to original sources
PubMed1980

Dietary selenium and age-related susceptibility of rat erythrocytes to oxidative damage.

The effects of age and dietary selenium on cellular susceptibility to oxidative stress were studied in rat erythrocytes. Young (26 or 40 days) and mature adult (11 or 15 months) male rats were fed a Torula yeast-based low selenium and low vitamin E diet supplemented with either 0, 1.0 to 2.0 ppm selenium (as sodium selenite) for 5 weeks. The rates of spontaneous hemolysis amd methemoglobin formation and levels of glutathione (GSH), glucose-6-phosphate (G6P) dehydrogenase, but not of GSH peroxidase, GSH reductase, superoxide dismutase and catalase were significantly higher in the erythrocytes of young rats than in those of the adults. Adult rats, however, had higher levels of plasma vitamin E and GSH peroxidase than those of the young group. Dietary selenium markedly increased activity of plasma GSH peroxidase and partially retarded the rates of hemolysis and methomoglobin formation, but it had no significant effect on the erythrocyte levels of GSH, GSH reductase, catalse, G6P dehydrogenase and superoxide dismutase or plasma vitamin E levels of young rats. Except of GSH peroxidase activity, dietary selenium had no significant effect on any other measurements made in the erythrocytes or plasma of adult rats. The results suggest that the ability of adult rats. The results suggest that the ability of adult rats to retain higher levels of vitamin E and selenium than the young rats may be partly responsible for the increased resistance of their erythrocytes against oxidative stress.

Aging↗
PubMed1980

Glucose and dietary vitamin E protection against catalase inactivation in the red cells of rats.

One-month-old male Sprague-Dawley rats were fed a basal vitamin E deficient diet with or without 50 ppm vitamin E supplementation for 7 months. The washed red cells were suspended in a saline-phosphate buffer, pH 7.4, that contained either 0, 0.011 or 0.055 M glucose and were incubated at 37 C with constant shaking. Catalase activity in the red cells of vitamin E deficient rats was decreased 74% (P less than 0.001) at the end of the 22-hour incubation, and only 9% of the initial value was retained at the end of 46 hours. In the red cells of the vitamin E supplemented group, 82% and 48% of catalase activity was retained at the end of 22 and 46 hours, respectively. Glucose in the medium significantly increased catalase activity during the early hours of incubation and retarded the enzyme inactivation at the end of 22 and 46 hours in both groups of animals. The activities of superoxide dismutase and glutathione peroxidase were not significantly altered by the presence of glucose or by the status of dietary vitamin E during the incubation. The results suggest that both glucose and dietary vitamin E provide protection against inactivation of catalase under the experimental conditions.

Animals↗
PubMed1979

Increased level of L-ascorbic acid in the plasma of poly-chlorobiphenyls-treated rats and its inhibition by dietary vitamin E.

One-month-old male rats were fed a basal vitamin E deficient diet with or without 100 ppm vitamin E supplementation for 11 weeks and were injected intraperitoneally with either 500mg/kg body weight of polychlorobiphenyls (PCB) in sesame oil or equivalent amount of sesame oil. Five days after PCB treatment, the level of total L-ascorbic acid in the plasma of vitamin E deficient rats increased 69% (p less than 0.001) as compared with 26% (p less than 0.01) of the supplemented group. The dehydro form of ascorbic acid increased 111% (p less than 0.001) and 33% (p less than 0.01), respectively, in the plasma of PCB treated rats maintained on the vitamin E deficient and supplemented diets. The levels of reduced ascorbic acid and of vitamin E in plasma were not significantly altered by PCB in both groups of animals. The results suggest that dietary vitamin E may modify cellular susceptibility to PCB toxicity.

Animals↗
PubMed1979

Effect of dietary selenium and vitamin E on the antioxiant defense systems of rat erythrocytes.

The effect of dietary selenium and vitamin E on the important cellular antioxidant defense systems was studied in rat erythrocytes. Weanling male Sprague-Dawley rats were fed a basal selenium and vitamin E deficient diet and supplemented with either none or 0.5 ppm selenium and either none or 45 ppm vitamin E for 35 or 40 days. Depletion of dietary selenium resulted in marked decrease of glutathione (GSH) peroxidase in the red cells, but the levels of GSH, catalase and superoxide dismutase were not significantly altered. The red cells of rats fed the basal diet deficient in both selenium and vitamin E had significantly lower levels of GSH and GSH peroxidase, but not of catalase and superoxide dismutase, than in those fed the basal diet and supplemented with either selenium, vitamin E or both. The results suggest that depletion of dietary selenium and vitamin may have a precipitate effect on lowering the levels of GSH and GSH peroxidase in rat erytyrocytes.

Animals↗
PubMed1977

Lactate dehydrogenase activity and isoenzyme pattern in lungs, erythrocytes, and plasma of ozone-exposed rats and monkeys.

The effect of low levels of ozone exposure (8 hr daily for 7 days) on lactate dehydrogenase (LDH) activity and isoenzyme pattern was studied in the lungs, plasma, and erythrocytes of rats and monkeys. Exposure to 0.8 or 0.5 ppm ozone resulted in a significant increase in total LDH activvity in the lungs but not in the plasma and erythrocytes of rats. The LDH-5 fraction of the LDH isoenzymes was significantly decreased in terms of percentage distribution in the lungs and plasma of rats exposed to 0.8 ppm ozone, whereas the LDH-4 in the lungs and plasma and LDH-3 in the lungs were increased. At 0.5 ppm ozone, the isoenzyme distribution was not significantly changed in lungs, plasma, or erythrocytes. In monkeys, no significant change in either total LDH activity or isoenzyme pattern was observed in lungs, plasma, or erythrocytes after exposure to 0.8 ppm ozone.

Animals↗
PubMed1977

Effect of dietary vitamin E on lipid synthesis by rat lung in vitro.

The effect of dietary vitamin E on lipid synthesis from U-14 C-D-glucose and 1-14C-acetate was studied in rat lungs in vitro. One-month-old Sprague-Dawley male rats were fed either a basal vitamin E-deficient diet or one supplemented with 45 ppm vitamin E ad libitum for two months. Glucose oxidation to CO2 by lungs was significantly (p less than 0.05) decreased by the exclusion of vitamin E from the diet. Oxidation of acetate to CO2 was not affected by the presence of vitamin E in the diet. The extent of labeled carbons from both glucose and acetate incorporated into total lipids was significantly lower in the lungs of vitamin E-deficient animals than in those of the supplemented group. However, the relative amounts of phospholipids, neutral lipids are free fatty acids in total lipids, and of glyceryl moiety and fatty acids in total lipids and in phospholipid fraction were not significantly altered by the status of dietary vitamin E. The results suggest a general depression of lipid synthesis in the lungs of vitamin E-deficient rats.

Acetates↗
PubMed1977

Dietary vitamin E and levels of reduced glutathione, glutathione peroxidase, catalase and superoxide dismutase in rat blood.

The effects of dietary vitamin E on the important cellular antioxidant defense systems were studied in rat blood. One-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet and supplemented with either none or 45 ppm vitamin E for 4 months. The activity of glutathione (GSH) peroxidase was decreased significantly (p less than 0.05) in the red blood cells and plasma of vitamin E-deficient rats. The level of GSH in the red cells of vitamin E-deficient rats was also significantly decreased. No detectable GSH was found in the plasma of both groups of animals. The activities of catalase and superoxide dismutase were not significantly altered by the status of dietary vitamin E. Similar results were obtained when 2-month-old male rats were fed the respective diets for 3 months. The results suggest that the decreased levels of GSH and GSH peroxidase in the red cells of animals fed a vitamine E-deficient diet may in part contribute to their increased susceptibility to hemolytic agents.

Animals↗
PubMed1975

Distribution of tocopherols in human plasma and red blood cells.

The content of various tocopherols was determined in normal plasma and red blood cells. alpha-Tocopherol concentrations ranged form 6.6 to 15.0 (mean 9.6) mug/ml in plasma and from 0.9 to 1.8 (mean 1.4) mug/ml in red blood cells. gamma-Tocopherol ranged from 0.7 to 2.7 (mean 1.6) mug/ml in plasma and fron 0.1 to 0.4 (mean 0.24) mug/ml in red blood cells. Only a minute amount (smaller than 0.3 mug/ml) of each of alpha-tocotrienol, beta-tocopherol, gamma-tocotrienol and delta-tocopherol was found in plasma but none in red blood cells. No delta-tochotrienol was detected in either plasma or red blood cells. Of the total tocopherols, alpha form accounted 83 per cent in plasma and 87 per cent in red blood cells and gamma from represented 13 per cent in each system. The recovery of added 14-C-alpha-tocopherol averaged 87 per cent and 69 per cent, respectively, for plasma and red blood cells. All alpha-tocopherol in the red blood cells was found to be localized in the membrane fraction.

Carbon Radioisotopes↗