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Biomedical subjects

C K Chow

Publications and source records attributed to C K Chow.

At least 73 records · Page 4Linked to original sources
PubMed1988

Induction of eosinophilic enteritis and eosinophilia in rats by vitamin E and selenium deficiency.

Eosinophilic enteritis and eosinophilia, in addition to muscular dystrophy and occasionally liver necrosis, were experimentally induced in male Sprague-Dawley rats with a vitamin E- and selenium-deficient diet (basal diet) for 9 weeks. Cecum and ileum were affected more frequently and severely than other segments of the gastrointestinal tract. Eosinophils were multifocally or diffusely distributed in the intestinal wall but were most severe in the muscular layer and in the submucosa. Eosinophils were also present in stomach, liver with massive hepatocellular necrosis, and skeletal muscle with marked myonecrosis. Eosinophilic enteritis and eosinophilia were not observed in rats fed the basal diet supplemented with either vitamin E (100 or 200 ppm) or selenium (0.1 or 1.0 ppm). Eosinophilic enteritis, eosinophilia, and muscular dystrophy regressed when vitamin E- and selenium-deficient rats were subsequently fed either the vitamin E- or selenium-supplemented diet for 4-5 weeks. These findings suggest that vitamin E and selenium deficiency may play a role in the development of a diffuse type of eosinophilic enteritis and eosinophilia.

Animals↗
PubMed1988

Lipid peroxidation and endothelial cell injury: implications in atherosclerosis.

Vascular endothelial cells, which play an active role in the physiological processes of vessel tone regulation and vascular permeability, form a border separating deeper layers of the blood vessel wall and cellular interstitial space from the blood and circulating cells. Damage or dysfunction of endothelial cells may reduce the effectiveness of the endothelium to act as a selectively permeable barrier to plasma components, including cholesterol-rich lipoprotein remnants. This may be involved in the etiology of atherosclerosis. Experimental evidence indicates that free radical-mediated lipid peroxidation can induce endothelial cell injury/dysfunction. Reactive oxygen species, including peroxidized lipids capable of initiating cell injury, may be generated within endothelial cells, be present in plasma components, or be derived from neutrophils or other blood-borne cells. Lipid peroxidation could initiate or promote the process of atherosclerotic lesion formation by directly damaging endothelial cells, and by enhancing the adhesion and activation of neutrophils and the susceptibility of platelets to aggregate. Endothelial cell injury by lipid hydroperoxides also could increase the uptake of LDL into the vessel wall. These events and other cellular dysfunctions may individually or collectively initiate and/or help to sustain the development of atherosclerosis.

Arteriosclerosis↗
PubMed1988

Effect of dietary vitamin E level on the biochemical response of rat lung to ozone inhalation.

We examined the effects of dietary vitamin E level on rat lung response to ozone (O3) inhalation. In one study, we fed 1-month-old Sprague-Dawley (SD) rats a test diet containing 0 or 50 IU vitamin E/kg for 2 months, and then exposed one-half of the animals from each dietary group to 0.8 ppm (1,568 micrograms/m3) O3 intermittently (8 hours daily) and the other half to room air for 7 days. After O3 exposure, we found significant increases in marker enzyme activities in rat lungs from both dietary groups relative to corresponding air-exposed controls, but the magnitude of increases was greater for the 0 IU than the 50 IU group. In another study, we fed 1-month-old SD rats a test diet containing 10, 50, or 500 IU vitamin E/kg for 2 months and then exposed one-half of the animals from each dietary group to 0.8 ppm (1,568 micrograms/m3) O3 continuously and the other half to room air for 4 days. The O3 exposure increased the metabolic activities in rat lungs from all three dietary groups relative to corresponding air-exposed controls, but the magnitude of increases was greater for the 10 IU than the 50 IU or 500 IU group, and the difference between the 50 IU and 500 IU groups was small. Because a greater increase in lung metabolism after O3 exposure is thought to be associated with a greater tissue injury, the results suggest that an absence of dietary vitamin E exacerbates lung injury from O3 inhalation, while its presence protects from injury. However, the magnitude of this protective effect does not increase proportionately with increased dietary vitamin E supplementation beyond a certain level.

Administration, Inhalation↗
PubMed1986

Linoleic acid hydroperoxide increases the transfer of albumin across cultured endothelial monolayers.

Exposure to albumin-bound linoleic acid (60 to 150 microM) for 24 h significantly increased the rate of albumin transfer across cultured endothelial monolayers. The increase was dependent on the linoleic acid (18:2) concentration to which the cultures were exposed. Linoleic acid hydroperoxide (18:2-OOH) further accelerated the rate of albumin transfer over that of 18:2. A near maximum albumin transfer was observed after a 2-h incubation with 90 microM 18:2-OOH. Cells exposed to 18:2-OOH caused a marked release of lactate dehydrogenase into the media. On the other hand, 18:2 at concentrations as high as 150 microM, did not significantly affect lactate dehydrogenase release. These results suggest that exposure to 18:2, and in particular to 18:2-OOH, reduces the ability of the endothelium to act as a selective permeability barrier to plasma components.

Animals↗
PubMed1986

Lower levels of vitamin C and carotenes in plasma of cigarette smokers.

Plasma levels of vitamins A, C, and E, selenium, and carotenes were determined in 125 male cigarette smokers and 125 age- and race-matched nonsmokers. The smokers had a mean daily consumption of 30.6 cigarettes and a cumulative consumption of 22.8 pack years. Plasma levels of vitamin C and total carotenes were significantly (p less than 0.05) lower in smokers than those of nonsmokers, while levels of vitamin A, selenium, and vitamin E were not significantly different between these two groups. Similar results were found when only those subjects not taking any form of dietary supplements were included for analysis. Except for negative correlation between vitamin A and pack-year, no significant correlates were observed between plasma levels of these micronutrients and indices of smoking status or cigarette consumption in smokers. These data suggest that chronic cigarette smoking is associated with depressed levels of plasma vitamin C and carotenes; however, the relationship between smoking and these plasma micronutrients is still unclear.

Adult↗
PubMed1984

Determination of vitamin A and vitamin A acetate by high-performance liquid chromatography with fluorescence detection.

A rapid and sensitive high-performance liquid chromatographic method with fluorescence detection has been devised for the analysis of vitamin A (retinol) and its acetate. The method employs a C18 reversed-phase column and methanol as an eluent. The detection of these two compounds is monitored with fluorescence excitation at 348 nm and emission at 470 nm. Detector noise established the lower limit of quantitation at approximately 0.5 ng. Plasma samples were employed to evaluate the accuracy, reproducibility, and applicability of the method. Less than 1 ng of vitamin A in plasma (as low as 1 microliter) can be quantitated by this procedure.

Carotenoids↗
PubMed1984

The complete amino acid sequences of ribosomal proteins L17, L27, and S9 from Bacillus stearothermophilus.

The complete primary structures of proteins L17, L27 and S9 extracted from the Bacillus stearothermophilus ribosomes with 1 M NaCl and purified to homogeneity by column chromatography have been determined. The amino acid sequences of these proteins are compared to those of the homologous ribosomal proteins from Escherichia coli. The number of identical amino acid residues between the homologous proteins lies between 33-55%.

Amino Acid Sequence↗
PubMed1984

Dietary vitamin E and pulmonary biochemical responses of rats to cigarette smoking.

The effect of dietary vitamin E on cellular susceptibility to cigarette smoking was studied in rats. Young male rats maintained on a basal vitamin E-deficient diet with or without 100 ppm vitamin E supplementation for 4 or 5 weeks were exposed to either sham or cigarette smoke for up to 7 days. Higher animal mortality rate was observed in the animals fed the vitamin E-deficient diet than in the supplemented group when they were subjected to acute levels of cigarette smoking. Relative to the respective sham groups, a greater alteration of biochemical parameters, such as reduced glutathione (GSH) and related enzymes, was found in the lungs of smoked rats fed the deficient diet than in the supplemented group. Animal lungs exhibited a greater biochemical response to whole smoke than the gaseous phase of smoke. The results suggest that the nutritional status of vitamin E may influence the cellular susceptibility of rats to cigarette smoking.

Animals↗
PubMed1984

Effect of dietary vitamin E on nitrite-treated rats.

The effect of dietary vitamin E on cellular responses to nitrite was studied in rats. One-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet with or without 100 ppm vitamin E and 1000 ppm sodium nitrite (NaNO2) for 9 weeks. In addition to a high mortality rate, nitrite-fed rats maintained on a vitamin E-deficient diet exhibited a marked increase in liver necrosis, tubular nephrosis and myodegeneration, as well as greater biochemical and hematological alterations when compared to the control animals. No animal mortality or histopathologic lesions in any tissues were observed in rats receiving a vitamin E-supplemented diet with or without nitrite. The results suggest that depletion of vitamin E renders rats more susceptible to the adverse effect of nitrite, and that nitrite administration potentiates deficiency of vitamin E in rats.

Animals↗
PubMed1984

Pathogenesis of gastric ulceration produced by acetazolamide in rats.

The present experiment demonstrated that relatively high doses of acetazolamide (100 and 200 mg/kg s.c.) induced severe gastric hemorrhagic ulceration in rats. This ulceration was aggravated by oral administration of HC1, but was inhibited by NaHCO3. Further, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were affirmed by an increase in serotonin and histamine released from the stomach after acetazolamide treatment. Acetazolamide injection also increased the protein level, but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increases in serotonin and histamine released may also have been contributing factors for gastric ulcer formation.

Acetazolamide↗
PubMed1982

Dietary selenium, hepatic arylhydrocarbon hydroxylase and mutagenic activation of benzo(a)pyrene, 2-aminoanthracene and 2-aminofluorene.

The effect of dietary selenium (Se) on the hepatic aryl hydrocarbon hydroxylase (AHH) and mutagenic activation potential in young and adult rats was investigated. Animals were maintained on a low Se basal diet with or without 1 or 2 ppm Se supplementation (as sodium selenite) for 5 or 20 weeks. AHH inducibility was determined by an intraperitoneal injection of Aroclor 5 days prior to killing. A significant reduction in the AHH level was observed in low Se group of young untreated rats only. Dietary Se did not affect AHH inducibility by Aroclor treatment and the induced AHH levels were similar in both dietary groups. 5 weeks on low dietary Se did not alter the AHH levels in untreated or treated adult rats. The levels of Se-dependent glutathione peroxidase (GSH-P) were decreased more drastically in the young than adult rats by low dietary Se. Studies on the metabolic activation potential of liver enzymes from young rats on basal and Se-supplemented diets showed that dietary Se did not alter the activation of benzo(a)pyrene (BP) to mutagens although differences in the activation of 2-aminofluorene (2AF) and 2-aminoanthracene (2AA) were observed.

Animals↗
PubMed1981

Dietary selenium and levels of L-ascorbic acid in the plasma, livers, and lungs of polychlorinated biphenyls-treated rats.

Administration of polychlorinated biphenyls (PCB) (500 mg Aroclor, 1254/kg body weight) intraperitoneally significantly increased the levels of L-ascorbic acid in the plasma and livers, but not in the lungs of one-month-old male rats maintained on a basal low selenium diet with or without 2.0 ppm selenium (as sodium selenite) supplementation for 19 weeks prior to PCB treatment. The levels of L-ascorbic acid were not significantly altered by dietary selenium. In another experiment, 40 days or 15-month-old male rats were fed the same basal selenium diet with or without 1.0 ppm selenium for 1 month prior to PCB treatment. The plasma levels of ascorbic acid were found to increase significantly by PCB treatment, but not by the status of dietary selenium or by animal age. As expected, the activity of selenium dependent glutathione peroxidase was markedly decreased in the plasma, livers, and lungs of rats fed the low selenium diet. However, the enzyme activity was not significantly altered by PCB treatment in plasma, livers, and lungs of animals in both dietary groups.

Animals↗
PubMed1981

Influence of dietary selenium on the hepatic and pulmonary enzymes in polychlorobiphenyls-treated rats.

One-month-old male Sprague-Dawley rats maintained for 19 weeks on a low selenium diet with or without supplementation of 2.0 ppm selenium were injected intraperitoneally with either 500 mg PCB (Aroclor 1254)/kg body weight or placebo 5 days prior to sacrifice. In addition to aryl hydrocarbon hydroxylase (AHH) activity, PCB treatment also caused a significant increase in hepatic levels of thiobarbituric acid reactants (TBAR), reduced glutathione (GSH), GSH-peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase (G-6-PD), and GSH-S-transferase in rats on the low selenium diet. The non-selenium-dependent form of GSH peroxidase was mainly responsible for the increase of hepatic GSH peroxidase upon PCB treatment. Only the activities of AHH, GSH-S-transferase, and G-6-PD were significantly higher in the liver of PCB-treated rats fed the selenium-supplemented diet. In contrast, except for AHH activity, the lung GSH and related enzymes were not significantly affected by PCB in either of the two dietary groups. The results suggest that dietary selenium deprivation renders the livers of rats more sensitive to PCB effects.

Animals↗