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C K Chow

Publications and source records attributed to C K Chow.

At least 37 records · Page 2Linked to original sources
PubMed1997

Oxidative stress and antioxidant status in mouse liver: effects of dietary lipid, vitamin E and iron.

The purpose of this study was to determine the effects of dietary fat, vitamin E and iron on oxidative damage and antioxidant status. Male Swiss-Webster mice (1 mo old) were fed a basal vitamin E-deficient diet that contained either 8% fish oil + 2% corn oil or 10% lard with or without 1 g dl-alpha-tocopheryl acetate. The diets without vitamin E contained either 0.21 or 0.95 g ferric citrate/kg. Diets were fed for 4 wk/kg diet. Compared with the vitamin E-supplemented groups, mice fed diets without vitamin E (with or without supplemental iron) had significantly (P < 0.05) higher hepatic levels of thiobarbituric acid-reactive substances (TBARS), conjugated dienes and protein carbonyls when they were fed fish oil, but not lard. The levels of TBARS were further increased by iron supplementation in the mice fed fish oil. Significantly lower concentrations of alpha-tocopherol and higher glutathione (GSH) were found in the liver of mice fed fish oil and vitamin E than in those fed lard and vitamin E (P < 0.05). The activities of superoxide dismutase and glucose-6-phosphate dehydrogenase were lower in the fish oil-fed mice than in those fed lard (P < 0.05). The activities of Se-GSH peroxidase, non-Se-GSH peroxidase, catalase, and glutathione reductase were not altered by dietary fat or vitamin E/iron. The results obtained provide experimental evidence of the prooxidative effects of high dietary fish oil and iron, and suggest that vitamin E protects not only lipid-soluble compounds, but also water-soluble constituents, against oxidative damage. Further, dietary lipid plays a key role in determining cellular susceptibility to oxidative stress.

Analysis of Variance↗
PubMed1997

Syndrome of spotty skin pigmentation, myxomas, endocrine overactivity, and schwannomas (Carney complex): breast imaging findings.

PURPOSE: To study the imaging appearances of breast lesions in female patients with Carney complex. MATERIALS AND METHODS: Seven patients with Carney complex underwent mammography (n = 5), ultrasound (US) (n = 6), or magnetic resonance (MR) imaging (n = 6) in a prospective study. Previous breast images in three patients were reviewed. Mammograms in two additional patients were retrospectively reviewed. Thus, nine patients aged 16-61 were included in this study. RESULTS: Mammograms showed well-defined, iso- or hypodense masses; most were not calcified. Two lesions contained calcifications; both were biopsy-proved ductal adenomas. US demonstrated solid, hypoechoic, well-circumscribed masses in six patients and complex cystic masses (myxoid fibroadenomas) in one patient. MR imaging with a fat-suppressed, fast spin-echo, T2-weighted sequence demonstrated high-signal-intensity lesions (n = 5). Fat-suppressed, spoiled gradient-recalled-echo MR images demonstrated hypointense lesions with variable contrast material enhancement (n = 5). Five of seven patients in the prospective review had multiple breast lesions on at least one study. Mammograms and US scans were negative in three patients each. Chest and breast MR images were negative in only one patient. CONCLUSION: Female patients with Carney complex often have multiple breast masses with variable imaging appearances that probably represent myxoid fibroadenomas or ductal adenomas. MR imaging showed the most lesions. These lesions all demonstrate benign characteristics and should not prompt multiple biopsies.

Adolescent↗
PubMed1996

Red cell vitamin E and oxidative damage: a dual role of reducing agents.

The purpose of this study was to determine the role of reducing agents in maintaining the integrity of vitamin E-deficient red cells. Three groups of one-month-old male Wistar rats were fed a basal vitamin E-deficient diet supplemented with either 0, 10 or 100 mg d, 1-alpha-tocopheryl acetate per kg diet for up to 12 weeks. Washed red blood cells (5%) were resuspended in saline-phosphate buffer, pH 7.4, and were incubated at 37 degrees C with or without containing 12.5 mM 2, 2'-azobis (2amino- propane) dihydrochloride (AAPH), 2.8 mM glucose, 1 mM ascorbic acid, 10 mM hydrogen peroxide (H2O2), 250 microM dimethylsulfoxide (DMSO) or 2.8 mM deoxyribose (DR) for up to 20 hours. Addition of either glucose, AAPH, ascorbic acid or H2O2 markedly accelerated the rates of hemolysis and lipid peroxidation in the red cells of vitamin E-deficient rats. On the contrary, both glucose and ascorbic acid were protective against oxidative damage to the red cells of vitamin E-supplemented rats in a dose-dependent manner. Also, vitamin E-supplemented red cells were more resistant to AAPH and H2O2 than the deficient cells. DMSO or. DR had no significant effects on the rates of hemolysis or lipid peroxidation. Glucose, but not others, maintained or slowed down the loss of glutathione (GSH) during incubation. The results obtained suggest a dual role of ascorbic acid and GSH in the function of vitamin E in maintaining red cell integrity: these reducing agents may exert antioxidant function by participating in vitamin E regeneration when certain levels of vitamin E is maintained, but promote oxidative damage by enhancing free radical generation when vitamin E is low or depleted.

Amidines↗
PubMed1996

Antioxidant status and susceptibility of sickle erythrocytes to oxidative and osmotic stress.

The purpose of this study was to determine if differences in antioxidant status between the red blood cells (RBCs) of sickle cell anemia (SCA) patients and controls are responsible for the differential responses to oxidative and osmotic stress-induced hemolysis. Susceptibility to hemolysis was examined by incubating oxygenated and deoxygenated RBCs at 37 degrees C with 73 mM 2,2' azobis (2-amidinopropane) HCl (AAPH), a peroxyl radical generator, for up to 3.5 hours.f The ability of RBCs to maintain membrane integrity under osmotic stress was determined over a range of diluted saline-phosphate buffer. Sickled RBCs showed a lesser degree of AAPH-induced hemolysis than control groups and were more resistant to osmotic stress-induced hemolysis. SCA patients had higher levels of RBC vitamin E and RBC lipids, but lower RBC GSH, plasma lipids and plasma carotenes than those of the hospital controls. No significant differences were observed in the levels of retinol, vitamin C, vitamin E, MDA and conjugated dienes in plasma, or the levels of MDA and conjugated dienes in RBCs. The results obtained suggest that the differences in antioxidant status between sickled RBCs and controls do not appear to be responsible for their different susceptibility to oxidative or osmotic stress-induced hemolysis observed.

Adult↗
PubMed1996

Extraocular, limb and diaphragm muscle group-specific antioxidant enzyme activity patterns in control and mdx mice.

The mechanisms primarily responsible for the degenerative processes occurring in dystrophic skeletal muscle remain unresolved. The identification of the mechanisms that lead to the complete sparing of extraocular muscle in dystrophinopathies is of particular interest. A number of studies have provided evidence to suggest that the muscle pathology that characterizes muscular dystrophy may be, in part, free radical mediated. In the present study, we examined the antioxidant enzyme status of extraocular, diaphragm and gastrocnemius muscles in control strain and mdx mice. Our results revealed that in the control strain, both extraocular and diaphragm muscles had higher copper/zinc superoxide dismutase, manganese superoxide dismutase and selenium dependent glutathione peroxidase activities as compared to the gastrocnemius. Furthermore, the diaphragm had higher glutathione reductase activity as compared to the gastrocnemius. These findings indicate that the highly aerobic extraocular and diaphragm muscles have higher antioxidant enzyme capacity than the gastrocnemius, a muscle more dependent on anaerobic energy metabolism. Changes in the antioxidant enzyme status of the mdx mouse correlated, in part, with the degree of histopathological involvement of the three muscle groups assessed.

Animals↗
PubMed1995

Altered hepatic eicosanoid concentrations in rats treated with the peroxisome proliferators ciprofibrate and perfluorodecanoic acid.

Several hypolipidemic drugs, plasticizers, and other chemicals induce hepatic peroxisome proliferation and hepatocellular carcinomas in rodents. These agents induce and promote hepatocarcinogenesis by unknown mechanisms, since most studies have not found them to be genotoxic. Peroxisome proliferators increase the expression of several genes, including those for the enzymes of the peroxisomal beta-oxidation pathway and the cytochrome P-450 4A family, which metabolize lipids, including eicosanoids and their precursor fatty acids. The peroxisome proliferators ciprofibrate and perfluorodecanoic acid (PFDA) were therefore examined for their ability to alter hepatic eicosanoid concentrations. Rats received injections of 3 or 10 mg PFDA/kg body weight every 14 days or were fed 0.01% ciprofibrate for 10 days, 24 days, 6 weeks, 26 weeks, or 54 weeks. The activity of the peroxisomal enzyme fatty acyl CoA oxidase was significantly increased by both ciprofibrate and PFDA at all times. Hepatic concentrations of prostaglandins E2 and F2a (PGE2, PGF2a), thromboxane B2 (TXB2), and leukotriene C4 (LTC4) were measured by immunoassay. Concentrations of PGE2, PGF2a, and TXB2 were decreased in livers of rats receiving ciprofibrate or PFDA compared to livers of control rats, with ciprofibrate exerting a greater effect than PFDA at the doses used. Hepatic LTC4 concentrations were significantly increased by ciprofibrate at 10 days and PFDA at 54 weeks, and significantly decreased by PFDA at 26 weeks. These alterations in eicosanoid concentrations may be important in the natural history of peroxisome proliferator-induced hepatocarcinogenesis.

Acyl-CoA Oxidase↗
PubMed1995

Effect of dietary retinyl palmitate on the promotion of altered hepatic foci by 3,3',4,4'-tetrachlorobiphenyl and 2,2',4,4',5,5'-hexachlorobiphenyl in rats initiated with diethylnitrosamine.

The purpose of this study was to determine the effects of dietary vitamin A on the tumor promoting effect of 3,3',4,4'-TCB and 2,2',4,4',5,5'-HCB in a two-stage rat hepatocarcinogenesis model with diethylnitrosamine (DEN, 150 mg/kg) as the initiator. Two weeks after DEN injection rats were fed a purified diet containing either 2000 or 100,000 IU of vitamin A in the form of retinyl palmitate. Rats received four biweekly injections of 3,3',4,4'-TCB, 2,2',4,4',5,5'-HCB (300 mumol/kg), or both (150 mumol/kg each) in corn oil (10 ml/kg) for 8 weeks. Control animals received vehicle only. Six rats in each group that received no DEN treatment were used as additional control animals. Ten days after the last injection the rats were killed. In rats fed the low retinyl palmitate diet, treatment with 3,3',4,4'-TCB, 2,2',4,4',5,5'-HCB or both compounds lowered hepatic retinyl palmitate content. This effect was prevented by high dietary retinyl palmitate supplementation in rats treated with 2,2',4,4',5,5'-HCB, but not 3,3',4,4'-TCB or both compounds together. Histopathological examination of the liver showed that high dietary retinyl palmitate lessened the severity of hepatocellular necrosis and fatty changes induced by 3,3',4,4'-TCB alone or in combination with 2,2',4,4',5,5'-HCB. The latter did not cause significant pathological lesions to the liver. However, high dietary retinyl palmitate was not able to prevent thymic involution caused by 3,3',4,4'-TCB. The number and volume of altered hepatic foci were increased by 2,2',4,4',5,5'-HCB and particularly 3,3',4,4'-TCB; no synergistic effect was seen. Supplementation with high dietary retinyl palmitate diminished the number and volume of foci. These results show that supplementation with high dietary retinyl palmitate protects against hepatocellular necrosis, fatty changes, and preneoplastic changes induced by 3,3',4,4'-TCB as well as against preneoplastic changes induced by 2,2',4,4',5,5'-HCB. In addition, these two agents did not synergistically induce preneoplastic changes in DEN-induced rats.

Animals↗
PubMed1995

The idiopathic inflammatory myopathies: spectrum of MR imaging findings.

Magnetic resonance (MR) imaging is useful for demonstrating the soft-tissue and musculature changes seen in patients with idiopathic inflammatory myopathies (IIMs). These changes include edema within and around muscle, subcutaneous reticulation, muscle calcification, and fatty infiltration of muscle. Muscle edema is visible as areas of hyperintensity on short inversion time inversion recovery (STIR) images. Abnormal reticulation of the subcutaneous tissue can be due to subcutaneous edema or an infiltrating process; edema from inflammation appears as areas of low signal intensity on T1-weighted images and as areas of high signal intensity on STIR images. Intramuscular calcium deposition appears as hypointense areas with all pulse sequences. On T1-weighted images, fatty infiltration appears as areas of high signal intensity within muscles. Because of the improved visualization of muscle inflammation provided by STIR imaging and because MR imaging is noninvasive, it has become a useful modality for evaluating patients with IIMs.

Adult↗
PubMed1995

Oxidative damage and antioxidant status in the lungs and bronchoalveolar lavage fluid of rats exposed chronically to cigarette smoke.

The effect of chronic smoke exposure on oxidative damage and antioxidant status was studied in rats. Ten-week-old female Sprague-Dawley rats were exposed to fresh mainstream cigarette smoke or filtered room air twice daily, or maintained as room controls, for 65 weeks. Animals were sacrificed 18-20 hours after the last treatment. The bronchoalveolar lavage (BAL) fluid, lung tissues, and plasma were processed to assess oxidative damage and antioxidant status. Compared with sham and room control groups, the levels of conjugated dienes and alpha-tocopheryl quinone were significantly higher in the lung tissues of rats exposed to cigarette smoke. The levels of malondialdehyde, protein carbonyls, reduced glutathione (GSH), ascorbic acid and vitamin E, and activities of catalase and GSH peroxidase in the lung tissues were not significantly altered by smoke exposure. No significant differences in any measurements were found in BAL fluid and plasma among the experimental groups. The results obtained support the view that cigarette smoking increases oxidative stress and suggest a metabolic adaptation of antioxidant systems following chronic smoke exposure.

Animals↗
PubMed1994

Increased 8-hydroxydeoxyguanosine in hepatic DNA of rats treated with the peroxisome proliferators ciprofibrate and perfluorodecanoic acid.

In this study we examined the ability of peroxisome proliferators to induce oxidative DNA damage in the form of 8-hydroxydeoxyguanosine (OHdG). We studied the hypolipidemic drug ciprofibrate, which is among the most potent and efficacious of the peroxisome proliferators, and perfluorodecanoic acid (PFDA), which is an inhibitor of peroxisomal beta-oxidation. Rats were fed 0.01% ciprofibrate in the diet, or were injected with PFDA at doses of 3 or 10 mg/kg every 14 days (controls and ciprofibrate-fed rats were given equivalent doses of corn oil). Rats were maintained for 10 days, 24 days, 6 weeks, 26 weeks, or 54 weeks. DNA was isolated from the liver at these times and hydrolysed to nucleosides, and the levels of OHdG as well as normal nucleosides were analysed by high-performance liquid chromatography with electrochemical detection. Ciprofibrate increased OHdG concentrations at all times except for the initial 10-day timepoint. Both doses of PFDA increased OHdG levels at all times except the last timepoint, at which only the higher dose produced a significant increase. This study shows that both ciprofibrate and PFDA induce oxidative DNA damage in the form of OHdG. Furthermore, the inhibition of peroxisomal beta-oxidation by PFDA does not affect the development of OHdG.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1994

An improved method for the measurement of malondialdehyde in biological samples.

An improved method was developed for measuring malondialdehyde (MDA) as its thiobarbituric acid (TBA) complex. Samples were initially incubated with 1% potassium iodide and 0.1% butylated hydroxytoluene at 50 degrees C for 20 min, and then with 0.4% TBA at 60 degrees C for 60 min. The MDA-TBA complex formed was extracted with isobutyl alcohol and measured by high-performance liquid chromatography with fluorescence detection. The improved method allows for a more specific determination of MDA present in biological samples.

Chemistry Techniques, Analytical↗
PubMed1994

Effect of dietary carnosine on plasma and tissue antioxidant concentrations and on lipid oxidation in rat skeletal muscle.

The effect of dietary carnosine supplementation on plasma and tissue carnosine and alpha-tocopherol concentrations and on the formation of thiobarbituric acid reactive substances (TBARS) in rat skeletal muscle homogenates was evaluated. Plasma, heart, liver and hind leg muscle was obtained from rats fed basal semipurified diets or basal diets containing carnosine (0.0875%), alpha-tocopheryl acetate (50 ppm), or carnosine (0.0875%) plus alpha-tocopheryl acetate (50 ppm). Dietary carnosine supplementation did not increase carnosine concentrations in heart, liver and skeletal muscle. Dietary supplementation with both carnosine and alpha-tocopherol increased carnosine concentrations in liver 1.56, 1.51- and 1.51-fold as compared with diets lacking carnosine, alpha-tocopherol or both carnosine and alpha-tocopherol, respectively. Dietary supplementation with both carnosine and alpha-tocopherol also increased alpha-tocopherol concentrations in heart and liver 1-38-fold and 1.68-fold, respectively, as compared to supplementation with alpha-tocopherol alone. Dietary supplementation with carnosine, alpha-tocopherol or both carnosine and alpha-tocopherol was effective in decreasing the formation of TBARS in rat skeletal muscle homogenate, with dietary alpha-tocopherol and alpha-tocopherol plus carnosine being more effective than dietary carnosine alone. The data suggest that dietary supplementation with carnosine and alpha-tocopherol modulates some tissue carnosine and alpha-tocopherol concentrations and the formation of TBARS in rat skeletal muscle homogenates.

Animals↗
PubMed1994

Effect of the peroxisome proliferators ciprofibrate and perfluorodecanoic acid on hepatic cell proliferation and toxicity in Sprague-Dawley rats.

The objective of this study was to compare the effects of perfluorodecanoic acid (PFDA) and ciprofibrate on the induction of hepatic toxicity and on hepatocellular proliferation in rats. In the first study, rats were first subjected to partial hepatectomy and then injected with [3H]thymidine (20 microCi/injection) at 23, 24, 25, 47, 48 and 49 h afterwards. After a 2 week recovery period, rats were injected with one of four levels of PFDA (0.3, 1.0, 3.0 or 10 mg/kg/injection) in four i.p. doses every 14 days, or were fed 0.01% or 0.003% ciprofibrate. Six days after the last PFDA injection and three days before the animals were killed, an osmotic minipump containing 20 mg/ml 5-bromo-2'-deoxyuridine (BrdU) was implanted s.c. for the measurement of DNA synthesis. Peroxisomal fatty acyl-CoA oxidase activity was significantly enhanced in both PFDA and ciprofibrate-treated groups in a dose-dependent manner. Hepatotoxicity, measured as the loss of [3H]thymidine from hepatic DNA, was not significantly affected by any of the treatments. Hepatic DNA synthesis was significantly increased only in rats receiving the highest dose of PFDA. In order to determine the time course of ciprofibrate- and PFDA-induced cell proliferation, we conducted another study with more time points. Rats were fed 0.01% ciprofibrate or were injected every 14 days with 3 or 10 mg PFDA/kg body weight for 10 days, 24 days, 6 weeks, 26 weeks or 54 weeks. Cell proliferation was quantified as in the first study. Ciprofibrate increased cell proliferation at the early but not the later time points, whereas PFDA increased cell proliferation at most times throughout the study. This study demonstrates that PFDA and ciprofibrate do not selectively induce hepatic toxicity and that their effects on cell proliferation do not correlate with their carcinogenic or promoting activities.

Acyl-CoA Oxidase↗
PubMed1993

Cigarette smoking and oxidative damage in the lung.

Cigarette smoke contains a large variety of compounds, including many oxidants and free radicals that are capable of initiating or promotes oxidative damage. Also, oxidative damage may result from reactive oxygen species generated by the increased and activated phagocytes following cigarette smoking. In vitro studies are generally supportive of the hypothesis that cigarette smoke can initiate or promote oxidative damage. However, information obtained from in vivo studies is inconclusive. Contrary to expectations, the levels of lipid peroxidation products were found to be decreased or unchanged in the lungs of chronically smoked rats. Metabolic adaptation, such as accumulation of vitamin E in the lung, and increased activities of superoxide dismutase in alveolar macrophages and pulmonary tissues of chronically smoked animals may enable smoked subjects to counteract oxidative stress and to resist further damage to smoke exposure. However, it is also possible that the metabolic adaptation may be secondary to inflammatory response and injury repair process following smoking exposure. More studies are needed to better understand the role of oxidative damage in the etiology of smoking-related disorders.

Animals↗
PubMed1993

Dietary fat effects on hepatic lipid peroxidation and enzymes of H2O2 metabolism and NADPH generation.

The purpose of this study was to determine the effects of dietary fat quantity and fatty acid composition on hepatic H2O2-metabolizing systems, activities of NADPH-generating enzymes and lipid peroxidation. One-month-old male C57BL/6J mice were fed one of six diets: (i) 5% fat, rich in 18:2n-6 fatty acid (5% N-6); (ii) 20% fat, rich in 18:3n-3 (N-3); (iii) 20% fat, rich in 18:2n-6 (N-6); (iv) 20% fat, rich in 18:1n-9 (N-9); (v) 20% fat, rich in saturated fatty acids (SAT); and (vi) 20% fat, deficient in essential fatty acids (EFAD); for 11 wk. Comparisons between animal groups receiving different fat quantities showed that activities of glucose-6-phosphate dehydrogenase (G6PDH, EC 1.1.1.49) and malic enzyme (ME, EC 1.1.1.40) and the levels of conjugated dienes were significantly lower in the N-6 than in 5% N-6 group. Conversely, activities of catalase (CAT, EC 1.11.1.6) and selenium-glutathione peroxidase (SeGSHPx, EC 1.11.1.9) were higher in the N-6 than in 5% N-6 group. Among the five dietary groups receiving 20% fat but differing in fatty acid composition, CAT activity was lower in the N-9 group, SeGSHPx activity was lower in the EFAD group, and glutathione reductase (GSSGR, EC 1.6.4.2) activity was higher in the N-6 than in the N-3, N-9, SAT and EFAD group. The EFAD group had much higher levels of total lipids and conjugated dienes, as well as activities of NADPH-generating enzymes, including G6PDH, ME and isocitrate dehydrogenase (EC 1.1.1.42), than the other four high-fat groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗