Chronic alcoholism is considered a common cause of malnutrition. Especially, micronutrient deficiency may playa critical role in the incidence of alcoholic liver diseases. This study was conducted to investigate the effect of folate deficiency and ethanol consumption on cholesterol metabolism and the antioxidative system in rats. Plasma concentration of total cholesterol was increased by ethanol administration in folate-fed rats. HDL-cholesterol tended to be higher in the folate-fed group, but it was not significant. The plasma and hepatic levels of malondialdehyde were increased after chronic ethanol feeding, but dietary folate depressed the plasma malondialdehyde content of rats. Ethanol or folate feeding did not significantly change alcohol dehydrogenase activity. But folate feeding increased catalase activity in ethanol-fed rats. There was no significant change in superoxide dismutase activity among the experimental groups. Glutathione peroxidase activity tended to decrease by chronic ethanol feeding, but dietary folate did not affectthe glutathione peroxidase activity of chronic ethanol-fed rats. Glutathionine-S-transferase activity was not affected by ethanol feeding or folate deficiency. The plasma and hepatic levels of retinol decreased after chronic ethanol feeding. The hepatic level of retinol significantly decreased in ethanol-fed rats by folate deficiency. The plasma level of $\alpha$-tocopherol tended to be low in the folate deficient group with ethanol feeding, but there was no difference among the experimental groups in the hepatic level of $\alpha$-tocopherol. These results demonstrate that chronic ethanol consumption changes the plasma cholesterol metabolism and antioxidative system of rats, and optimal folate feeding in ethanol-fed rats exerts protective effects to some extent.
This study investigated anti-obesity and antioxidant effects of dietary non-fermented soybean crud residue (SCR) and fermented SCR by Monascus pilosus (FSCR) in high-fat induced-obese mice. SCR and FSCR were supplemented with high-fat diet at 2% (wt/wt) dose for 8 weeks. Both SCR and FSCR significantly lowered body weight, epididymal fat weight and weight gain rate compared to high-fat diet control (HC) group and FSCR group showed lowest weight gain rate. In addition, it was observed that serum and hepatic lipid profiles including triglyceride, total cholesterol, LDL-cholesterol and HDL-cholesterol were significantly improved by supplementing SCR or FSCR. Furthermore, SCR and FSCR administration showed increase of glutathione content and decrease of hepatic lipid peroxide content, serum aminotransferase activity, and hepatic xanthine oxidase activity. On the other hand, activities of reactive oxygen species scavenging enzyme such as superoxide dismutase, glutathione S-transferase and glutathione peroxidase in two test groups were higher than those of HC. Lastly, in comparison with SCR, FSCR was more effective in restoring obesity-related biomarkers to normal level in high-diet induced obese mice. In conclusion, the present study indicates that FSCR could have not only anti-obese effects such as inhibition of abdominal fat accumulation, but also protective effects of cardiovascular disease such as atherosclerosis by decreasing serum and hepatic lipid contents. Furthermore, these results suggest that experimental diets in this study could alleviate hepatic damage caused by overproduction of reactive oxygen spices (ROS) due to obesity via inhibition of ROS generating activities and induction of ROS scavenging activities.
It was undertake to investigate the factors involved in the micro thrombus formation in the plasma from the patients with cerebrovascular disease(CVD) and the in vitro actions of sodium nitroprusside on the platelet aggregate formation. 1) The microthrombus formation in the plasma from CVD was significantly enhanced, in comparison with that from the healthy volunteers. 2) Both lipid peroxide and cathepsin D in the plasma from CVD were higher than those levels from the healthy volunteers. 3) Whereas the platelets from healthy individuals showed less aggregation activity in response to ADP in the second phase those from CVD revealed the enhanced aggregating response to ADP. 4) When the bovine basilar artery, rabbit aorta and human umbilical artery were pretreated with $K^+-free$ PSS, ouabain, 13-hydroperoxylinoleic acid(13-HPLA) and cadmium they markedly enhanced the platelet aggregability respectively. 5) Platelet aggregation induced by $K^+-free$ PSS-treated bovine basilar artery was decreased by sodium nitroprusside in a dose-dependent manner, but not by either hydralazine. 6) Both dibutyryl cyclic AMP and 8-bromo cyclic GMP had the inhibitory action on the platelet aggregation. However, the latter had more prominent action than former. The antiaggregating effect by sodium nitroprusside was antagonized by pretreatment with methylene blue, but not by hemoglobin. These results provide the evidences for the therapeutic use of sodium nitroprusside in the emergency of cerebrovascular disease and in remains the further study of the clinical therapy with it.
In order to evaluate a potential role of mitochondria in the mediation of toxicity of paraquat (PQ), submitochondrial particle and microsome of mouse liver were compared by oxygen radical generation and lipid peroxidation. With NADH in submitochondrial particle and NADPH in microsome as electron donors, PQ stimulated production of superoxide anion and $H_2O_2$ in both fractions. Under the same conditions, PQ enhanced the generation of ethylene from methional suggestiong stimulation of OH production by PQ. But these effects by PQ were somewhat lower in submitochondrial particle than in microsome. In addition, lipid peroxidation(measured as MDA production) was stimulated by PQ in both fractions. The stimulation of lipid peroxidation in both fractions seemed to occur by the same mechanism probably through perferryl ion. This was supported by the following findings: i) The lipid peroxidation in both fractions was partially inhibited by SOD and completely inhibited by DETAPAC(an iron chelator) but not by catalase or OH scavenger. ii) Addition of $ADP-Fe^{3+}$ further increased PQ-induced lipid peroxidation but decreased ethylene production from methional suggesting no correlation between OH production and lipid peroxidation. The redox-cycling of PQ in mitochondria appeared to be linked to NADH dehydrogenase, not to CoQ since all of the observed stimulations by PQ in submitochondrial particle were inhibited by p-hydroxymercuribenzoate(a NADH dehydrogenase inhibitor) but not affected by other respiratory chain blockers. The above results demonstrate that redox-cycling properties of PQ leading to oxygen radical generation and lipid peroxidation can also occur in mitochondria in the same manner as in microsome. Therefore, the observed actions of PQ in mitochondria suggest that mitochondria may also contribute to toxicity of this drug in vivo.
The effect of antioxidants on the myocardial cellular damage which occurs during reoxygenation of hypoxic myocardium was examined in isolated rat hearts. The roles of oxygen free radical and lipid peroxidation in reoxygenation injury of myocardium were also investigated. In Langenorff preparation of isolated rat heart, which was made hypoxic by perfusion with the substrate free, hypoxic cardioplegic solution ($37^{\circ}C$, 90 min), the release of cytosolic enzymes (creatine phosphokinase, lactic dehydrogenase) and a lipid peroxidation product, malondialdehyde into the coronary effluent were abruptly increased by reoxygenation. The release of enzymes was closely parallel to that of MDA. These increases of enzymes and lipid peroxidation product were suppressed to various degrees in the presence of scavengers of superoxide anion (superoxide dismutase, 10,000 U), hydrogen peroxide (catalase, 25,000 U) and hydroxyl radical (dimethyl sulfoxide, 10%). A natural antioxidant, ${\alpha}-tocopherol$(4.5 uM) and a synthetic one, butylated hydroxytoluene (2 uM) suppressed the release of cytosolic enzymes with the concomittent reduction of lipid peroxidation as measured by malondialdehyde release into the coronary effluent. These effects of antioxidants were dose dependent, and were more pronounced when the antioxidants were administered throughout hypoxic and reoxygenation periods than given during reoxygenation period only. These results suggest that cytotoxic oxygen free radicals produced in the myocardium during reoxygenation may be responsible fur the myocardial cellular injury by enhancing the lipid peroxidation of cellular membranes. Furthermore, the antioxidants may exert protective effect against reoxygenation damage of hypoxic myocardium through the inhibition of lipid peroxidation reaction.
JE Yoi-Kwon;YU Young-Beob;KIM Gyeong-Eup;LEE Jong-Ho;JUNG Byung-Chun
Korean Journal of Fisheries and Aquatic Sciences
/
v.30
no.1
/
pp.72-78
/
1997
The levels of reducing sugars, organic acids and fatty acids, known as precursors of major flavors induced from dried sellfish, were analyzed to investigate their behaviors during drying process. Free reducing sugar contents were markedly decreased in all samples by boiling, Its content in Blue mussel and Short-necked calm samples significantly decreased after drying process. Among the eight different organic acids from blue mussel, Short-necked calm and Pacific oyster samples, succinic acid in blue mussel and short-necked calm samples was measured with $74.9\%\;and\;67.4\%$, respectively. In the sample of Pacific oyster, succinic acid content was found to be $38.4\%$, but pyroglutamic acid content was the highest level with $41.6\%$. Contents of organic acids with exception succinic acid were significantly reduced in all three samples of sun-dried or hot-air dried. The content of succinic acid in the samples of sun-dried and hot-air dried pacific oyster reduced to $53.0\%\;and\;44.2\%$, respectively, but relatively small decrease $(29.0\%\;and\;10.0\%)$ was observed in sun-dried and hot-air dried short-necked calm samples, respectively. Content of polar lipid with the major fatty acids profile of C16:0, C16:1, C20:5 and C22:6 was consisted of $59.1\%,\;66.7\%\;and\;42.4\%$, respectively, in blue mussel, short-necked calm and pacific oyster samples and the content of polyene fatty acids was appeared to be $40.5\%,\;48.6\%\;and\;48.9\%$, respectively. Relatively high peroxide value in all boiled-dried products samples was found to be $41.64\~86.80\;meq/kg$ sample. Carbonyl value in boiled-dried products samples was found to be $15.55\~27.99\;meq/kg$, but its value in broiled products samples was significantly high level of $127.6\~136.5\;meq/kg$.
The present study was directed to investigate the antioxidative effects of onion and mustard powder extracts on fish oil. The oxidative changes of sardine oil with and without onion and mustard powder extract were estimated by measuring peroxide value (POV), thiobarbituric acid (TBA) value, weighing method, acid value (AV) and fatty acid composition, periodically. The results obtained are summarized as follows ; From view point of POV, fat soluble fraction of onion and mustard powder showed much inhibitory effect on the oxidation of sardine oil, marked induction period to be prolonged about 18 and 20 days, respectively. But the POV in fat soluble fraction of mustard powder increased remarkably in the early stage of storage, so it did not show inhibitory effect on the oxidation of sardine oil. In the TBA value of sardine oil during storage, the water soluble fraction of onion and mustard powder were more slowly increased than other fractions. The weighing change of sardine oil, contained in the water soluble fraction of mustard powder, was slower than other fractions, marking $0.5\%$ of weight gain during 30 day storage. On the other hand water and $80\%$ ethanol soluble fractions of onion were marked $2.3\%\;and\;5.8\%$ of weight gain during 30 day storage. In the oxidative degradation of docosahexaenoic acid, water soluble fractions of mustard powder and onion extracts showed the strongest inhiditory effect.
For an effective utilization, quality stability of instant powdered oyster soup made of canned oyster processing waste water (IPSW) was determined. Instant powdered soup from oyster hot-water extracts (IPSE) was also prepared by mixing hot-water extract powder (15 g) with table salt (5 g), cream powder (19 g), milk replacer (12 g), wheat flour (20 g), corn flour (15 g), starch (5 g), glucose (7.5 g) and onion powder (1.5 g). In preparing IPSW, mixed powder from wash water and boiling liquid waste, instead of powder from hot-water extracts and table salt, was added (powder from boiling liquid waste: powder from wash water= 12: 8) and other additives were added in proportion to those in the IPSE. The moisture content, water activity, peroxide value and fatty acid composition showed little changes during storage of the IPSW. The pH, volatile basic nitrogen content and brown pigment formation increased slightly, while white index decreased slightly during storage of IPSW. No significant difference was observed in the changes of food component during storage between IPSW and IPSE. According to a sensory evaluation, the change in quality of IPSW was negligible during 12 months of storage. from the results of the chemical experiment and sensory evaluation, IPSW packed with laminated film bag (OPP, $20{\mu}m/PE,\;20{\mu}m/paper,\;45g/m^3/PE,\;20{\mu}\;m/Al,\;7{\mu}\;m/PE,\;20{\mu}m$) was revealed to be preserved in good quality during 12 months of storage.
Water supplied through dental unit waterlines (DUWLs) has been shown to contain high number of bacteria. To reduce the contamination of DUWLs, it is essential to develop effective disinfectants. It is, however, difficulty to obtain proper DUWL samples for studies. The purpose of this study was to establish a simple laboratory model for reproducing DUWL biofilms. The bacteria obtained from DUWLs were cultured in R2A liquid medium for 10 days, and then stored at $-70^{\circ}C$. This stock was inoculated into R2A liquid medium and incubated in batch mode. After 5 days of culturing, it was inoculated into the biofilm formation model developed in this study. Our biofilm formation model comprised of a beaker containing R2A liquid medium and five glass rods attached to DUWL polyurethane tubing. Biofilm was allowed to form on the stir plate and the medium was replaced every 2 days. After 4 days of biofilm formation in the laboratory model, biofilm thickness, morphological characteristics and distribution of the composing bacteria were examined by confocal laser microscopy and scanning electron microscopy. The mean of biofilm accumulation was $4.68{\times}10^4$ colony forming unit/$cm^2$ and its thickness was $10{\sim}14{\mu}m$. In our laboratory model, thick bacterial lumps were observed in some parts of the tubing. To test the suitability of this biofilm model system, the effectiveness of disinfectants such as sodium hypochlorite, hydrogen peroxide, and chlorhexidine, was examined by their application to the biofilm formed in our model. Lower concentrations of disinfectants were less effective in reducing the count of bacteria constituting the biofilm. These results showed that our DUWL biofilm laboratory model was appropriate for comparison of disinfectant effects. Our laboratory model is expected to be useful for various other purposes in further studies.
Background : Arsenic trioxide ($As_2O_3$) has been used to treat acute promyelocytic leukemia, and it induces apoptosis in a variety of solid tumor cell lines including non-small cell lung cancer cells. However, nonsteroidal antiinflammatory drugs (NSAID) can enhance tumor response to chemotherapeutic drugs or radiation. It was previously demonstrated that a combination treatment with $As_2O_3$ and sulindac induces the apoptosis of NCI-H157 human lung carcinoma cells by activating the caspase cascade. This study aimed to determine if a combination treatment augmented its apoptotic potential through other pathways except for the activation of the caspase cascade. Material and Methods : The NCI-H157 cells were treated with $As_2O_3$, sulindac and antioxidants such as glutathione (GSH) and N-acetylcysteine (NAC). The cell viability was measured by a MTT assay, and the level of intracellular hydrogen peroxide ($H_2O_2$) generation was monitored fluorimetrically using a scopoletin-horse radish peroxidase (HRP) assay. Western blotting and mitochondrial membrane potential transition analysis were performed in order to define the mechanical basis of apoptosis. Results : The viability of the cells was decreased by a combination treatment of $As_2O_3$ and sulindac, and the cells were protected using antioxidants in a dose-dependent manner. The increased $H_2O_2$ generation by the combination treatment was inhibited by antioxidants. The combination treatment induced changes in the mitochondrial transmembrane potential as well as the expression of the Bcl-2 family proteins, and increased cytochrome c release into the cytosol. However, the antioxidants inhibited the effects of the combination treatment. Conclusion : Combination treatment with $As_2O_3$ and sulindac induces apoptosis in NCI-H157 human lung carcinoma cells via ROS generation with a mitochondrial dysfunction.
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