• Journal of Nutrition and Health
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• v.42 no.1
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• pp.5-13
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• 2009

Mushrooms have become a largely untapped source of powerful new pharmaceutical products that poses anti-inflammatory, and antimutagenic, and antioxidant activities. The antioxidant effects of the mushroom may be partly explained by protecting cellular components against free radical. The aim of this study was to investigate the protective effect of chaga mushroom against diabetes, via the mitigation of oxidative stress and reduction of blood glucose, in streptozotocin-induced diabetic rats. Rats were rendered diabetic by intravenous administration of STZ through tail at a dose of 50 mg/kg. Animals were allocated into four groups with 8 rats each. The control and diabetic control group were fed with standard rat feed. The other diabeic groups, the low chaga extract group and the high chaga extract group were fed ad libitum using 0.5 g/kg and 5 g/kg of chaga mushroom extract, respectively, for 4 weeks. The blood glucose levels in the two chaga extract groups showed a tendency to decrease but did not reach statistical significance after the supplementation. Leukocyte DNA damage, expressed as tail length, was found to be significantly lower in the high chaga extract group than in the diabetic control group (p > 0.05). Plasma level of total radical-trapping antioxidant potential (TRAP) was tend to be higher in the high chaga extract group compared with the diabetic control group. Erythrocyte antioxidant enzyme activities of two groups did not differ. Although we did not obtain beneficial effect on lowering blood glucose levels in the STZ-induced diabetic rats, this results suggest that the chaga mushroom extracts may initially act on protecting endogenous DNA damage in the short-term experiment.

• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.30-38
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• 2005

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.

• Journal of the Korean Society of Food Science and Nutrition
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• v.39 no.2
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• pp.227-236
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• 2010

This study was carried out to investigate the anti-oxidative and anti-inflammatory actions of Hericium erinaceus mycelia in BALB/C mice injected with lopopolysaccharide (LPS), called endotoxin. Mice (6 weeks of age) weighing approximately $24.73\pm0.11$ g were divided into 5 groups and were fed on the experimental diets containing Hericium erinaceus mycelia powder (HMP) for 1 week. Experimental groups were NC (normal control), HMP-C (HMP control), LC (LPS control), HMP 3%, and HMP 10%. Endotoxin shock was induced by intraperitoneal injection of LPS (100 mg/kg BW). NC and HMP-C groups were injected with saline solution (100 mg/kg BW). Food efficiency ratio were significantly (p<0.05) decreased in the HMP supplementation groups. Total fat and $\beta$-glucan excretion were higher in HMP supplementation groups than NC and LC groups, while plasma TG level was not different among groups. Plasma ALT levels were significantly (p<0.05) lower in the HMP supplementation groups than in LC group at 8 hr after LPS injection, while tumor necrosis factor-$\alpha$ and interleukine-6 levels of plasma were not different among groups. Hepatic superoxide dismutase, glutathione-reductase (GSH-red), and glutathione-peroxidase activities were higher in the HMP supplementation groups than in LC group at 4 hr after intraperitoneal injection of LPS. Hepatic GSH levels and protein expression of GSH-red was significantly (p<0.05) higher in the HMP supplemented groups than in LC group at 1 hr, 4 hr and 8 hr after LPS injection. From the above results, it is concluded that Hericium erinaceus mycelia may ameliorate hepatic oxidative stress by LPS through the elevation of hepatic glutathione level and antioxidant enzyme activities, which support the hepatoprotective effect of Hericium erinaceus mycelia.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.6
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• pp.807-813
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• 2014

The objective of the present study was to investigate the protective effects of anthocyanin-enriched extract from radiation-induced blackberry (Rubus fruticosus L.) mutant (${\gamma}$-B201) against carbon tetrachloride ($CCl_4$)-induced liver injury in Spargue-Dawley (SD) rats. The in vivo results show that ${\gamma}$-B201 attenuated the levels of serum aspartate aminotransferase, alanine aminotransferase, and liver lipid peroxidation in $CCl_4$-treated SD rats. Histopathological examination of rat livers showed that ${\gamma}$-B201 reduced the incidence of liver lesions induced by $CCl_4$. Moreover, ${\gamma}$-B201 prevented DNA damage in $CCl_4$-treated SD rats. Furthermore, administration of ${\gamma}$-B201 significantly increased the activity of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), in $CCl_4$-treated rat livers. In conclusion, the present study suggests that ${\gamma}$-B201 blackberry extract protects the liver from $CCl_4$-induced hepatic damage through an antioxidant mechanism. Therefore, ${\gamma}$-B201 blackberry may be functional food material for human health.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.6
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• pp.1065-1070
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• 2002

The purpose of this study was investigated the effects of YK-209 mulberry leaves on antioxidative defense system of liver in diabetic rats induced with streptozotocin (STZ). Male Sprague-Dawley rats weighing 100$\pm$10 g were randomly assigned to one normal and four STZ-induced diabetic groups; YK-209 mulberry leaves free diet (DM group),0.1% YK-209 mulberry leaves diet (DM-0.1Y group),0.2% YK-209 mulberry leaves diet (DM-0.2Y group) and 0.4% YK-209 mulberry leaves diet (DM-0.4Y group). Diabetes was induced by intravenous Injection of 55 mg/kg body weight of STZ in sodium citrate buffer (pH 4.3) via tail vein after 4 weeks feeding of experimental diets. Rats were sacrificed at the 9th day of diabetic states. Liver weight in all four diabetic groups were higher than normal group, but YK-209 mulberry supplementation groups were lower than DM group. Hepatic superoxide dismutase (SOD) activity was significantly decreased in all diabetic groups, compared with normal group. Hepatic glutathione peroxidase (GSHpx) activity was 7.3% decreased in DM group, compared with normal group, but those of DM-0.1Y and DM-0.2Y groups were maintained the normal level. The hepatic thiobarbituric acid reactive substances was markedly increased by 144% in DM group, compared with normal group, but those of DM-0. 1Y, DM-0.2Y groups were maintained the normal level. The contents of lipofuscin in liver were increased by 100% in DM group compared with normal group, but those of DM-0. 1Y, DM-0.2Y and DM-0.4Y groups were decreased to 42% 43% and 44%, respectively, compared with DM group. The hepatic superoxide radical (0$^2$-) contents in DM group were increased to 81%, compared with normal group, but those of DM-0.1Y and DM-0.4Y groups were similar to those of normal group. The present result indicate that YK-209 mulberry leaves regarded to suppress lipid peroxidation as an free radical scavenger system by the inhibition of oxidative stress.

• Journal of Nutrition and Health
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• v.44 no.1
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• pp.5-15
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• 2011

Although iron is an essential mineral, excess iron intake during pregnancy may increase oxidative stress in tissues. This study was conducted to investigate the effects of iron overload during pregnancy on iron status and oxidative stress in maternal rats. Ten week-old female Sprague-Dawley rats were mated with male rats. Non-pregnant (control) and pregnant rats were fed diets containing normal Fe (35 mg/kg diet), high Fe (350 mg/kg diet), or excess Fe (1,050 mg/kg diet) during pregnancy. Rats were sacrificed on pregnancy day 19. No significant difference in weight gain, diet intake, or litter size was observed according to iron intake levels. Furthermore, serum iron, hemoglobin, and hematocrit were not different among the rats administered the three levels of Fe both in the control and pregnant groups. However, the iron levels were lower in pregnant rats than those in the control. The liver and spleen iron contents increased significantly in the excess Fe group. An increase in liver ferritin levels with increasing iron intake was observed. Protein carbonyl content, as a marker of oxidative stress, increased significantly in liver with increasing iron intake but not malondialdehyde. Glutathione peroxidase activity in the liver of pregnant rats fed excess iron decreased significantly. Bcl-2 protein expression in the liver declined remarkably with increasing maternal iron intake in pregnant rats. Taken together, iron overload during pregnancy had little effect on hematology. However, the deposits of iron in the liver and the decline in antioxidant enzyme activity implied increased oxidative stress in tissues of the excess Fe group. These results suggest that excess iron intake during pregnancy increases oxidative stress in maternal tissues and may also affect fetal tissues.

• Korean Journal of Poultry Science
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• v.49 no.2
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• pp.115-124
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• 2022

The objective of this study was to investigate the effects of dietary coenzyme Q10 (CoQ10) sources on the antioxidant defense system in the blood and liver of laying hens. Thirty-six 40-wk old Lohmann Brown hens were randomly assigned to three groups based on body weight, with four cages with three layers each. Laying hens were divided into one of the following groups: control (CON), powdered CoQ10 (PCoQ, 100 mg/kg diet), and emulsified CoQ10 (ECoQ, 100 mg/kg diet). All hens were fed a control diet or a control diet supplemented with powdered or emulsified CoQ10 ad libitum for five weeks. There were no differences in body weight, weight gain, and organ weights among the treatment groups, including the liver and spleen. The blood total antioxidant power (TAP) in the ECoQ group increased (P<0.05) by approximately 2-fold compared to that in the CON group. However, there was no significant difference in blood TAP levels between the PCoQ and ECoQ groups, although a decreasing trend (P<0.13) was observed for levels of TAP in the ECoQ group. The mRNA expression and specific activities of superoxide dismutase, glutathione peroxidase, and catalase in the liver were not affected by dietary CoQ10 or type of CoQ10. However, hepatic lipid peroxidation in the ECoQ group was lower (P<0.05) than in the CON group. In conclusion, emulsified CoQ10 increased blood TAP and decreased hepatic lipid peroxidation without affecting antioxidant enzymes, suggesting that emulsified CoQ10 might be more applicable as an active antioxidant supplement than powdered type in laying hens.

• Tuberculosis and Respiratory Diseases
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• v.58 no.1
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• pp.31-42
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• 2005

Background : Peroxiredoxins (Prxs) are a relatively newly recognized, novel family of peroxidases that reduce $H_2O_2$ and alkylhydroperoxide into water and alcohol, respectively. There are 6 known isoforms of Prxs present in human cells. Normally, Prxs exist in a head-to-tail homodimeric state in a reduced form. However, in the presence of excess $H_2O_2$, it can be oxidized on its catalytically active cysteine site into inactive oxidized forms. This study surveyed the types of the Prx isoforms present in the pulmonary epithelial, macrophage, endothelial, and other cell lines and observed their response to oxidative stress. Methods : This study examined the effect of exogenous, excess $H_2O_2$ on the Prxs of established cell lines originating from the pulmonary epithelium, macrophages, and other cell lines, which are known to be exposed to high oxygen partial pressures or are believed to be subject to frequent oxidative stress, using non-reducing SDS polyacrylamide electrophoresis (PAGE) and 2 dimensional electrophoresis. Result : The addition of excess $H_2O_2$ to the culture media of the various cell-lines caused the immediate inactivation of Prxs, as evidenced by their inability to form dimers by a disulfide cross linkage. This was detected as a subsequent shift to its monomeric forms on the non-reducing SDS PAGE. These findings were further confirmed by 2 dimensional electrophoresis and immunoblot analysis by a shift toward a more acidic isoelectric point (pI). However, the subsequent reappearance of the dimeric Prxs with a comparable, corresponding decrease in the monomeric bands was noted on the non-reducing SDS PAGE as early as 30 minutes after the $H_2O_2$ treatment suggesting regeneration after oxidation. The regenerated dimers can again be converted to the inactivated form by a repeated $H_2O_2$ treatment, indicating that the protein is still catalytically active. The recovery of Prxs to the original dimeric state was not inhibited by a pre-treatment with cycloheximide, nor by a pretreatment with inhibitors of protein synthesis, which suggests that the reappearance of dimers occurs via a regeneration process rather than via the de novo synthesis of the active protein. Conclusion : The cells, in general, appeared to be equipped with an established system for regenerating inactivated Prxs, and this system may function as a molecular "on-off switch" in various oxidative signal transduction processes. The same mechanisms might applicable other proteins associated with signal transduction where the active catalytic site cysteines exist.

• Journal of the Korean Society of Food Science and Nutrition
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• v.40 no.2
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• pp.321-326
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• 2011

The aim of the present study was to investigate antihyperglycemic effect of Gleditschiae Spina (GS) in streptozotocin (STZ)-nicotinamide (NA)-induced type 2 diabetic rats. The rats were divided into four groups: normal control (NC), diabetic control (DC), diabetic rats supplemented with acarbose (AC, 4 mg/kg), and with GS ethanol extracts (GSE, 50 mg/kg). Weekly fasting blood glucose (FBG) for 10 weeks and oral glucose tolerance test (OGTT) at 10th week were monitored using glucose oxidase-peroxidase reactive strips. The FBG level was significantly reduced in AC group after 8 weeks and in GSE group at the end of period. The AUCs for the glucose response from OGTT and blood glucose level after sacrifice were significantly lower in the AC and GSE groups than the DC group. GSE supplementation significantly increased plasma total radical-trapping antioxidant potential (TRAP) in STZ-NA-induced diabetic rats, compared with DC group. The present study indicates that GSE could ameliorate type 2 diabetes and be comparable to acarbose, a standard hypoglycemic drug. Also, we suggest that GSE may possess antioxidant activity against the STZ-NA-induced oxidative stress.

• Tuberculosis and Respiratory Diseases
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• v.43 no.1
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• pp.46-53
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• 1996

Background: Endotoxin or lipopolysaccharide(LPS) can prime phagocytic cells such as polymorphonuclear leukocytes, monocytes or animal peritoneal macrophages to generate increased amounts of secretory products such as oxygen free radicals and tumor necrosis factor, which play an important role in developing adult respiratory distress syndrome in gram negative sepsis. Human alveolar macrophages(HAM) are continuously exposed to various stimuli inhaled into the alveoli, and the response to LPS might be different in HAM. Therefore, we investigated the effect of LPS pre-exposure on HAM adhered to plastic surface and A549 cell(type II human alveolar epithelial cell line) monolayer. Methods: HAM were isolated from bronchoalveolar lavage fluid from normal lung of the patients with localized lung cancer and esophageal cancer. LPS was exposed to HAM for 2hrs before or after adherence to plastic surface of 24-well Linbro plate and A549 cell monolayer. And then HAM was stimulated with PMA(phorbol myristate acetate) or fMLP(N-formyl-methionylleucyl-phenylalanine). The amount of hydrogen peroxide($H_2O_2$) production in the supernatant was measured on the principle of peroxidase-dependent oxidation of phenol red by hydrogen peroxide. Results: LPS pre-exposure could not enhance $H_2O_2$ production in neither HAM adhered to plastic surface nor one to A549 cell monolayer. But LPS even in the absence of PMA or fMLP stimulation directly increased $H_2O_2$ release in HAM if added after the adherence to A549 cell monolayer. Conclusion: Endotoxin does not prime HAM, but may directly activate HAM adhered to alveolar epithelial cells. Further investagation will be necessary.