• Molecular & Cellular Toxicology
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• 제5권3호
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• pp.230-236
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• 2009

Acrolein, a known toxin in cigarette smoke, is the most abundant electrophilic $\alpha$, $\beta$-unsaturated aldehyde to which humans are exposed in a variety of environmental pollutants, and is also product of lipid peroxidation. Increased unsaturated aldehyde levels and reduced antioxidant status plays a major role in the pathogenesis of various diseases such as diabetes, Alzheimer's and atherosclerosis. The findings reported here show that low concentrations of acrolein induce heme oxygenase-1 (HO-1) expression in RAW 264.7 macrophages. HO-1 induction by acrolein and signal pathways was measured using reverse transcription-polymerase chain reaction, Western blot and immunofluorescence staining analyses. Inhibition of extracellular signal-regulated kinase activity significantly attenuated the induction of HO-1 protein by acrolein, while suppression of Jun N-terminal kinase and p38 activity did not affect induction of HO-1 expression. Moreover, rottlerin, an inhibitor of protein kinase $\delta$, suppressed the upregulation of HO-1 protein production, possibly involving the interaction of NF-E2-related factor 2 (Nrf2), which has a key role as a HO-1 transcription factor. Acrolein elevated the nuclear translocation of Nrf2 in nuclear extraction. The results suggest that RAW 264.7 may protect against acrolein-mediated cellular damage via the upregulation of HO-1, which is an adaptive response to oxidative stress.

• 대한지역사회영양학회지
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• 제7권6호
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• pp.844-851
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• 2002

Smoking can increase oxidative stress and thereby change the antioxidant defense system in the body. To investigate the relationship between male adolescent smoking and antioxidant status, we surveyed the eating habits and dietary intake of 82 smokers and 44 nonsmokers recruited from a male technical high school. In addition, antioxidant enzyme activity and lipid peroxide values were determined in both the plasma and the erythrocytes. Although the frequency of food intake was not significantly different, most nutrient intake was unexpectedly higher in smokers than in nonsmokers. In comparison with the Korean RDA, especially the average intake of Ca, Fe and vitamin $B_2$ didn t reach 75% of the Korean RDA in either smokers or nonsmokers. An analysis of antioxidant enzyme activity showed that plasma catalase. superoxide dismutase (SOD), glutathione peroxidase (GSH-px), erythrocyte catalase and GSH-px activities showed no significant difference between smokers and nonsmokers. However, the erythrocyte SOD activity of smokers (1.57 unit/mgHb) was significantly lower than that of nonsmokers (2.00 unit/mg Hb). In addition, the plasma ceruloplasmin concentration of smokers (28.68 mg/$d\ell$) was significantly higher than that of nonsmokers (26.30 mg/$d\ell$), whereas the specific ceruloplasmin ferroxidase activity of smokers (0.31 unit/mg) was lower than that of nonsmokers (0.35 unit/mg). The plasma and erythrocyte thlobarbituric acid reactive substance (TBARS) of smokers (2.57 $\mu$mol/L, 0.32 $\mu$mol/gHb) were also significantly higher than those of nonsmokers (2.25 $\mu$mol/L, 0.27 $\mu$mol/gHb). The overall data indicate that adolescent smoking might decrease the antioxidant capacity of the body, in part, by lowering the erythrocyte SOD activity and the specific ceruloplasmin ferroxidase activity.

• Nutrition Research and Practice
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• 제4권5호
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• pp.393-399
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• 2010

Enteral nutritional support has been used via tube feeding for dysphagic stroke patients. We performed long and short term trials to evaluate the effects of commercial enteral nutritional supports on nutrition and health in stroke patients (mRS = 3~5) and quality of life in their caregivers. For a long term study, we recruited chronic (${\geq}$ 1 yrs) stroke patients (n = 6) and administered them 6 cans/day (1,200 kcal) of the commercial enteral formula N for 6 months according to IRB-approved protocol. We collected peripheral blood at 0, 2, 4 and 6 months. For a short term study, we recruited acute (${\leq}$ 3 months) stroke patients (n = 12) and randomly administered them two different commercial enteral formulas, N or J, for 2 weeks. We collected their blood at 0, 4, 7 and 14 day of the administration. Blood samples were analyzed to quantify 19 health and nutritional biomarkers and an oxidative stress biomarker, malondialdehyde (MDA). In order to evaluate quality of life, we also obtained the sense of competence questionnaire (SCQ) from all caregivers at 'before' and 'after trials'. As results, the enteral formula, N, improved hemoglobin and hematocrit levels in the long term trial and maintained most of biomarkers within normal ranges. The SCQ levels of caregivers were improved in the long term treatment (P < 0.05). In a case of the short term study, both of enteral formulas were helpful to maintain nutritional status of the patients. In addition, MDA levels were decreased in the acute patients following formula consumption (0.05 < P < 0.1). Most of health and nutrition outcomes were not different, even though there is a big difference in price of the two products. Thus, we evaluate the formula N has equal nutritional efficacy compared to the formula J. In addition, long term use of enteral formula N can be useful to health and nutrition of stroke patients, and the quality of life for their caregivers.

• Journal of Nutrition and Health
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• 제38권4호
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• pp.297-306
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• 2005

It is known that dehydroepiandrosterone (DHEA) shows a dual effect, prooxidant or antioxidant, depending on the do-sage or physiological status of animals. The purpose of this study was to determine the effects of DHEA administration at low dose on lipid peroxidation, protein carbonylation and fatty acid composition in liver. Sprague Dawley male rats were fed either com oil diet containing $15\%$ com oil or fish oil diet containing $2\%$ corn oil + $13\%$ sardine oil, with or without $0.2\%$ DHEA for 9 weeks. Atherogenic index and hepatic triglyceride and cholesterol levels were significantly reduced by DHEA administration in rats fed with fish oil diet. Hepatic lipid peroxide product (TBARS) and protein carbonyl levels were significantly higher in rats fed with fish oil diet than in rats fed with corn oil diet. However, DHEA administration significantly reduced the hepatic thiobarbituric acid-reactive substance (TBARS) and conjugated diene levels in rats fed with fish oil diet. Contents of C16 : 0, C16 : 1, C20 : 5 and C22 : 6 in hepatic microsome were higher in rats fed with fish oil diet than in rats fed with corn oil diet, and contents of C18 : 2 and C20 : 4 were lower than in rats fed with com oil diet. DHEA administration significantly increased C16 : 0 and C18 : 3 contents and reduced C18 : 2 content in rats fed with com oil diet, while it increased C16 : 0 and C18 : 1 and reduced C20 : 5 and C22 : 6 in rats fed with fish oil diet. On overall, DHEA administration increased saturated fatty acid (SFA) and reduced polyunsaturated fatty acid (PUFA) in hepatic microsome, thereby PUFA/SFA ratio was significantly (p < 0.0001) reduced without the change of n-3/n-6 ratio. Taken together, low dose of DHEA administration lowered PUFA/SFA ratio in hepatic microsomal membranes and also showed antioxidative effect especially in fish oil-induced highly oxidative stress condition through blocking increases of C20 : 5 and C22 : 6 contents.

• Molecules and Cells
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• 제38권5호
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• pp.452-456
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• 2015

Obesity is the fifth leading risk for death globally, and a significant challenge to global health. It is a common, complex, non-malignant disease and develops due to interactions between the genes and the environment. DNA methylation can act as a downstream effector of environmental signals; analysis of this process therefore holds substantial promise for identifying mechanisms through which genetic and environmental factors jointly contribute to disease risk. To assess the effects of excessive weight and obesity on gene-specific methylation levels of promoter regions, we determined the methylation status of four genes involved in inflammation and oxidative stress [interleukin 6 (IL6), tumor necrosis factor ${\alpha}$ ($TNF{\alpha}$), mitochondrial transcription factor A (TFAM), and glucose transport 4 (GLUT4)] in blood cell-derived DNA from healthy women volunteers with a range of body mass indices (BMIs) by methylation-specific PCR. Interestingly, the samples from obese individuals ($BMI{\geq}30kg/m^2$) showed significantly increased hypermethylation for IL6 gene compared to normal weight ($BMI<23kg/m^2$) and overweight sample ($23kg/m^2{\leq}BMI<30kg/m^2$) (P = 0.034 and P = 0.026). However there was no statistically significant difference in promoter methylation of the other 3 genes between each group. These findings suggest that aberrant DNA methylation of IL6 gene promoter may play an important role in the etiology and pathogenesis of obesity and IL6 methylation could be used as molecular biomarker for obesity risk assessment. Further studies are required to elucidate the potential mechanisms underlying this relationship.

• 한국임상수의학회지
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• 제26권3호
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• pp.200-204
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• 2009

This study was performed to evaluate the effects of reduced L-glutathione on the oxidant/antioxidant status(superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase(GPx), protein carbonyl and lipid hydroperoxide(LPO) concentration), renal function(blood urea nitrogen(BUN) and serum creatinine levels), and microscopy of renal tissues in pigs undergoing unilateral renal ischemia-reperfusion(I/R). Sixteen Landrace and Yorkshire mixed-breed pigs were divided randomly into two groups: untreated control group and reduced L-glutathione-treated group(4 mg/kg IV). Each group had 8 pigs. Pigs were unilaterally nephrectomized and the kidney was subject to 30 min of renal pedicle occlusion. Blood samples for biochemical assay were collected on days 1, 3, 5, 7, and 14 post nephrectomy. Renal I/R injury were evaluated histopathologically by the microscopic observation of renal tissue sections and biochemically by the measurement of the plasma creatinine and urea levels. Parameters of oxidative stress such as SOD, GPx, CAT, protein carbonyl and LPO were measured. The elevation of creatine and BUN levels was lower in the treated group, compared with the control group. The activities of antioxidant-enzyme were higher in the treated group, compared with the control group. In histological findings, the severity of damage in the reduced L-glutathione treated group was less when compared to the control group.

• 대한생식의학회:학술대회논문집
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• 대한불임학회 2000년도 제39차 춘계 학술대회
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• pp.13-28
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• 2000

Human spermatozoa exhibit a capacity to generate ROS and initiate peroxidation of the unsaturated fatty acids in the sperm plasma membrane, which plays a key role in the etiology of male infertility. The short half-life and limited diffusion of these molecules is consistent with their physiologic role in key biological events such as acrosome reaction and hyperactivation. The intrinsic reactivity of these metabolites in peroxidative damage induced by ROS, particularly $H_2O_2$ and the superoxide anion, has been proposed as a major cause of defective sperm function in cases of male infertility. The number of antioxidants known to attack different stages of peroxidative damage is growing, and it will be of interest to compare alpha-tocopherol and ascorbic acid with these for their therapeutic potential in vitro and in vivo. Both spermatozoa and leukocytes generate ROS, although leukocytes produce much higher levels. The clinical significance of leukocyte presence in semen is controversial. Seminal plasma confers some protection against ROS damage because it contains enzymes that scavenge ROS, such as catalase and superoxide dismutase. A variety of defense mechanisms comprising a number of antioxidants can be employed to reduce or overcome oxidative stress caused by excessive ROS. Determination of male infertility etiology is important, as it will help us develop effective therapies to overcome excessive ROS generation. ROS can have both beneficial and detrimental effects on the spermatozoa and the balancing between the amounts of ROS produced and the amounts scavenged at any moment will determine whether a given sperm function will be promoted or jeopardized. Accurate assessment of ROS levels and, subsequently, OS is Vital, as this will help clinicians both elucidate the fertility status and identify the subgroups of patients that respond or do not respond to these therapeutic strategies. The overt commercial claims of antioxidant benefits and supplements for fertility purposes must be cautiously looked into, until proper multicentered clinical trials are studied. From the current data it appears that no Single adjuvant will be able to enhance the fertilizing capacity of sperm in infertile men, and a combination of the possible strategies that are not toxic at the dosage used would be a feasible approach.

• Environmental Analysis Health and Toxicology
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• 제26권
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• pp.6.1-6.8
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• 2011

Objectives: The present study investigated the potential adverse effects of multi-wall carbon nanotubes (MWCNTs) on pregnant dams and embryonic development following maternal exposure in rats. Methods: MWCNTs were orally administered to pregnant rats from gestational day (GD) 6 through 19 at dose levels of 0, 8, 40, 200, and 1000 mg/kg/day. During the test period, clinical signs, mortality, body weights, food consumption, serum biochemistry, oxidant-antioxidant status, gross findings, organ weights, and Caesarean section findings were examined. Results: All animals survived to the end of the study. A decrease in thymus weight was observed in the highest dose group. However, maternal body weight, food consumption, serum biochemical parameters, and oxidant-antioxidant balance in the kidneys were not affected by treatment with MWCNTs. No treatment-related differences in gestational index, embryo-fetal mortality, or fetal and placental weights were observed between treated and control groups. Conclusions: The results show that 14-day repeated oral dosing of MWCNTs during pregnancy induces minimal maternal toxicity at 1000 mg/kg/day in rats. Under these experimental conditions, the no-observed-adverse-effect level of MWCNTs is considered to be 200 mg/kg/day for dams and 1000 mg/kg/day for embryonic development.

• The Korean Journal of Physiology and Pharmacology
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• 제24권5호
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• pp.403-412
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• 2020

Diabetic nephropathy (DN) is a hyperglycemia-induced progressive development of renal insufficiency. Excessive glucose can increase mitochondrial reactive oxygen species (ROS) and induce cell damage, causing mitochondrial dysfunction. Our previous study indicated that cilostazol (CTZ) can reduce ROS levels and decelerate DN progression in streptozotocin (STZ)-induced type 1 diabetes. This study investigated the potential mechanisms of CTZ in rats with DN and in high glucose-treated mesangial cells. Male Sprague-Dawley rats were fed 5 mg/kg/day of CTZ after developing STZ-induced diabetes mellitus. Electron microscopy revealed that CTZ reduced the thickness of the glomerular basement membrane and improved mitochondrial morphology in mesangial cells of diabetic kidney. CTZ treatment reduced excessive kidney mitochondrial DNA copy numbers induced by hyperglycemia and interacted with the intrinsic pathway for regulating cell apoptosis as an antiapoptotic mechanism. In high-glucose-treated mesangial cells, CTZ reduced ROS production, altered the apoptotic status, and down-regulated transforming growth factor beta (TGF-β) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB). Base on the results of our previous and current studies, CTZ deceleration of hyperglycemia-induced DN is attributable to ROS reduction and thereby maintenance of the mitochondrial function and reduction in TGF-β and NF-κB levels.

• Journal of Nutrition and Health
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• 제51권1호
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• pp.1-13
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• 2018

Purpose: This review article provides an overview of the trends of research papers on the health benefits of kimchi and kimchi lactic acid bacteria published from 1995 to 2017. Methods: All publications from 1995 to 2017 regarding kimchi and kimchi lactic acid bacteria were collected, reviewed, and classified. This review article covers the publications of the health benefits of kimchi and kimchi lactic acid bacteria on experimental, clinical trials, and epidemiology studies. Results: The number of publications on kimchi over the period were 590: 385 publications in Korean and 205 publications in English. The number of publications on the health benefits of kimchi and kimchi lactic acid bacteria were 95 in Korean and 54 in English. The number of publications on kimchi and kimchi lactic acid bacteria were 84 and 38, respectively, in the experimental models. Ten research papers on kimchi in clinical trials and 7 publications in epidemiology were found. Kimchi or kimchi lactic acid bacteria had protective effects against oxidative stress, mutagenicity, toxicity, cancer, dyslipidemia, hypertension, immunity, and inflammation in in vitro, cellular, and in vivo animal models. Moreover, kimchi had effects on the serum lipids, intestinal microbiota, iron status, obesity, and metabolic parameters in human clinical trials. In epidemiology, kimchi had effects on hypertension, asthma, atopic dermatitis, rhinitis, cholesterol levels, and free radicals. Conclusion: This review focused on the publications regarding the health benefits of kimchi and kimchi lactic acid bacteria, suggesting the future directions of studies about kimchi and kimchi lactic acid bacteria by producing a database for an evaluation of the health benefits of kimchi.