• Asian Pacific Journal of Cancer Prevention
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• 제15권3호
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• pp.1125-1131
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• 2014

Background: Schistosomiasis is a parasitic disease causing chronic ill health in humans with a serious consequences for socio-economic development in tropical and subtropical regions. There is also evidence linking Schistosoma mansoni to colonic carcinoma occurrence. The aim of this study was to evaluate some inflammatory and oxidative stress biomarkers, as well as L-fucose as linkers between intestinal schistosomiasis and colonic dysplasia development in mice. Materials and Methods: This study was conducted upon 80 mice that were divided the control group (10 non infected mice) and infected group which was subdivided into 7 sub-groups (10 mice each) according to the time of sacrifaction in the post infection (p.i.) period, 10 mice being sacrificed every two weeks from 6 weeks p.i. to 18 weeks p.i. Tumor necrosis factor alpha (TNF-${\alpha}$), inducible nitric oxide synthase (iNOS), and pentraxin 3 (PTX3) levels were estimated by immunoassay. The L-fucose level, and thioredoxin reductase (TrxR) and lactate dehydrogenase (LDH) activities were also evaluated in colonic tissue. Results: The current study revealed statistically significant elevation in the studied biochemical markers especially at 16 and 18 weeks p.i. The results were confirmed by histopathological examination that revealed atypical architectural and cytological changes in the form of epithelial surface serration and nuclear hyper-chromatizia at 14, 16 and 18 weeks p.i. Conclusions: inflammation, oxidative stress and L-fucose together may form an important link between Schistosomal mansoni infection and colonic dysplasia and they can be new tools for prediction of colonic dysplasia development in experimental schistosomiasis.

• Nutrition Research and Practice
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• 제9권2호
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• pp.165-173
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• 2015

BACKGROUND/OBJECTIVES: This study addressed the question whether the composition of supposedly 'healthy' or 'unhealthy' dietary regimes has a calorie-independent short-term effect on biomarkers of metabolic stress and vascular risk in healthy individuals. SUBJECTS/METHODS: Healthy male volunteers (age $29.5{\pm}5.9years$, n = 39) were given a standardized baseline diet for two weeks before randomization into three groups of different dietary regimes: fast food, Mediterranean and German cooking style. Importantly, the amount of calories consumed per day was identical in all three groups. Blood samples were analyzed for biomarkers of cardiovascular risk and metabolic stress after two weeks of the baseline diet and after two weeks of the assigned dietary regime. RESULTS: No dietary intervention affected the metabolic or cardiovascular risk profile when compared in-between groups or compared to baseline. Subjects applied to the Mediterranean diet showed a statistically significant increase of uric acid compared to baseline and compared to the German diet group. Plasma concentrations of urea were significantly higher in both the fast food group and the Mediterranean group, when compared to baseline and compared to the German diet group. No significant differences were detected for the levels of vitamins, trace elements or metabolic stress markers (8-hydroxy-2-deoxyguanosine, malondialdehyde and methylglyoxal, a potent glycating agent). Established parameters of vascular risk (e.g. LDL-cholesterol, lipoprotein(a), homocysteine) were not significantly changed in-between groups or compared to baseline during the intervention period. CONCLUSIONS: The calorie-controlled dietary intervention caused neither protective nor harmful short-term effects regarding established biomarkers of vascular or metabolic risk. When avoiding the noxious effects of overfeeding, healthy individuals can possess the metabolic capacity to compensate for a potentially disadvantageous composition of a certain diet.

• Ocean and Polar Research
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• 제30권1호
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• pp.109-117
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• 2008

해양환경 건강성 평가에서 바이오마커의 적용은 상대적으로 새로운 분야이다. 국립학술원 및 세계보건기구에 따르면 바이오마커는 노출바이오마커, 영향바이오마커 및 민감바이오마커 등 3가지로 나누어진다. 해양생태계에 대한 환경오염물질의 노출 및 영향을 평가하기 위하여 다음과 같은 바이오마커들이 시험되고 있다: 해독, 산화스트레스, 분해산물, 스트레스 반응, 세포사멸, 물질대사, 신경반응, 생식, 스테로이드 호르몬, 항산화물질, 유전적 변형. 1990년대 초부터 여러 바이오마커 연구그룹들은 해양생물의 건강지수를 개발하여 해양환경의 상태를 평가하기 위한 수단으로 활용해 왔다. 바이오마커 지수는 생물학적 효과에 대한 모니터링활동으로부터 얻어진 자료의 해석에 사용될 수 있다. 본 총설에서는 이제까지 보고된 바이오마커 지수 관련 연구 중 대표적인 건강평가지수(Health assessment Index), 바이오마커 지수(Biomarker Index), 생물영향평가지수(Bioeffect Assessment Index) 및 일반화된 선형모델(Generalized Linear Model) 등의 연구를 요약하였다. 오염된 지역에 서식하는 해양생물의 바이오마커 반응 측정 및 바이오마커 지수 개발은 다양한 측면의 해양생태계 위해성 평가를 위해 고안된 환경모니터링 프로그램에 공헌할 수 있는 정보를 제공해 줄 수 있을 것이다.

• 대한본초학회지
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• 제30권4호
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• pp.37-44
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• 2015

Objectives : The present study was designed to evaluate the anti-inflammatory and anti-oxidative stress activities through regulation of Nrf2-mediated genes by Rhei rhizoma and Glycyrrhiza rhizoma combined extract (RGE) in reflux esophagitis.Methods : The antioxidant activity of RGE in vitro was measured in terms of radical scavenging capacity such as DPPH and ABTS. RGE was administered at 350 mg/kg body weight prior to induction of reflux esophagitis. Reflux esophagitis was induced that tied the pylorus and the transitional junction between the forestomach and the corpus in Sprague-Dawley rats.Results : RGE scavenged DPPH and ABTS effectively and IC₅₀of RGE each were 4.9 μg/ml and 45.6 μg/ml. Our results show that RGE administration markedly ameliorated mucosal damage upon histological evaluation. In serum and esophagus tissue, RGE significantly suppressed the oxidative stress biomarkers. Reflux esophagitis induced rats exhibited down-regulation of antioxidant-related proteins in the esophagus; however, the levels with treatment of RGE were significantly higher than those of vehicle reflux esophagitis rats. RGE treatment caused significant reductions in activation of NF-κB transcription factor. Thus, RGE significantly exhibited potent anti-inflammatory activities by suppressing the protein expression levels of pro-inflammatory proteins such as COX-2 and iNOS and inflammatory cytokines such as TNF-αin the esophagus tissue.Conclusions : Reflux esophagitis caused considerable levels of oxidative stress in the esophageal mucosa and the administration of RGE reduced the esophageal mucosa damage through the regulation of Nrf2 and NF-κB pathways. Our findings can considered as supplementary therapy in the prevention or treatment of reflux esophagitis.

• 한국어류학회지
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• 제22권1호
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• pp.1-8
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• 2010

고수온 환경 ($25^{\circ}C$와 $30^{\circ}C$)에 노출시킨 넙치의 산화 스트레스 정도를 알아보기 위하여 넙치의 간 조직에서 항산화 효소 [superoxide dismutase (SOD)와 catalase(CAT)] mRNA의 발현량 및 그 활성을 측정한 결과, $20^{\circ}C$ 대조구보다 $25^{\circ}C$와 $30^{\circ}C$ 실험구에서 증가하는 경향을 보였다. 또한 지질 과산화 지표로 사용되는 lipid peroxidation(LPO)을 측정한 결과, $25^{\circ}C$와 $30^{\circ}C$ 실험구에서 증가하는 경향을 나타내었다. LPO의 증가는 SOD 및 CAT의 증가와 밀접한 관련이 있으며, 체내의 $H_O_2$ 농도 또한 $25^{\circ}C$와 $30^{\circ}C$ 실험구에서 증가하는 것으로 보아 고수온 환경이 넙치의 산화 스트레스를 유발하고 있는 것으로 사료된다. 고수온 환경에 노출시킨 넙치의 혈중 alanine aminotransferase (AlaAT)와 aspartate aminotransferase (AspAT) 값을 측정 한 결과, AlaAT와 AspAT 모두 유의적으로 증가하는 경향을 보였다. 또한 면역 지표로 사용되는 lysozyme 활성도가 $20^{\circ}C$ 대조구보다 $30^{\circ}C$ 실험구에서 유의적으로 낮은 값을 나타낸 점으로 보아, 고수온 환경에 노출된 넙치에서는 간 세포의 손상뿐만 아니라 면역력 또한 저해되고 있는 것으로 사료된다. 고수온 환경에 노출시킨 넙치에서 항산화 효소인 SOD와 CAT mRNA 발현량 및 활성이 증가하였을 뿐만 아니라 활성산소와 LPO 값 또한 증가된 점으로 보아, 고수온 환경은 넙치의 체내에서 산화 스트레스를 유발시키는 동시에 면역 기능을 저해시키고 있는 것으로 사료된다.

• Journal of Nutrition and Health
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• 제48권6호
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• pp.468-475
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• 2015

우리나라 일부 건강한 유아를 대상으로 Mn-SOD Val16Ala, GSTP1 Ile105Val, GSTT1 present/null, GSTM1 present/null 유전자 다형성 분포를 살펴본 결과, Mn-SOD Val/Val형, GSTP1 Ile/Ile형, GSTT1 null 형, GSTM1 null 형이 주된 (major) 유전자형인 것으로 나타났다. 이 중 Mn-SOD Val/Val형은 Val/Ala 또는 Ala/Ala형에 비해 소변 8-OHdG 수준이 유의적이지는 않으나 높은 경향을 나타내었고, GSTP1 Ile/Ile형은 Ile/Val 또는 Val/Val형에 비해 소변 8-OHdG 수준이 유의적으로 낮았다. 간접흡연에의 노출 여부와 간접흡연-유전자 다형성의 상호 작용이 산화손상지표에는 유의적인 영향을 미치지 않는 것으로 나타났다. 이상의 결과로 볼 때 건강한 유아에서 GSTP1 Val allele 보유한 경우 산화적 손상에 대해 취약할 수 있음을 제시하며, 추후 대규모 연구를 통한 검증 및 이들 유전자형을 보유한 대상자를 위한 효과적인 영양 중재방안에 대한 고려가 필요할 것으로 사료된다.

• 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 Preventive Medicine and Public Health
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• 제36권4호
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• pp.314-322
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• 2003

Objectives : In this study, the exposure status of the hazardous substances from incinerators, such as polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), were studied , and the relationship between the exposure of these hazardous substances and their heath effects on the workers and residents near municipal solid waste (MSW) incinerators and an industrial incinerator investigated. Methods : Between July 2001 and Jure 2002, 13 workers at two MSW incinerators, 16 residents from the area around the two MSW incinerators, 6 residents from the control area, and further 10 residents near an industrial incinerator, estimated to emit higher levels of hazardous substances, were interviewed. Information, including sociodemographic information, personal habits, and work history, detailed gynecologic and other medical history were collected through interviews. Blood samples were also collected from 45 subjects, and analyzed for PCDD/DFs, by high resolution gas chromatography -high resolution mass spectrometry, using the US EPA 1613 method. In addition to the questionnaire survey, urinary concentrations of 8-hydroxydeoxyguanosine (8-OH-dG) and malondialdehyde (MDA) were measured as oxidative injury biomarkers. The urinary concentrations of 8-OH-dG were determined by in vitro ELISA, and the MDA by HPLC, using u adduct with thiobarbituric acid. Results : The PCDD/DFs concentrations in the residents near the industrial incinerator were higher than those in the controls, workers and residents near the MSW incinerators. The average TEQ (Toxic Equivalencies) concentrations of the PCDD/DFs in residents near the industrial incinerator were 53.4pg I-TEQs/g lipid. The estimated daily intakes were within the tolerable daily intake range (1-4 pg I-TEQ/Kg bw/day) suggested by WHO (1997) in only 30% to the people near the industrial incinerator. Animal studies have already shown that even a low body border of PCDD/DFs, such as 10 ng TEQ/kg bw, can cause oxidative damage in laboratory animals. Our study also showed that the same body burden of PCDD/DFs can cause oxidative damage to humans. Conclusions : The exposures to PCDD/DFs and the oxidative stress of residents near the industrial incinerator, were higher than those in the controls, workers and residents near the MSW incinerators. Proper protection strategies against these hazardous chemicals are needed. Because a lower body burden of PCDD/Fs, such as 10ng TEQ/kg bw, can cause oxidative damage, the tolerable daily intake range should be restrictedly limited to 1pg I-TEQ/kg bw/day.

• Molecules and Cells
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• 제39권1호
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• pp.72-76
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• 2016

Cell death pathways such as apoptosis can be activated in response to oxidative stress, enabling the disposal of damaged cells. In contrast, controlled intracellular redox events are proposed to be a significant event during apoptosis signaling, regardless of the initiating stimulus. In this scenario oxidants act as second messengers, mediating the post-translational modification of specific regulatory proteins. The exact mechanism of this signaling is unclear, but increased understanding offers the potential to promote or inhibit apoptosis through modulating the redox environment of cells. Peroxiredoxins are thiol peroxidases that remove hydroperoxides, and are also emerging as important players in cellular redox signaling. This review discusses the potential role of peroxiredoxins in the regulation of apoptosis, and also their ability to act as biomarkers of redox changes during the initiation and progression of cell death.

• Advances in Traditional Medicine
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• 제5권2호
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• pp.137-143
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• 2005

Doxorubicin induces oxidative stress leading to cardiotoxicity causing electrocardiogram abnormalities and increases in biomarkers associated with toxicity. Green tea extract (GTE) is reported to possess antioxidant activity mainly via its polyphenolic constituent, catechins. This study was intended to determine the effect of various doses of GTE (25, 50 and 100 mg/kg/day p.o. for 30 days) on doxorubicin-induced electrocardiographic and biochemical changes in rat heart. The latter included lactate dehydrogenase, creatine kinase, and glutamic oxaloacetate transaminase in serum and superoxide dismutase, catalase, and reduced glutathione, as well as membrane bound enzymes like $Na^+K^+ATPase,\;Ca^{2+}ATPase,\;Mg^{2+}ATPase$ and decreased lipid peroxidation in heart tissue Results demonstrated that rats which received GTE were less susceptible to such changes indicating protection afforded by GTE.