Journal of Preventive Medicine and Public Health

Original Articles

The Association Between Oxidative Stress and Depressive Symptom Scores in Elderly Population: A Repeated Panel Study: Changwoo Han, Youn-Hee Lim, Yun-Chul Hong; J Prev Med Public Health. 2016;49(5):260-274. Published online August 23, 2016; DOI: https://doi.org/10.3961/jpmph.16.029

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Objectives
Previous epidemiological studies about oxidative stress and depression are limited by hospital-based case-control design, single-time measurements of oxidative stress biomarkers, and the small number of study participants. Therefore, in this study, we analyzed the association between biomarker of oxidative stress and depressive symptom scores using repeatedly measured panel data from a community-dwelling elderly population.
Methods
From 2008 to 2010, a total of 478 elderly participants residing in Seoul, Korea, were evaluated three times. Participants underwent the Korean version of the Short Form Generic Depression Scale (SGDS-K) test for screening depression, and urinary malondialdehyde (MDA) levels were measured as an oxidative stress biomarker. We used a generalized estimating equation with a compound symmetry covariance structure to estimate the effects of oxidative stress on depressive symptom scores.
Results
A two-fold increase in urinary MDA concentration was significantly associated with a 33.88% (95% confidence interval [CI], 21.59% to 47.42%) increase in total SGDS-K scores. In subgroup analyses by gender, a two-fold increase in urinary MDA concentration was significantly associated with increased SGDS-K scores in both men and women (men: 30.88%; 95% CI, 10.24% to 55.37%; women: 34.77%; 95% CI, 20.09% to 51.25%). In bivariate analysis after an SGDS-K score ≥8 was defined as depression, the third and the fourth urinary MDA quartiles showed a significantly increased odds ratio(OR) of depression compared to the lowest urinary MDA quartile (third quartile OR, 6.51; 95% CI, 1.77 to 24.00; fourth quartile OR, 7.11; 95% CI, 1.99 to 25.42).
Conclusions
Our study suggests a significant association between oxidative stress and depressive symptoms in the elderly population.

Summary

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Placental Superoxide Dismutase, Genetic Polymorphism, and Neonatal Birth Weight.: Yun Chul Hong, Kwan Hee Lee, Moon Whan Im, Young Ju Kim, Eun Hee Ha; J Prev Med Public Health. 2004;37(4):306-311. Published online November 30, 2004

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Abstract PDF: BACKGROUND
The roles of antioxidants in the placenta and genetic susceptibility to oxidant chemicals in relation to neonatal birth weight have not been elucidated. We determined whether the level of placental manganese superoxide dismutase (MnSOD) and its genetic polymorphism plays any role in oxidative stress and neonatal birth weight. METHODS: We measured placental MnSOD and determined MnSOD genetic polymorphism among 108 pregnant women who were hospitalized for delivery and their singleton live births in Korea. Main outcome measurements are maternal urinary malondialdehyde (MDA) and birth weight. RESULTS: Maternal urinary concentrations of MDA were significantly associated with neonatal birth weight (P=0.04). The enzyme level of placental MnSOD was also significantly associated with MDA concentration (P=0.04) and neonatal birth weight (P< 0.01). We observed dose-response relationships between placental MnSOD and maternal urinary MDA, and neonatal birth weight after adjusting for maternal weight, height, age, and neonatal sex. After controlling for covariates, MnSOD variant genotype increased maternal urinary MDA concentrations (P< 0.01) and reduced birth weight by 149 gm (P=0.08). CONCLUSIONS: This study demonstrates that the placental level of MnSOD during pregnancy significantly affects fetal growth by reducing oxidative stress, and that genetic polymorphism of MnSOD probably modulate the effects of oxidants on fetal growth.; Summary

Review

Gene-Diet Interaction on Cancer Risk in Epidemiological Studies.: Sang Ah Lee; J Prev Med Public Health. 2009;42(6):360-370.; DOI: https://doi.org/10.3961/jpmph.2009.42.6.360

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Abstract PDF

Genetic factors clearly play a role in carcinogenesis, but migrant studies provide unequivocal evidence that environmental factors are critical in defining cancer risk. Therefore, one may expect that the lower availability of substrate for biochemical reactions leads to more genetic changes in enzyme function; for example, most studies have indicated the variant MTHFR genotype 677TT is related to biomarkers, such as homocysteine concentrations or global DNA methylation particularly in a low folate diet. The modification of a phenotype related to a genotype, particularly by dietary habits, could support the notion that some of inconsistencies in findings from molecular epidemiologic studies could be due to differences in the populations studied and unaccounted underlying characteristics mediating the relationship between genetic polymorphisms and the actual phenotypes. Given the evidence that diet can modify cancer risk, gene-diet interactions in cancer etiology would be anticipated. However, much of the evidence in this area comes from observational epidemiology, which limits the causal inference. Thus, the investigation of these interactions is essential to gain a full understanding of the impact of genetic variation on health outcomes. This report reviews current approaches to gene-diet interactions in epidemiological studies. Characteristics of gene and dietary factors are divided into four categories: one carbon metabolism-related gene polymorphisms and dietary factors including folate, vitamin B group and methionines; oxidative stress-related gene polymorphisms and antioxidant nutrients including vegetable and fruit intake; carcinogen-metabolizing gene polymorphisms and meat intake including heterocyclic amins and polycyclic aromatic hydrocarbon; and other gene-diet interactive effect on cancer.

Summary

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Evaluation Studies

Stability and Intra-Individual Variation of Urinary Malondialdehyde and 2-Naphthol.: Kyoung Ho Lee, Daehee Kang; J Prev Med Public Health. 2008;41(3):195-199.; DOI: https://doi.org/10.3961/jpmph.2008.41.3.195

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Abstract PDF

OBJECTIVES
Malondialdehyde (MDA), a lipid peroxidation by-product, has been widely used as an indicator of oxidative stress. Urinary 2-naphthol, a urinary PAH metabolite, is used as a marker of ambient particulate exposure and is associated with lung cancer and chronic obstructive pulmonary disease. However, the stability and intra-individual variation associated with urinary MDA and 2-naphthol have not been thoroughly addressed. The objective of this study was to assess the stability and intraindividual variation associated with urinary MDA and 2-naphthol. METHODS: Urine samples were collected from 10 healthy volunteers (mean age 34, range 27~42 years old). Each sample was divided into three aliquots and stored under three different conditions. The levels of urinary MDA and 2-naphthol were analyzed 1) just after sampling, 2) after storage at room temperature (21degrees C) for 16 hours, and 3) after storage in a -20degrees C freezer for 16 hours. In addition, an epidemiological study was conducted in 44 Chinese subjects over a period of 3 weeks. The urinary MDA and 2-naphthol were measured by HPLC three times. RESULTS: There was no difference in the levels of urinary MDA and 2-naphthol between the triplicate measurements (n=10, p=0.84 and p=0.83, respectively). The intra-class correlation coefficients (ICC) for urinary MDA and 2-naphthol were 0.74 and 0.42, respectively. However, the levels of PM2.5 in the air were well correlated with the levels of both MDA and 2-naphthol in the epidemiological study. CONCLUSIONS: These results suggest that urinary MDA and 2-naphthol remain stable under variable storage conditions, even at room temperature for 16 hours, and indicate that these markers can be used in epidemiological studies involving various sample storage conditions. The intra-CC of urinary 2-naphthol and MDA were acceptable for application to epidemiological studies.

Summary

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Phong K. Thai, Andrew P.W. Banks, Leisa-Maree L. Toms, Phil M. Choi, Xianyu Wang, Peter Hobson, Jochen F. Mueller
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English Abstract

Associations of Non Alcoholic Fatty Liver with the Metabolic Syndrome and Serum Carotenoids.: Sun kyun Park, Hyun Jung Lee, Duk Hee Lee, Sung Kook Lee, Byung Yeol Chun, Sung Ae Kim, Hye Sung Lee, Hyo Kyung Son, Sung Hi Kim; J Prev Med Public Health. 2008;41(1):39-44.; DOI: https://doi.org/10.3961/jpmph.2008.41.1.39

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Abstract PDF

OBJECTIVES
This study was conducted to investigate the associations of non alcoholic fatty liver with metabolic syndrome and the serum carotenoids. METHODS: This study was conducted in a general hospital in South Korea from November, 2004 to August, 2005. The study subjects were 350 sampled persons who were aged from 40 years and older (males: 180, females: 170). They were grouped into the normal, mild and severe groups according to fat accumulation in their livers, as determined by ultrasonography. We analyzed the association between non alcoholic fatty liver and metabolic syndrome by multiple logistic regression analysis and we analyzed the association between non alcoholic fatty liver and the serum carotenoids by a general linear model(ANCOVA). RESULTS: After adjustment for the effect of potential covariates, the prevalence of metabolic syndrome was associated with fat accumulation in the liver (p trend <0.001). If the odds ratio of normal group is 1.00, then that of the mild group is 2.80 (95% C.I=1.17-6.71) and that of the severe group is 7.29 (95% C.I=2.76-19.30). The prevalence of metabolic alterations fitting the criteria of metabolic syndrome, according to the class of fat accumulation in the liver, was significantly increased, except for criteria of high blood pressure, a large waist circumference and low HDL (high density lipoprotein) cholesterol level (p trend <0.001). The level of serum beta-carotene was decreased according to the class of fat accumulation in the liver (p trend=0.036), but the levels of serum alpha-carotene, lycopene, bata-cryptoxanthin and lutein were not decreased. CONCLSIONS: This study shows that non alcoholic fatty liver was associated with metabolic syndrome and with the serum beta-carotene level.

Summary

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In Vitro

Exposure Assessment of PCDD/Fs and Monitoring of Health Effects on Workers and Residents near the Waste Incinerators in Korea.: Jong Han Leem, Yun Chul Hong, Kwan Hee Lee, Ho Jang Kwon, Jae Yeon Jang; Korean J Prev Med. 2003;36(4):314-322.

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Abstract PDF: 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 June 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 an 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 burden of PCDD/DFs, such as 10ng 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.; Summary

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