Increase of urinary malondialdehyde level by bisphenol A exposure: a longitudinal panel study

Background To verify oxidative stress as a possible mechanism that establishes a relationship between exposure to bisphenol A (BPA) and adverse health outcomes in the elderly Korean population, we evaluated the relation between visit-to-visit variations in urinary BPA and oxidative stress biomarker. Methods To assess the relation between BPA and urinary malondialdehyde (MDA) as an oxidative stress biomarker, we used a mixed effect model after controlling for age, sex, BMI, drinking status, exercise, urinary cotinine level, PM10 on lag day 2, and mean temperature and dew point on the day. The relation between exposure to BPA and MDA level by sex of participants and polymorphisms of oxidative stress-related genes (COX2, EPHX1, HSP70-hom, PON1, eNOS, CAT, DRD2, SOD2, and MPO) was also evaluated. Results A significant association was found for BPA with MDA in both male and female elderly participants (male, β = 0.19 and p = 0.0003; female, β = 0.18 and p < .0001; and total, β = 0.18 and p < .0001). Furthermore, the association of BPA with MDA was found regardless of any genotype of the nine oxidative stress-related genes. Conclusions The results of our study suggest a strong association of BPA with oxidative stress, not related with sex and oxidative stress-related gene polymorphisms

Computer use at work is associated with self-reported depressive and anxiety disorder

Adjusted OR* of DAD considering the combined effect of computer use and occupational group, education, and job status. (DOC 61 kb

Production of Transgenic Cloned Miniature Pigs with Membrane-bound Human Fas Ligand (FasL) by Somatic Cell Nuclear Transfer

Cell-mediated xenograft rejection, including NK cells and CD8+ CTL, is a major obstacle in successful pig-to-human xenotransplantation. Human CD8+ CTL and NK cells display high cytotoxicity for pig cells, mediated at least in part by the Fas/FasL pathway. To prevent cell-mediated xenocytotoxicity, a membrane-bound form of human FasL (mFasL) was generated as an inhibitor for CTL and NK cell cytotoxicity that could not be cleaved by metalloproteinase to produce putative soluble FasL. We produced two healthy transgenic pigs harboring the mFasL gene via somatic cell nuclear transfer (SCNT). In a cytotoxicity assay using transgenic clonal cell lines and transgenic pig ear cells, the rate of CD8+ CTL-mediated cytotoxicity was significantly reduced in transgenic pig&#x27;s ear cells compared with that in normal minipig fetal fibroblasts. Our data indicate that grafts of transgenic pigs expressing membrane-bound human FasL control the cellular immune response to xenografts, creating a window of opportunity to facilitate xenograft survival

Exposures to Particulate Matter and Polycyclic Aromatic Hydrocarbons and Oxidative Stress in Schoolchildren

BACKGROUND: Air pollution is known to contribute to respiratory and cardiovascular mortality, and morbidity. Oxidative stress has been suggested as one of the main mechanisms for these effects on health. OBJECTIVE: The aim of this study was to analyze the effects of exposure to particulate matter (PM) with aerodynamic diameters &lt;= 10 mu m (PM(10)) and &lt;= 2.5 mu M (PM(2.5)) and polycyclic aromatic hydrocarbons (PAHs) on urinary malondialdehyde (MDA) levels in schoolchildren. METHODS: The study population consisted of 120 schoolchildren. The survey and measurements were conducted in four cities two in China (Ala Shan and Beijing) and two in Korea (Jeju and Seoul) between 4 and 9 June 2007. We measured daily ambient levels of PM and their metal components at the selected schools during the study period. We also measured urinary 1-hydroxypyrene (1-OHP) and 2-naphthol, to assess PAH exposure, and MDA, to assess oxidative stress. Measurements were conducted once a day for 5 consecutive days. We constructed a linear mixed model after adjusting for individual variables to estimate the effects of PM and PAH on oxidative stress. RESULTS: We found statistically significant increases in urinary MDA levels with ambient PM concentrations from the current day to the 2 previous days (p &lt; 0.0001). Urinary 1-OHP level also showed a positive association with urinary MDA level, which was statistically significant with or without PM in the model (p &lt; 0.05). Outdoor PM and urinary 1-OHP were synergistically associated with urinary MDA levels. Some metals bound to PM(10) (aluminum, iron, strontium, magnesium, silicon, arsenic, barium, zinc, copper, and cadmium) and PM(2.5) (magnesium, iron, strontium, arsenic, cadmium, zinc, aluminum, mercury, barium, and copper) also had significant associations with urinary MDA level. CONCLUSION: Exposure to PM air pollution and PAHs was associated with oxidative stress in schoolchildren.Environmental SciencesPublic, Environmental &amp; Occupational HealthToxicologySCI(E)40ARTICLE4579-58311

Associations of air pollution exposure with blood pressure and heart rate variability are modified by oxidative stress genes: A repeated-measures panel among elderly urban residents

Background Oxidative stress has been suggested as a major cause of elevated blood pressure (BP) and reduced heart rate variability (HRV) due to air pollution. We hypothesized that the associations of air pollution exposure with BP and HRV are modified by oxidative stress gene polymorphisms. Methods Between 2008 and 2010, we conducted up to 5 surveys of 547 elderly participants, measured their BP and HRV, and genotyped 47 single nucleotide polymorphisms (SNPs) in 18 oxidative stress genes. Linear mixed models were constructed to evaluate the associations of particulate matter ≤10 μm, nitrogen dioxide, and sulfur dioxide with BP and HRV, as well as the modifications of these associations by the genotyped SNPs. Results Single-SNP analyses revealed interactions between air pollution and 15 SNPs (for BP) and 33 SNPs (for HRV) (all, P for interaction < 0.05). When we generated genetic risk scores for BP and HRV, using the SNPs with interactions in the single-SNP models, we found that associations of air pollution exposure with BP and HRV were modified by the genetic risk scores (P for interaction < 0.05). Conclusions These results strongly suggest that the associations of air pollution with BP and HRV are mediated by oxidative stress pathways