Dietary β-Carotine to Reduce Lipid Peroxidation Induced by PAH Exposure of Pregnant Women

Abstract

ISEE-885 Objective: Prenatal exposure to oxidative stress may explain the adverse pregnancy outcomes and fetal origin of adult disease. The purpose of this study was to investigate the association between the exposure to polycyclic aromatic hydrocarbons (PAHs) and oxidative stress for pregnant women and the modification effect by nutritional factors. Material and Methods: A total of 519 pregnant women who had lived in Seoul, Cheonan and Ulsan, Korea were enrolled from July 2006 through January 2007. We measured urinary 2-naphthol concentrations to represent exposure to PAH and analyzed biomarkers such as urinary Malondialdehyde (MDA) and serum total reactive oxygen species (total ROS) for measurement of oxidative stress. Dietary intake was calculated using 24 hours recall. Other individual characteristics such as exercise, smoking, and alcohol consumption were obtained by a questionnaire completed at the beginning of the study. Results: Mean urinary concentrations of 2-naphthol, MDA, and serum total ROS were 13.41 ± 15.52 mmol/mol creatinine, 2.39 ± 1.86 μmol/g creatinine, and 197.77 ± 64.53 mmol respectively. Urinary concentrations of 2-naphthol were significantly associated with urinary MDA levels (P = 0.002), but not with total ROS concentrations (P = 0.097). Urinary 2-naphthol concentrations remained to be significantly associated with urinary MDA levels after adjusting for age, height, weight, urinary cotinine level, and alcohol consumption. We searched for nutritional factors affecting the relationship and found β-carotine uptake significantly decreases urinary MDA levels associated with urinary 2-naphthol concentrations. Conclusions: Polycyclic aromatic hydrocarbons (PAHs) are important carcinogens which are found in cigarette smoking, coke oven emissions, and diesel exhaust. These results suggest that exposure to PAH affects lipid peroxidation for pregnant women and dietary β-carotine uptake decreases the lipid peroxidation caused by PAH exposure.