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Polybrominated diphenyl ethers cause oxidative stress in human umbilical vein endothelial cells

Department of Bioenvironmental Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan, Department of Maternity Nursing, Chiba Prefectural University of Health Sciences, Chiba, Japan

Hideki Fukata

Department of Bioenvironmental Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan, Center for Preventive Medical Science, Chiba University, Chiba, Japan

Koji Sato

Department of Public Health, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata, Japan

Hiroyuki Aburatani

Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan

Hidetaka Takigami

Research Center for Material Cycles and Waste Management, National Institute for Environmental Studies, Ibaraki, Japan

Chisato Mori

Department of Bioenvironmental Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan, Center for Preventive Medical Science, Chiba University, Chiba, Japan, Center for Environment, Health and Field Science, Chiba University, Chiba, Japan, cmori{at}faculty.chiba-u.jp

Polybrominated diphenyl ethers (PBDEs) are used as flame retardants to prevent combustion in consumer products, such as electronics, construction materials, and textiles and, therefore, have become important commercial substances. PBDEs were also detected in maternal blood, breast milk, umbilical cord blood, and cord tissue, thereby indicating that fetuses were also exposed to PBDEs. The purpose of this study is to identify the effect of PBDEs on human umbilical vein endothelial cells (HUVECs). Cultured HUVECs were exposed to a commercial mixture of penta-BDE (DE71), octa-BDE (DE79), and deca-BDE (DE83). Each gene expression that was altered in DNA microarray was confirmed by real-time reverse transcription—polymerase chain reaction and Western blotting analysis. The results indicated that gene expressions concerning antioxidant system, i.e., thioredoxin family, 24-dehydrocholesterol reductase (DHCR24), and tumor suppressor protein p53, were altered by PBDEs exposure in HUVECs. Moreover, it was demonstrated that thioredoxin-interacting protein (TXNIP) was a target gene in exposure to DE71 and DE79 in HUVECs, by drastically decreasing time-dependent TXNIP expression in HUVECs.

Key Words: polybrominated diphenyl ethers (PBDEs) • human umbilical vein endothelial cells (HUVECs) • thioredoxin-interacting protein (TXNIP) • fetal exposure

This version was published on November 1, 2009

Human & Experimental Toxicology, Vol. 28, No. 11, 703-713 (2009)
DOI: 10.1177/0960327109350669


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