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

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

Hum Exp Toxicol

Department of Bioenvironmental Medicine, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan.

Published: November 2009

AI Article Synopsis

  • Polybrominated diphenyl ethers (PBDEs) are commonly used flame retardants found in consumer products, but they can accumulate in human tissues, indicating potential exposure for fetuses.
  • This study investigates the impact of PBDEs on human umbilical vein endothelial cells (HUVECs) by analyzing changes in gene expression after exposure to a commercial mixture of PBDEs.
  • The results revealed alterations in genes related to the antioxidant system and tumor suppression, particularly highlighting the significant decrease in the expression of thioredoxin-interacting protein (TXNIP) due to exposure to specific PBDE mixtures.

Article Abstract

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.

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Source
http://dx.doi.org/10.1177/0960327109350669DOI Listing

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