Tetrabromobisphenol A induces cellular damages in pancreatic β-cells in vitro. Issue 7 (7th June 2017)

• Record Type: Journal Article
• Authors: Suh, Kwang Sik; Choi, Eun Mi; Rhee, Sang Youl; Oh, Seungjoon; Kim, Sung Woon; Pak, Youngmi Kim; Choe, Wonchae; Ha, Joohun; Chon, Suk
• Is Part Of: Journal of environmental science and health. Volume 52:Issue 7(2017)
• Page Start: 624
• Page End: 631
• Publication Date: 2017-06-07
• Subjects: Mitochondrial function -- tetrabromobisphenol A -- pancreatic β-cell-derived RIN-m5F cells; Environmental engineering -- Periodicals; Environmental sciences -- Periodicals; Ecology -- periodicals; Hazardous Substances -- periodicals; 628
• DOI: 10.1080/10934529.2017.1294964
• Languages: English
• ISSNs: 1093-4529

Abstract

ABSTRACT: Tetrabromobisphenol A (TBBPA) is a well-known organobrominated flame retardant. TBBPA has been detected in the environment. The roles played by environmental pollutants in increasing the prevalence of metabolic syndrome are attracting increasing concern. In the present work, we investigated the effects of TBBPA on rat pancreatic β-cells (the RIN-m5F cell line). RIN-m5F cells were incubated with different concentrations of TBBPA for 48 h, and cell viability and the extent of apoptosis were determined. We also measured the levels of inflammatory cytokines, reactive oxygen species (ROS), mitochondrial adenosine triphosphate (ATP), and cardiolipin, as well as the extent of cytochrome c release from mitochondria. TBBPA reduced the ATP level, induced cardiolipin peroxidation and cytochrome c release, and triggered apoptotic cell death. Moreover, TBBPA increased the levels of inflammatory cytokines (TNF-α and IL-1β), nitric oxide, intracellular ROS, and mitochondrial superoxide. Together, our results indicate that TBBPA damages pancreatic β-cells by triggering mitochondrial dysfunction and inducing apoptosis.