Flame retardant tris(1, 3-dichloro-2-propyl)phosphate (TDCPP) toxicity is attenuated by N-acetylcysteine in human kidney cells. (2017)

• Record Type: Journal Article
• Authors: Killilea, David W.; Chow, Darryl; Xiao, Sheng Qi; Li, Charles; Stoller, Marshall L.
• Is Part Of: Toxicology reports. Volume 4(2017)
• Page Start: 260
• Page End: 264
• Publication Date: 2017
• Subjects: Tris(1, 3-dichloro-2-propyl)phosphate (PubChem CID: 26177) -- N-acetylcysteine (PubChem CID: 12035); ATSDR Agency for Toxic Substances and Disease Registry -- DMEM Dulbecco's Modified Eagle Medium -- DMSO dimethyl sulfoxide -- EDTA ethylenediamine tetraacetic acid -- FBS fetal bovine serum -- NAC N-acetylcysteine -- SFFCPF San Francisco Firefighters Cancer Prevention Foundation -- TDCPP tris(1, 3-dichloro-2-propyl)phosphate -- Tris tris(2, 3-dibromopropyl)phosphate -- TR thyroid hormone receptor; flame retardant -- cytostasis -- cell toxicity -- antioxidant -- cell cycle; Toxicology -- Periodicals; Clinical toxicology -- Periodicals; Drug-Related Side Effects and Adverse Reactions; Hazardous Substances; Poisoning; Toxicology; Electronic journals; Periodicals; Periodicals; 571.9505
• DOI: 10.1016/j.toxrep.2017.05.003
• Languages: English
• ISSNs: 2214-7500

Abstract

Graphical abstract: Highlights: The toxicity of the flame retardant TDCPP was studied in a human kidney cell type. TDCPP was cytostatic at low micromolar concentrations, and toxic at high micromolar. N -acetylcysteine attenuated TDCPP toxicity, suggesting a role for oxidative stress. Abstract: Prolonged exposure to the flame retardants found in many household products and building materials is associated with adverse developmental, reproductive, and carcinogenic consequences. While these compounds have been studied in numerous epidemiological and animal models, less is known about the effects of flame retardant exposure on cell function. This study evaluated the toxicity of the commonly used fire retardant tris(1, 3-dichloro-2-propyl)phosphate (TDCPP) in cell line derived from the kidney, a major tissue target of organohalogen toxicity. TDCPP inhibited cell growth at lower concentrations (IC50 27 μM), while cell viability and toxicity were affected at higher concentrations (IC50 171 μM and 168 μM, respectively). TDCPP inhibited protein synthesis and caused cell cycle arrest, but only at higher concentrations. Additionally, the antioxidant N -acetylcysteine (NAC) reduced cell toxicity in cells treated with TDCPP, suggesting that exposure to TDCPP increased oxidative stress in the cells. In summary, these data show that low concentrations of TDCPP result in cytostasis in a kidney cell line, whereas higher concentrations induce cell toxicity. Furthermore, TDCPP toxicity can be attenuated by NAC, suggesting that antioxidants may be effective countermeasures to some organohalogen exposures.