Ns (IC50 171 M and 168 M, respectively). TDCPP inhibited protein synthesis and
Ns (IC50 171 M and 168 M, respectively). TDCPP inhibited protein synthesis and caused cell cycle arrest, but only at higher concentrations. Also, the antioxidant N-acetylcysteine (NAC) reduced cell toxicity in cells treated with TDCPP, suggesting that exposure to TDCPP enhanced oxidative tension within the cells. In summary, these data show that low concentrations of TDCPP result in cytostasis within a Alkaline Phosphatase/ALPL Protein Synonyms kidney cell line, whereas higher concentrations induce cell toxicity. Additionally, TDCPP toxicity might be attenuated by NAC, suggesting that antioxidants could be efficient countermeasures to some organohalogen exposures.1. INTRODUCTION Flame retardants are a diverse group of chemical substances which can be developed to slow or avoid the spread of fire. These compounds are added into quite a few household items, but could be gradually released in to the environment because the products age, or a lot more rapidly when the products are damaged by flood or fire. The halogenated phosphate triester tris(1,3dichloro propyl) phosphate (TDCPP) is often a high volume additive flame retardant with main application in polyurethane foams, resins, plastics, textile coatings, and rubber [1]. Actually, TDCPP along with other flame retardants can comprise as considerably as 5 in the total weight in foam solutions [1]. A recent study located TDCPP in dust from 96 of US households at 2 ppm, with some as high as 50 ppm [2]. In addition, research monitoring TDCPP levels in people today have found detectable to alarming levels of TDCPP in breast milk, adipose tissue, semen and urine [3]. Consequently, much more research are needed to understand the dangers and consequences of exposure to TDCPP and other organohalogens. Although the environmental penetrance of TDCPP is widespread, the compound frequently is regarded to possess low toxicity byregulatory agencies, which includes the Environmental Protection Agency, International Agency for Analysis on Cancer, or National Toxicology System [9]. California’s Proposition 65 does list TDCPP as a possible carcinogen, but the No Substantial Risk Level (NSRL) is listed as 5.4 g/ day as a “safe harbor value” for market [10]. In contrast, reports in animal models have shown that TDCPP can disrupt improvement, reproduction, and endocrine functions, as well as escalating risk for some kinds of cancers [11,12]. The mechanisms of TDCPP actions are mammalian and some mammalian systems [136]. To study TDCPP toxicity, the usage of a cell culture model is effective due to the degree of handle for dose, duration, and target varieties. Many research of TDCPP toxicity have been reported from culture model systems, but only several of those MFAP4 Protein Gene ID employed human cells [171]. From the human cell research, only Ren and colleagues utilized cells that were derived from the kidney, despite the fact that they had been applied primarily as a transfection method to test organohalogens on thyroid hormone receptor (TR) signaling. The lack of reports with kidney cells is surprising because the kidney is actually a essential target for organohalogen toxicity because of the accumulation of chemical compounds before excretion. Moreover, research in animal have specificallyAbbreviations: 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(2,3dibromopropyl)phosphate; TR, thyroid hormone receptor Correspo.
