1-2-5-6-tetrabromocyclooctane and 1-2-dibromo-4-(1-2-dibromoethyl)cyclohexane

Due to the regulation of hexabromocyclododecane (HBCD), much attention has been paid to its potential substitutes, 1,2-dibromo-4-(1,2-dibromoethyl) cyclohexane (DBE-DBCH) and 1,2,5,6-tetrabromocyclooctane (TBCO). DBE-DBCH and TBCO contain several diastereomers and enantiomers, which may exhibit different environmental behaviors and biological effects. In this study, the accumulation and depuration of individual DBE-DBCH and TBCO diastereomers by earthworms (Eisenia fetida) from diastereomer-contaminated soils were evaluated. The accumulation and depuration kinetics of DBE-DBCH and TBCO diastereomers followed one-compartment first-order kinetics. The biota soil accumulation factor (BSAF) of β-DBE-DBCH (2.74 g

Topics: Animals; Cyclohexanes; Cyclooctanes; Flame Retardants; Hydrocarbons, Brominated; Oligochaeta; Soil; Soil Pollutants

With the listing of the of cycloaliphatic brominated flame retardants (CBFR) hexabromocyclododecane (HBCD) as a persistent organic pollutant (POP) by the Stockholm Convention, much attention has been paid to the environmental behaviors and biological effects of HBCD, as well as its potential alternatives, such as 1,2-dibromo-4-(1,2-dibromoethyl) cyclohexane (TBECH) and 1,2,5,6-tetrabromocyclooctane (TBCO). In this study, the neurotoxicity of HBCD, TBECH, and TBCO in human SH-SY5Y cells were compared. The results showed that HBCD, TBECH, and TBCO induced cytotoxicity, including dose-dependent cell viability decreases, cell membrane permeability increases, cytoskeleton development damage, and apoptosis induction, with the cytotoxicity in the order of HBCD > TBCO > TBECH. The expression levels of apoptotic proteins (caspase-3, Bax, caspase-9, Bcl-2, and cytochrome c (Cyt c)) followed the same order, which indicated that mitochondrial apoptotic pathway may be one of the mechanisms responsible for their neurotoxicity. In order to study the mechanisms of cytotoxicity, CBFRs-induced reactive oxygen species (ROS) and the intracellular calcium levels were determined. The ROS levels were significantly elevated for three CBFRs treatment, suggesting that oxidative stress contributes to their cytotoxicity. The intracellular calcium concentrations were significantly enhanced for HBCD and TBCO treatment, but not for TBECH, indicating that in addition to ROS, cytotoxicity of HBCD and TBCO may follow Ca

Topics: Cyclohexanes; Cyclooctanes; Flame Retardants; Humans; Hydrocarbons, Brominated; Neuroblastoma