Microbial dysbiosis induced in Cyprinus carpio by tetrabromobisphenol A exposure: Mediation through gut barrier impairment and oxidative stress.

Tetrabromobisphenol A (TBBPA) is a high-production chemical widely used in printed circuit boards and other polymeric materials for inflaming. As an environmental pollutant, it is widely found in various abiotic and biological media. Usually, the TBBPA could enter the body through skin contact, respiratory exposure and the dietary intake, among which respiratory exposure may be a most important exposure route. Previous studies reported that TBBPA possesses the endocrine, liver and kidney toxicity. However, few studies focused on the effects of TBBPA on respiratory toxicity. Therefore, it is urgent to study the toxic effects of TBBPA on respiratory system. In this study, human bronchial cells Beas2B and pulmonary epithelial cells 16HBE were used as subjects to study the exposure toxicity of TBBPA. Firstly, the viability and permeability of cells were assayed during the TBBPA exposure process. When TBBPA was in low concentration range (0−0.4 μmol/L), 24 h of exposure cannot significantly affect cell viability. When concentration of TBBPA was greater than 10 μmol/L, the inhibitory effect on cell activity was obviously observed. When concentration of TBBPA was up to 50 μmol/L, the cell viabilities of 16HBE and Beas2B cells decreased to 80.9% and 86.2%. It is worth noting that, as compared with bronchial epithelial cell 16HBE, lung epithelial cell Beas2B has a higher tolerance to TBBPA, which may be due to the different cell structures. In addition, the oxidation stress of cells was also determined by assaying the cell intracellular reactive oxygen species (ROSs), antioxidant enzymatic activity of superoxide dismutase (SOD) and catalase (CAT) during the whole expose duration. The results showed that the levels of intracellular ROSs obviously increased in both cells, indicating that peroxidation occurred in the cells during TBBPA exposure. Correspondingly, the enzymatic activities of SOD and CAT also increased, indicating that oxidative stress happened in cells. After that, flow cytometry was applied to analyze cell apoptosis. The results showed that partial apoptosis occurred after 24 h of TBBPA exposure, indicating that TBBPA could induce cell apoptosis. Besides, with the increase of exposure concentration, the apoptosis rate of the two kinds of cells also increased. Furthermore, the q-PCR was used to determine the apoptosis-related gene expression. The results revealed that the expression levels of apoptosis-related genes p53, Survivin , bax , bcl-2 , caspase-3 , caspase-9 were all up-regulated to different degrees, further confirming that cells were apoptotic caused by TBBPA. Further, compared with the 12-h exposure data, 24-h exposure would stimulate more intense expression up-regulation. In all, this research mainly investigated the toxicity of typical generation bromide flame retardants TBBPA on human bronchial epithelial cells 16 HBE and lung epithelial cells Beas2B. Results showed that the exposure of TBBPA could cause damage to cell viability and elicit oxidative stress in cells, which could further induce cell apoptosis. The results of cytotoxicity related to human respiratory system in this work can provide a scientific basis for revealing the health risk of toxic organic pollutants to human respiratory system.

Tetrabromobisphenol A (TBBPA) is a flame retardant that can contaminate the environment and human being, acting as an endocrine disruptor. Several studies propose a correlation between TBBPA exposure and adverse health outcomes, however, at vascular level TBBPA effects are still poorly understood. Thus, considering that the vascular tonus is regulated by vasoactive substances (serotonin and histamine) which are involved in some pathological processes, this work aimed to analyse the direct effects and the 24 h exposure of TBBPA on the human umbilical artery (HUA) and to investigate its signalling pathway. Using organ bath technique, endothelium-denuded HUA rings were contracted with serotonin (5-HT, 1 μM), histamine (His, 10 μM) and potassium chloride (KCl, 60 mM), and the exposure (0–24 h) of different concentrations of TBBPA (1, 10 and 50 μM) were evaluated. Besides, the vascular mode of action of TBBPA was studied through the analysis of cyclic guanosine monophosphate and calcium channels activity, pathways involved in relaxation and contraction of HUA, respectively. Our results demonstrated that the direct effects of TBBPA induce a vasorelaxation of HUA. The maximum relaxant effect was observed at 100 μM of TBBPA with 63.74%, 64.24% and 30.05%, for 5-HT-, His- or KCl-contracted arteries respectively. The 24 h TBBPA exposure altered the vasorelaxant response pattern of sodium nitroprusside and nifedipine. This effect is due to the involvement of TBBPA with the NO/sGC/cGMP/PKG pathway and the interference in calcium influx. Furthermore, using the real-time quantitative polymerase chain reaction, TBBPA clearly modulates L-type calcium and large-conductance Ca2+ 1.1 α- and β1 -subunit channels, and soluble guanylyl cyclase and protein Kinase G. So, at vascular level TBBPA induces changes in HUA after TBBPA exposure.

TBBPA caused multiple intestinal injuries via ROS/NF-κB signal in common carp

Aim: This study investigated hexabromocyclododecane (HBCDD) and tetrabromobisphenol A (TBBPA) concentrations in indoor dust from houses, offices, and cars and estimated toddler and adult exposure to HBCDD and TBBPA through dust ingestion. Methods: The concentrations of HBCDD and TBBPA were measured in 47 indoor dust samples collected from the Bangkok metropolitan area, Thailand. All samples were analyzed for HBCDD and TBBPA using LC-MS/MS. The estimated daily intake (EDI) through dust ingestion was calculated from the median and 95th percentile concentrations of HBCDD and TBBPA. Results: HBCDD was detected in 47% of samples, and TBBPA was detected in all samples. The median concentrations of HBCDD were 6.7 ng g-1, <0.7 ng g-1, and <0.7 ng g-1 in cars, houses, and offices, respectively. The isomer composition of ∑HBCDD in dust was: α-HBCDD (40%-54%), γ-HBCDD (19%-40%), and β-HBCDD (17%-28%). In contrast, TBBPA was observed at higher concentrations, with median values of 674, 67, and 22 ng g-1 in offices, houses, and cars, respectively. Under a median exposure scenario, toddlers were exposed to 0.05 ng kg-1 bw day-1 for HBCDD and 0.25 ng kg-1 bw day-1 for TBBPA, with adults exposed to 0.01 and 0.06 ng kg-1 bw day-1 for HBCDD and TBBPA respectively. Conclusion: Concentrations of HBCDD in dust from Thai cars, homes, and offices are lower than those of TBBPA following the listing of HBCDD in the Stockholm Convention on Persistent Organic Pollutants and limited use of HBCDD in Thailand in applications such as building insulation foam. Concentrations of TBBPA in office dust significantly exceeded (P < 0.05) those in house and car dust owing to the greater number of electronic appliances and poor natural ventilation in offices. EDIs for Thai toddlers exceeded those of adults under both median and high-end exposure scenarios. However, EDIs of HBCDD and TBBPA for the general Thai population were below the corresponding oral reference dose guidelines.

Breast adipose metabolites mediates the association of tetrabromobisphenol a with breast cancer: A case-control study in Chinese population

Toxicological evaluation of TBBPA by common carp (Cyprinus carpio) about the in vivo/vitro disturbance of the AHR pathway

Bioaccumulation and physiological effects of tetrabromobisphenol A in coontail Ceratophyllum demersum L.

Tetrabromobisphenol A reduces male rats reproductive organ coefficients and disrupting sexual hormone by causing oxidative stress

TBBPA exposure during a sensitive developmental window produces neurobehavioral changes in larval zebrafish

Toxicological assessment and underlying mechanisms of tetrabromobisphenol A exposure on the soil nematode Caenorhabditis elegans.

TBBPA and lead co-exposure induces grass carp liver cells apoptosis via ROS/JAK2/STAT3 signaling axis

Embryonic exposure to tetrabromobisphenol A and its metabolites, bisphenol A and tetrabromobisphenol A dimethyl ether disrupts normal zebrafish ( Danio rerio) development and matrix metalloproteinase expression

Ecotoxicity of Caenorhabditis elegans following a step and repeated chronic exposure to tetrabromobisphenol A

Photoaging enhances combined toxicity of microplastics and tetrabromobisphenol A by inducing intestinal damage and oxidative stress in Caenorhabditis elegans

We studied the tetrabromobisphenol A (TBBPA) and bisphenol A (BPA) patterns and their sources and transport in different land-use soils from Longtang, South China, a typical electronic waste recycling center. We also studied the reductive debromination of TBBPA in paddy soils. TBBPA and BPA concentrations (on a dry weight basis) were undetected-220 and 0.50-325ng/g, respectively, and both increased, by similar factors, in the following order: pond sediments < paddy soils = vegetable soils < wasteland < dismantling sites < former open burning sites. BPA concentrations were higher than TBBPA concentrations in all six land-use soils, and they correlated significantly. TBBPA and BPA were transported through the soil profiles, being found at relatively high concentrations in soil 0-40cm deep, but only at low concentrations in soil 40-80cm deep. The surface soil concentrations appear to have been strongly affected by crude recycling activities, and former open burning and dismantling sites were the main point sources. The areas surrounding the open burning sites and dismantling sites have been contaminated not only by the dumping of waste residues but also by fly ash deposition, even though the agricultural soils are far from the point pollution sources. Some BPA in the soils is likely to be the reductive debromination product of TBBPA because the long rainy season promotes TBBPA transformation and because BPA can persist for a long time. Incubation experiments confirmed that TBBPA could be transformed into BPA and that BPA could accumulate in waterlogged paddy soils, and this may be why BPA concentrations were higher than TBBPA concentrations in the Longtang area.