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TCBPA
ENVIRONMENTAL POLLUTION · 2022 · IF 9.988

TBBPA and its alternative TCBPA induced ROS-dependent mitochondria-mediated apoptosis in the liver of Rana nigromaculata

Xiuying Jia,Ruopeng Yan,Huikang Lin,Zhiquan Liu,Lilai Shen,Hongmei Yang,Haoying Wu,Xiaodong Shan,Hangjun Zhang

Tetrabromobisphenol A (TBBPA), which is the most widely employed brominated flame retardant , and its alternative tetrachlorobisphenol A (TCBPA) are widely distributed in aquatic environments. In the present study, the hepatotoxicity induced by TBBPA and TCBPA was investigated in Rana nigromaculata , and the potential mechanisms were investigated with a particular focus on ROS (reactive oxygen species) -dependent mitochondria-mediated apoptosis. Healthy adult frogs were exposed to 0, 0.001, 0.01, 0.1, and 1 mg/L waterborne TBBPA and TCBPA for 14 days. The results showed that liver weight was significantly increased by 51.52%–98.99% in the 0.01, 0.1, and 1 mg/L TBBPA and TCBPA groups relative to the control. Histological examination revealed that the structure of the liver, to some extent, was influenced by TBBPA and TCBPA with nuclear shrinkage and mitochondrial swelling. Meanwhile, TBBPA and TCBPA have significantly increased the alanine transaminase level in serum and the content of ROS, while inhibiting the activity of superoxide dismutase in the liver. In addition, DNA fragments were observed in the TBBPA and TCBPA groups relative to the control. Expression of Cytochrome C was significantly increased by 1.13-, 1.38-, 1.60-, and 2.46-fold in 0.001, 0.01, 0.1, and 1 mg/L TBBPA, and by 1.26-, 1.51-, 2.14-, and 2.98- fold in 0.001, 0.01, 0.1, and 1 mg/L TCBPA, respectively, which indicated that TCBPA may be more toxic than TBBPA. Similarly, the ratio of Bax/Bcl-2 was increased in a dose-dependent manner. These results indicated that apoptosis in the ROS-dependent mitochondrial pathway mediates hepatotoxicity caused by TBBPA and TCBPA. The present study will facilitate an understanding of the toxicity mechanism of flame retardants.

CAS / MDL: 67-68-5 79-94-7
研究领域: 环境毒理学 · 水生生物学 · 分子生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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ENVIRONMENTAL POLLUTION · 2018 · IF 4.358

Differences in reproductive toxicity of TBBPA and TCBPA exposure in male Rana nigromaculata

Hangjun Zhang,Wenli Liu,Bin Chen,Jianbo He,Feifei Chen,Xiaodong Shan,Qiongxia Du,Ning Li,Xiuying Jia,Juan Tang

Tetrabromobisphenol A (TBBPA) and tetrachlorobisphenol A (TCBPA) are persistent toxic environmental pollutants that cause severe reproductive toxicity in animals. The goal of this study was to compare the reproductive toxic effects of TBBPA and TCBPA on male Rana nigromaculata and to expound on the mechanisms leading to these effects. Healthy adult frogs were exposed to 0, 0.001, 0.01, 0.1, and 1 mg/L of TBBPA and TCBPA for 14 days. Sperm numbers were counted by erythrometry. Sperm mobility and deformities were observed under a light microscope (400 × ). We used commercial ELISA kits to determine the serum content of testosterone (T), estradiol (E2), luteinizing hormone (LH) and follicle stimulating hormone (FSH). Expression of androgen receptor (AR) mRNA was detected using real-time qPCR. Sperm numbers and sperm mobility were significantly decreased and sperm deformity was significantly increased in a concentration dependent manner following exposure to TBBPA and TCBPA. Sperm deformity was significantly greater in the 1 mg/L TCBPA (0.549) treatment group than in the 1 mg/L TBBPA (0.397) treatment group. Serum T content was significantly greater in the 0.01, 0.1 and 1 mg/L TBBPA and TCBPA experimental groups compared with controls, while E2 content was significantly greater in only the 1 mg/L TBBPA and TCBPA experimental groups. Expression levels of LH and FSH significantly decreased in the 1 mg/L TBBPA and TCBPA treatment groups. AR mRNA expression decreased markedly in all the treated groups. Our results indicated that TBBPA and TCBPA induced reproductive toxicity in a dose-dependent manner, with TCBPA having greater toxicity than TBBPA. Furthermore, changes in T, E2, LH, and FSH levels induced by TBBPA and TCBPA exposure, which led to endocrine disorders, also caused disturbance of spermatogenesis through abnormal gene expressions of AR in the testes .

研究领域: 环境毒理学 · 内分泌学 · 生殖生物学
✓ 已验证 DOI PubMed 高影响因子
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Journal of Environmental Chemical Engineering · 2024 · IF 7.4

Photocatalytic magnetic bimetallic ferrite synergistically activates ammonium persulfate for the efficient degradation of tetrachlorobisphenol A(TCBPA)

Yawen Wu,Xueying Hou,Rui Guo

The presence of tetrachlorobisphenol A(TCBPA) in the environment is continually increasing, which has potential negative effects on human health. Therefore, it is important to develop new materials that can degrade these compounds using various modification techniques. Recently, the photocatalytic degradation of organic pollutants using peroxides has been widely used as the focus of several research studies. This study synthesized Zr-doped NiFe 2 O 4 (Zr-NiFe 2 O 4 ) metal complex materials using a co-precipitation method and applied them to catalyze the degradation of a typical halogenated bisphenol A pollutant using different phase-catalyzed peroxydisulfate (PS) compounds. The results showed that Zr-NiFe 2 O 4 significantly enhances the nitrogen-active adaptive catalytic action between the reactive species and (NH 4 ) 2 S 2 O 8 , exhibiting an excellent catalytic performance (99 %). The degradation rate could reach 90 % after 30 mins with the low concentration of TCBPA (20 mg•L –1 ). Furthermore, the degradation of TCBPA in the Zr-NiFe 2 O 4 /LED/(NH 4 ) 2 S 2 O 8 system occurred over a wide pH range of 3–11. The results of leaching metals were detected that the concentrations of the leached zirconium, nickel and iron ions declined to 0.018 mg•L −1 . In addition, the tri-metal synergistic effect of Zr-NiFe 2 O 4 not only significantly improved the TCBPA removal efficiency, but also enhanced the long-term stability of the composite material. Mechanistic studies revealed that ·OH and SO 4 ·– were involved in the TCBPA degradation process with ·OH being the primary active species, and the possible degradation pathways were deduced using mass spectrometry. The on-line infrared test experiments showed the disappearance of the hydroxyl and double bond within approximately 120 seconds. Moreover, the magnetic properties of Zr-NiFe 2 O 4 met the water recovery requirements, effectively reducing secondary pollution, and aligned with the practical needs for water treatment, providing data for the construction of efficient magnetic catalysts.

研究领域: 环境科学 · 材料科学
✓ 已验证 产品关联 DOI 高影响因子
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PLACENTA · 2025 · IF 2.5

Gestational TCBPA exposure impairs placental function and fetal Development: Mechanisms of syncytialization disruption and fetal growth restriction

Siyu Wang,Shufang Wang,Xin Zhang,Zhiyuan Lyu,Cong Lu,Zeyi Long,Xihua Chen,Taifeng Zhuang,Xiangbo Xu

Introduction Tetrachlorobisphenol A (TCBPA), a BPA alternative, has been identified as a potential toxin, yet its reproductive toxicity remains poorly understood. This study aimed to investigate the effects of gestational TCBPA exposure on fetal development and placental function, focusing on syncytialization and TauT expression. Methods Pregnant ICR mice were divided into three groups: TCBPA-treated (50 mg/kg/day), vehicle-treated (corn oil), and control (water). Treatments were administered until embryonic day 12.5 (E12.5) and 18.5 (E18.5). Embryos and placentas were collected at E12.5 for histological, immunofluorescence, western blotting, and quantitative PCR analyses of placental development and fetal growth. In vitro BeWo cell experiments were conducted to assess TCBPA's effects on syncytialization. Results Gestational TCBPA exposure led to fetal growth restriction (FGR) and impaired placental development, including reduced labyrinth area, disorganized vascular patterns, and disrupted syncytialization. Key syncytialization markers, such as Syncytin1 and β-hCG, were significantly reduced, while E-Cadherin was elevated. Both the localization and expression levels of syncytiotrophoblast polarity markers MCT1 and MCT4 were decreased. Mechanistically, TCBPA downregulated the PPARγ/RXRα/SP-1 signaling pathway and reduced TauT expression. In vitro, TCBPA disrupted syncytialization in BeWo cells. Discussion Gestational TCBPA exposure disrupts placental function, particularly syncytialization, resulting in fetal growth restriction. The downregulation of Syncytin-1, β-hCG, TauT, and the altered localization and expression of MCT1 and MCT4 point to key mechanisms underlying TCBPA-induced placental dysfunction. These findings highlight the reproductive risks of TCBPA and emphasize the need for further investigation and caution in its use during pregnancy.

CAS / MDL: 79-95-8
✓ 已验证 产品关联 DOI PubMed 高影响因子
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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY · 2019 · IF 4.527

Typical halogenated flame retardants affect human neural stem cell gene expression during proliferation and differentiation via glycogen synthase kinase 3 beta and T3 signaling

Shaojun Liang,Shengxian Liang,Hui Zhou,Nuoya Yin,Francesco Faiola

2′,2′,4,4′-tetrabromo diphenyl ether (BDE-47), one of the most abundant congeners of commercial pentaBDE utilized as flame retardants , has been phased out of production due to its potential neural toxicity and endocrine disrupting activities, and yet still present in the environment. Several alternatives to BDE-47, including tetrabromobisphenol A (TBBPA), tetrabromobisphenol S (TBBPS), tetrachlorobisphenol A (TCBPA) and decabromodiphenyl ether (BDE-209), are presently employed without restrictions and their potential toxic effects on human neural development are still unclear. In this study, we utilized a human neural stem cell (hNSC)-based system to evaluate the potential developmental neurotoxic effects of the above-mentioned five chemicals, at environment and human exposure relevant concentrations. We found that those compounds slightly altered the expression of hNSC identity markers ( SOX2 , SOX3 and NES ), without impairing cell viability or proliferation, in part by either modulating glycogen synthase kinase 3 beta (GSK3β) signaling (TBBPS, TCBPA and BDE-47), and slightly disturbing the NOTCH pathway (TBBPA, TBBPS and TCBPA). Moreover, the five chemicals seemed to alter hNSC differentiation by perturbing triiodothyronine (T3) cellular signaling. Thus, our findings suggest that the five compounds, especially TBBPS, TCBPA, and BDE-47, may affect hNSC self-renewal and differentiation abilities and potentially elicit neural developmental toxicity.

CAS / MDL: 6893-02-3
研究领域: 神经科学 · 毒理学 · 细胞生物学 · 分子生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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