HBCD, TBECH, and BTBPE exhibit cytotoxic effects in human vascular endothelial cells by regulating mitochondria function and ROS production. Issue 8 (11th May 2021)

• Record Type: Journal Article
• Authors: Shi, Jun; Wang, Xueting; Chen, Lulu; Deng, Huiping; Zhang, Min
• Is Part Of: Environmental toxicology. Volume 36:Issue 8(2021)
• Page Start: 1674
• Page End: 1682
• Publication Date: 2021-05-11
• Subjects: 1 1, 2‐bis‐(2, 4, 6‐tribromophenoxy)ethane -- 1, 2, 5, 6‐tetrabromocyclooctane -- 1, 2‐dibromo‐4‐(1, 2‐dibromopropyl)cyclohexane -- brominated flame retardants -- ROS -- vascular toxicity; Water quality bioassay -- Periodicals; Water -- Pollution -- Toxicology -- Periodicals; Microbiological assay -- Periodicals; Toxicity testing -- Periodicals; Environmental toxicology -- Periodicals; Environmental Pollution -- Periodicals; Environmental Pollutants -- Periodicals; Environmental Monitoring -- Periodicals; Écotoxicologie -- Périodiques; Pollution -- Périodiques; 615.902
• DOI: 10.1002/tox.23163
• Languages: English
• ISSNs: 1520-4081

Abstract

Abstract: Brominated flame retardants (BFRs), such as, 1, 2, 5, 6‐tetrabromocyclooctane (HBCD), 1, 2‐dibromo‐4‐(1, 2‐dibromopropyl)cyclohexane (TBECH), and 1 1, 2‐bis‐(2, 4, 6‐tribromophenoxy)ethane (BTBPE), have garnered increasing attention due to their potent biological effects. In the present study, the toxicity of HBCD, TBECH, and BTBPE in human vascular endothelial cells (ECs) was explored. The data showed that HBCD, TBECH, and BTBPE induced cytotoxicity, namely dose–dependent cell viability reduction, cell membrane permeability and apoptosis increase, migration, and lumen formation inhibition. Moreover, HBCD was found to be more toxic than BTBPE or TBECH. Exposure to HBCD, TBECH, and BTBPE led to the production of reactive oxygen species, mitochondrial superoxide generation, and mitochondrial membrane potential collapse, implying that reactive stress caused the cytotoxicity. The ATP content, glutathione content, superoxide dismutase, and MDA activities were reduced, indicating that mitochondrial dysfunction may be the key mechanisms responsible for apoptosis. The present study suggested that mitochondria are a new target of BFRs in ECs and further deepened our understanding of the developmental toxicity of BFRs.