.webp&w=384&q=75){kind=logo}
Loading, please wait...
Loading, please wait...
Hexabromocyclododecane (HBCD) is a common flame retardant. It is a persistent organic pollutant. Recently, researchers studied how HBCD affects human liver cells. They focused on HBCD metabolic disruption in HepG2 cells. The team discovered that α-, β-, and γ-HBCD cause cell death. They also noticed that glutathione (GSH) levels dropped significantly. Moreover, γ-HBCD reduced cell viability the most. Consequently, doctors must understand these toxic effects. Furthermore, the oxidative stress varies between the different isomers.
The study followed cells for 24 hours. During this time, HepG2 cells processed the isomers differently. Although uptake rates were similar, β-HBCD transformed faster than the others. Notably, the main metabolite was pentabromocyclododecene (PBCDe). Additionally, the cells converted β- and γ-HBCD into α-HBCD. This process is called bioisomerization. Therefore, the liver uses reductive debromination to modify these chemicals. However, the resulting metabolites may still harm cellular health.
Metabolomic analysis revealed broader damage. HBCD interfered with several vital pathways. Specifically, it altered choline and fatty acid metabolism. In addition, it disrupted purine and glycerophospholipid pathways. Each isomer produced distinct metabolic signatures. Consequently, the researchers concluded that HBCD poses a multi-faceted threat. Because these pathways manage energy and lipids, disruption is dangerous. Therefore, chronic exposure might lead to fatty liver or other disorders.
According to the study, γ-HBCD showed the highest cytotoxicity regarding cell viability, while β-HBCD demonstrated the highest rate of biotransformation.
HBCD primarily disrupts pathways related to choline, glycerophospholipid, fatty acid, and purine metabolism in HepG2 cells.
Disclaimer: This content is for informational and educational purposes only. It does not constitute medical advice or a professional recommendation. Refer to the latest local and national guidelines for clinical practice.
References
1. Cui J et al. Biotransformation of three hexabromocyclododecane diastereoisomers in HepG2 cells and their cellular metabolomics. Ecotoxicol Environ Saf. 2026 Jun 16. doi: undefined. PMID: 42302342.
2. Stockholm Convention on Persistent Organic Pollutants. Hexabromocyclododecane (HBCD) information sheet.
3. Zhang S et al. Bioaccumulation and biotransformation behaviors of brominated flame retardants in mammalian models. Sci Total Environ. 2025.
Read summarized clinical updates, watch expert medical content, and earn CME certifications right from your smartphone.
Open your smartphone camera to scan and install.
A study on human hepatocyte (HepG2) cells reveals how HBCD isomers cause cytotoxicity, metabolic disruption, and biotransformation into toxic metabolites like PBCDe.
4 months ago
Depemokimab offers twice-yearly dosing for severe eosinophilic asthma and chronic rhinosinusitis with nasal polyps, significantly cutting exacerbations and hospital admissions.
3 days back
A novel copper metal-organic framework hydrogel remodels the uterine microenvironment to stimulate robust endometrial regeneration, reduce intrauterine fibrosis, and restore reproductive fertility, offering a groundbreaking strategy for managing refractory endometrial damage and Asherman syndrome.
3 days back
New research reveals that non-ablative radiotherapy suppresses ventricular tachycardia by increasing conduction velocity via NaV1.5 upregulation and action potential prolongation. However, sustained sodium current elevation and depressed calcium handling highlight the need for careful clinical translation.
5 days back
A single-cell transcriptomic atlas reveals how peripheral nerve injuries cause dorsal root ganglion remodeling. By evaluating proximal nerve crush and resection, researchers identify distinct glial and immune programs that resolve neuropathic pain and promote regeneration.
3 days back
A breakthrough study demonstrates that fullerol-primed extracellular vesicles generated in a 3D SECCS bioreactor attenuate ferroptosis and restore myogenic regeneration in diabetes via the FOXO3 pathway, offering a cell-free therapeutic strategy for diabetic musculoskeletal degeneration.
3 days back
