Hexachlorobenzene and chlorpyrifos, environmental pollutants that disrupt the endocrine system, promote angiogenesis associated with endometriosis
Lab / animal
OA: closed
CC0
AI-generated summary
Environmental pollutants hexachlorobenzene and chlorpyrifos were found to promote angiogenesis, a process linked to the development and progression of endometriosis.
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Abstract
Endometriosis defined by the growth of endometrial tissues outside the uterus, affects women of reproductive age. A critical process in endometriosis progression, angiogenesis involves endothelial cell migration, proliferation and tube formation, with vascular endothelial growth factor (VEGF) playing a powerful role. Exposure to endocrine-disrupting pollutants, like Hexachlorobenzene (HCB) andChlorpyrifos (CPF), is linked to a higher risk of reproductive diseases including endometriosis. Both HCB and CPF are weak aryl hydrocarbon receptor (AhR) ligands. These study examined HCB and CPF mechanisms of action in endometriosis-associated angiogenesis in vitro. Our results show that HCB (0.005, 0.05 and 5 μM) and CPF (0.5-50 μM) induced VEGF secretion in human stromal endometrial cells (T-HESCs). Moreover, HCB- or CPF-conditioned media (HCB-CM, CPF-CM) from T-HESCs boosted endothelial cell (EA.hy926) proliferation and survival. In addition, wound healing assays rendered an increase in EA.hy926 cell migration after exposure to HCB-CM (0.005-0.5 μM) or CPF-CM (5 μM), while tube-like structures revealed an increase in neovasculogenesis after HCB-CM (0.5 μM) or CPF-CM (5 μM). Our findings show that HCB- and CPF-induced angiogenesis was mediated by AhR and VEGF receptor-2. These results demonstrate that both pesticides increase VEGF secretion in endometrial cells and triggers angiogenesis, a critical event in endometriosis progression.
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SciLite annotations
chemicals 4
hexachlorobenzene
chlorpyrifos
hexachlorobenzene
chlorpyrifos
organisms 3
noordeloos 2009062
human
tetraodon pardalis
Source provenance
- europepmc
- last seen: 2026-10-17T06:09:56.316927+00:00
- openalex
- last seen: 2026-09-04T06:09:26.363916+00:00
- pubmed
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