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Retracted

Combined Effect of Silica Nanoparticles and Benzo[a]pyrene on Cell Cycle Arrest Induction and Apoptosis in Human Umbilical Vein Endothelial Cells

Datos Bibliográficos

ID17801191
AutoresCollins Otieno Asweto (0000-0003-3514-9836, Capital Medical University), Collins Asweto (Capital Medical University), Jing Wu (0000-0002-6559-4335, Capital Medical University), Hejing Hu (Capital Medical University), Lin Feng (0000-0001-7062-1281, Capital Medical University), Xiaozhe Yang (0000-0002-0190-5114, Capital Medical University), Junchao Duan (0000-0002-1455-304X, Capital Medical University, autor de correspondencia), Zhiwei Sun (0000-0003-4470-9743, Capital Medical University, autor de correspondencia)
Año2017
Volumen14
Número3
Páginas289-289
Fecha de publicación2017-03-09
Peer ReviewedSí
Open AccessSí
TipoARTICLE
RevistaInternational Journal of Environmental Research and Public Health (JOURNAL)
Identificadores de la revistaISSN: 1661-7827 • E-ISSN: 1660-4601
EditorialMultidisciplinary Digital Publishing Institute (PUBLISHER • CH)
DOI10.3390/ijerph14030289
PMID28282959
OpenAlexW2593927517
IdiomaEN
Citas recibidas1
Referencias citadas43

Particulate matter (PM) such as ultrafine particulate matter (UFP) and the organic compound pollutants such as polycyclic aromatic hydrocarbon (PAH) are widespread in the environment. UFP and PAH are present in the air, and their presence may enhance their individual adverse effects on human health. However, the mechanism and effect of their combined interactions on human cells are not well understood. We investigated the combined toxicity of silica nanoparticles (SiNPs) (UFP) and Benzo[a]pyrene (B[a]P) (PAH) on human endothelial cells. Human umbilical vascular endothelial cells (HUVECs) were exposed to SiNPs or B[a]P, or a combination of SiNPs and B[a]P. The toxicity was investigated by assessing cellular oxidative stress, DNA damage, cell cycle arrest, and apoptosis. Our results show that SiNPs were able to induce reactive oxygen species generation (ROS). B[a]P, when acting alone, had no toxicity effect. However, a co-exposure of SiNPs and B[a]P synergistically induced DNA damage, oxidative stress, cell cycle arrest at the G2/M check point, and apoptosis. The co-exposure induced G2/M arrest through the upregulation of Chk1 and downregulation of Cdc25C, cyclin B1. The co-exposure also upregulated bax, caspase-3, and caspase-9, the proapoptic proteins, while down-regulating bcl-2, which is an antiapoptotic protein. These results show that interactions between SiNPs and B[a]P synergistically potentiated toxicological effects on HUVECs. This information should help further our understanding of the combined toxicity of PAH and UFP

Apoptosis · Benzo(a)pyrene · Biology · Carcinogen · Cell cycle · Cell cycle checkpoint · DNA · DNA damage · Downregulation and upregulation · In vitro · Oxidative stress · Reactive oxygen species · Toxicity · Umbilical vein · Air Quality and Health Impacts · Carcinogens and Genotoxicity Assessment · Chemistry · Toxic Organic Pollutants Impact · Biochemistry · Cell Biology

  • Retracted

    Open Access•Collins Otieno Asweto, Jing Wu et al.•International Journal of…•2025

  • Particulate Matter Air Pollution and Cardiovascular Disease

    Robert D Brook, Sanjay Rajagopalan et al.•Circulation•2010

  • Air pollution

    Open Access•Michelle L Block, Lilian Calderón‐Garcidueñas et al.•Trends in Neurosciences•2009

  • Air pollution and lung cancer incidence in 17 European cohorts

    Open Access•Ole Raaschou‐Nielsen, Ole Raaschou-Nielsen et al.•The Lancet Oncology•2013

Obras citantes distintas1
Citas por año1
Intervalo de citas2025 - 2025 (1)
Velocidad de citaciónrecent
Altamente citadoNo
Tipos de citaNeutras: 1
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