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Environ Pollut. 2015 Aug;203:175-182. doi: 10.1016/j.envpol.2015.03.051. Epub 2015 Apr 20.

Induction of c-Jun by air particulate matter (PM₁₀) of Mexico city: Participation of polycyclic aromatic hydrocarbons.

Author information

1
Subdirección de Investigación Básica, Instituto Nacional de Cancerología, Av. San Fernando No. 22, Col Sección XVI. C.P. 14080. Delegación Tlalpan, México, D.F., Mexico.
2
Department of Paediatrics, University of Alberta, 3-591 ECHA, 11405 87th Ave, NW, Edmonton T6G 1C9, Canada.
3
Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, A.P. 70228. Ciudad Universitaria. 04510, México, D.F., Mexico.
4
Laboratorio de Genómica Funcional del Cáncer, Instituto Nacional de Medicina Genómica, Periférico Sur, No.4809. Col. Arenal Tepepan, C.P. 14610. Delegación Tlalpan, México, D.F., Mexico.
5
Instituto Mexicano del Petróleo, Eje Central Lázaro Cárdenas 152. San Bartolo Atepehuacan, C.P. 07730, México, D.F., Mexico.
6
Subdirección de Investigación Básica, Instituto Nacional de Cancerología, Av. San Fernando No. 22, Col Sección XVI. C.P. 14080. Delegación Tlalpan, México, D.F., Mexico. Electronic address: claudia.garciac@salud.gob.mx.

Abstract

The carcinogenic potential of urban particulate matter (PM) has been partly attributed to polycyclic aromatic hydrocarbons (PAHs) content, which activates the aryl hydrocarbon receptor (AhR). Here we report the effect of PM with an aerodynamic size of 10 μm (PM10) on the induction of AhR pathway in A549 cells, evaluating its downstream targets CYP1B1, IL-6, IL-8 and c-Jun. Significant increases in CYP1B1 protein and enzyme activity; IL-6 and IL-8 secretion and c-Jun protein were found in response to PM10. The formation of PAH-DNA adducts was also detected. The involvement of AhR pathway was confirmed with Resveratrol as AhR antagonist, which reversed CYP1B1 and c-Jun induction. Nevertheless, in IL-6 and IL-8 secretion, the Resveratrol was ineffective, suggesting an effect independent of this pathway. Considering the role of c-Jun in oncogenesis, its induction by PM may be contributing to its carcinogenic potential through induction of AhR pathway by PAHs present in PM10.

KEYWORDS:

Particulate matter; aryl hydrocarbon receptor; cJun; carcinogenic potential; polycyclic aromatic hydrocarbons

PMID:
25909326
DOI:
10.1016/j.envpol.2015.03.051
[Indexed for MEDLINE]

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