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Environ Toxicol Pharmacol. 2017 Jun;52:114-120. doi: 10.1016/j.etap.2017.04.001. Epub 2017 Apr 3.

Silica nanoparticles and lead acetate co-exposure triggered synergistic cytotoxicity in A549 cells through potentiation of mitochondria-dependent apoptosis induction.

Author information

1
Evaluation and Research Center for Toxicology, Institute of Disease Control and Prevention, Academy of Military Medical Sciences, 20 Dongdajie Street, Fengtai District, Beijing 100071, PR China; Department of Pharmacology, Basic Medical College, Jiamusi University, Jiamusi 154007, PR China.
2
Evaluation and Research Center for Toxicology, Institute of Disease Control and Prevention, Academy of Military Medical Sciences, 20 Dongdajie Street, Fengtai District, Beijing 100071, PR China.
3
Evaluation and Research Center for Toxicology, Institute of Disease Control and Prevention, Academy of Military Medical Sciences, 20 Dongdajie Street, Fengtai District, Beijing 100071, PR China. Electronic address: wangyimei2006@126.com.
4
Evaluation and Research Center for Toxicology, Institute of Disease Control and Prevention, Academy of Military Medical Sciences, 20 Dongdajie Street, Fengtai District, Beijing 100071, PR China. Electronic address: pengsq@hotmail.com.

Abstract

The adverse effects of PM2.5 are the results of combined toxicities of finer particles and their adsorbed toxic pollutants. Nevertheless, the combined toxicity of finer particles and air pollutants still remains unclear. The present study was therefore undertaken to investigate the combined cytotoxicity of silica nanoparticles (nano-SiO2, a typical atmospheric ultrafine particle) and lead acetate (Pb, a representative air pollutant) in A549 cells focusing on mitochondria-dependent apoptosis induction. The results showed that Pb exposure alone induced mitochondria-dependent apoptosis in A549 cells, as evidenced by increased apoptotic rate and Bax/Bcl-2 ratio, up-regulated caspases 3 and 9 expressions as well as decreased mitochondrial membrane potential. Non-cytotoxic concentration of nano-SiO2 exposure alone did not trigger apoptosis in A549 cells, but potentialized the apoptotic changes when co-exposure with Pb. Factorial analyses revealed synergistic interactions were responsible for the potentiation of joint apoptotic responses.

KEYWORDS:

Apoptosis; Combined toxicity; Lead; PM2.5; Silica nanoparticles; Synergism

PMID:
28411581
DOI:
10.1016/j.etap.2017.04.001
[Indexed for MEDLINE]

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