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Open Access Open Badges Research article

Atrazine-induced apoptosis of splenocytes in BALB/C mice

Xiaofeng Zhang1, Mingqiu Wang2, Shuying Gao1, Rui Ren1, Jing Zheng3 and Yang Zhang1*

Author affiliations

1 Department of Toxicology, College of Public Health, Harbin Medical University, Harbin, Heilongjiang Province, 150081, PR China

2 Institute of Toxicology, Centre of Disease Control of Heilongjiang Province, Harbin, Heilongjiang Province, 150030, PR China

3 Institute of Monitoring for Public Health, Centre of Disease Control of Heilongjiang Province, Harbin, Heilongjiang Province, 150030, PR China

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Citation and License

BMC Medicine 2011, 9:117  doi:10.1186/1741-7015-9-117

Published: 27 October 2011



Atrazine (2-chloro-4-ethytlamino-6-isopropylamine-1,3,5-triazine; ATR), is the most commonly applied broad-spectrum herbicide in the world. Unintentional overspray of ATR poses an immune function health hazard. The biomolecular mechanisms responsible for ATR-induced immunotoxicity, however, are little understood. This study presents on our investigation into the apoptosis of splenocytes in mice exposed to ATR as we explore possible immunotoxic mechanisms.


Oral doses of ATR were administered to BALB/C mice for 21 days. The histopathology, lymphocyte apoptosis and the expression of apoptosis-related proteins from the Fas/Fas ligand (FasL) apoptotic pathway were examined from spleen samples.


Mice administered ATR exhibited a significant decrease in spleen and thymus weight. Electron microscope histology of ultrathin sections of spleen revealed degenerative micromorphology indicative of apoptosis of splenocytes. Flow cytometry revealed that the percentage of apoptotic lymphocytes increased in a dose-dependent manner after ATR treatment. Western blots identified increased expression of Fas, FasL and active caspase-3 proteins in the treatment groups.


ATR is capable of inducing splenocytic apoptosis mediated by the Fas/FasL pathway in mice, which could be the potential mechanism underlying the immunotoxicity of ATR.