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- Title
Atrazine induces endoplasmic reticulum stress-mediated apoptosis of T lymphocytes via the caspase-8-dependent pathway.
- Authors
Lee, Eun‐Jin; Jang, Youngsaeng; Kang, Kwonyoon; Song, Da‐Hyun; Kim, Rihyun; Chang, Hee‐Won; Lee, Dong Eil; Song, Claire Ka‐Eun; Choi, Bongkun; Kang, Min‐Ji; Chang, Eun‐Ju
- Abstract
ABSTRACT Atrazine (ATR) is one of the most commonly applied broad-spectrum herbicides. Although ATR is well known to be a biologically hazardous molecule with potential toxicity in the immune system, the molecular mechanisms responsible for ATR-induced immunotoxicity remain unclear. In this study, we found that the immunotoxic properties of ATR were mediated through the induction of apoptotic changes in T lymphocytes. Mice exposed to ATR for 4 weeks exhibited a significant decrease in the number of spleen CD3+ T lymphocytes, while CD19+ B lymphocytes and nonlymphoid cells were unaffected. ATR exposure also led to inhibition of cell growth and induction of apoptosis in human Jurkat T-cells. Importantly, ATR triggered the activation of caspase-3 and the cleavage of caspase-8 and PARP, whereas it did not affect the release of cytochrome c from the mitochondria in Jurkat T-cells. In addition, ATR activated the unfolded protein response signaling pathway, as indicated by eIF2 α phosphorylation and CHOP induction. Our results demonstrate that ATR elicited an immunotoxic effect by inducing ER stress-induced apoptosis in T-cells, therefore providing evidence for the molecular mechanism by which ATR induces dysregulation of the immune system. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 998-1008, 2016.
- Subjects
HERBICIDE research; ATRAZINE; MOLECULES; TOXICOLOGY; IMMUNE system
- Publication
Environmental Toxicology, 2016, Vol 31, Issue 8, p998
- ISSN
1520-4081
- Publication type
Article
- DOI
10.1002/tox.22109