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Cytotoxic effects and apoptosis induction of atrazine in a grass carp ( Ctenopharyngodon idellus ) cell line
Author(s) -
Liu XinMei,
Shao JianZhong,
Xiang LiXin,
Chen XiaoYong
Publication year - 2006
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.20159
Subject(s) - atrazine , apoptosis , grass carp , dna fragmentation , fragmentation (computing) , tunel assay , programmed cell death , intracellular , reactive oxygen species , biology , microbiology and biotechnology , cytotoxic t cell , chemistry , cell culture , biochemistry , fish <actinopterygii> , ecology , pesticide , genetics , fishery , in vitro
Atrazine is a widely used herbicide that was considered to be an endocrine disrupter capable of interfering with the synthesis and action of natural hormones. In the present study, we found that atrazine was able to cause apoptosis in grass carp ( Ctenopharyngodon idellus ) cells from cell line ZC7901. By fluorescent and transmission electron microscopy, the atrazine‐incubated cells displayed a series of morphological changes, including condensation of the nucleus, margination of chromatin to form dense granular caps, and formation of apoptotic bodies. Moreover, DNA fragmentation was detected by the TUNEL reaction and agarose gel electrophoresis. These typical characteristics of cells undergoing apoptosis indicated the occurrence of apoptosis in ZC7901. Apoptosis induced by atrazine was dose‐ and time‐dependent and was involved in mitochondrial membrane potential (ΔΨ m ) disruption, elevation in intracellular Ca 2+ , generation of reactive oxygen species, and intracellular ATP depletion. This study provides the first evidence that atrazine was able to induce apoptosis in fish cells, which indicated the existence of a novel cytotoxic mechanism caused by atrazine and may improve our understanding of the complex relationship between contaminants and aquatic organisms. © 2006 Wiley Periodicals, Inc. Environ Toxicol 21: 80–89, 2006.