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Cell alterations but no DNA strand breaks induced in vitro by cylindrospermopsin in CHO K1 cells
Author(s) -
Fessard Valérie,
Bernard Cécile
Publication year - 2003
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.10136
Subject(s) - cylindrospermopsin , chinese hamster ovary cell , comet assay , dna damage , apoptosis , biology , dna , microbiology and biotechnology , dna repair , in vitro , genotoxicity , programmed cell death , cell , biochemistry , chemistry , cell culture , toxicity , genetics , cyanobacteria , organic chemistry , bacteria
Cylindrospermopsin has been involved in some cyanobacterial blooms associated with animal and human intoxications in different countries. Liver is the main target organ even though thymus and kidney are also affected. Its toxic effect has been shown to be induced by protein synthesis inhibition. However, further research about its toxicological potential is required, as revealed by the U.S. Unregulated Contaminant Monitoring Regulation (US UCMR) meeting in 2001. Induction of DNA damage by cylindrospermopsin has been reported by some authors either by a direct effect on DNA or by an indirect effect on associated macromolecules. This study focused on evaluating its in vitro genotoxic potential using the comet assay coupled to various cell alteration measurements. No DNA damage was detected by the alkaline comet assay on Chinese hamster ovary (CHO) K1 cells after 24 h of treatment with cylindrospermopsin concentrations of 0.5 and 1 μg mL −1 . However, inhibition of cell growth was noticed as well as cell blebbing and rounding. These morphological effects were linked to cytoskeletal reorganization (mainly microfilaments) but not to apoptosis. This study concluded that cylindrospermopsin does not obviously react directly with DNA in CHO K1 cells. But the hypothesis of its metabolization into a genotoxic product must be explored further. © 2003 Wiley Periodicals, Inc. Environ Toxicol 18: 353–359, 2003.