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Alteration of proteins expression in apoptotic FL cells induced by MCLR
Author(s) -
Xing MingLuan,
Wang XiaoFeng,
Xu LiHong
Publication year - 2008
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.20355
Subject(s) - apoptosis , microcystin lr , downregulation and upregulation , hepatotoxin , biology , programmed cell death , chop , microbiology and biotechnology , chemistry , biochemistry , toxicity , cyanobacteria , gene , genetics , bacteria , organic chemistry
Microcystins (MCs) are a family of monocyclic heptapeptide hepatotoxins produced by freshwater species of cyanobacteria. Microcystin‐LR (MCLR) is the most frequently studied and most toxic in over 80 MC congeners. Great deals of studies have demonstrated that MCLR can induce apoptosis in a wide variety of cell types. Although much evidence indicates that mitochondria play a pivotal role in MCLR‐induced apoptosis, the complicated apoptosis mechanisms induced by MCLR have not been completely characterized. It is possible that there are other apoptotic pathways existing in MCLR‐induced apoptosis. The present study was undertaken to determine the expression of PP2A, CHOP, Bax, Bcl‐2, and p53 proteins in MCLR‐induced apoptosis in FL cells. The results showed that MCLR could induce apoptosis in FL cells and the process was accompanied with the upregulation of PP2A, Bax, and p53 proteins and the downregulation of Bcl‐2 proteins. In addition, the CHOP protein was upregulated at most treatment groups and decreased at the highest concentration group. These results, especially the alteration of PP2A and CHOP proteins might provide new insights into MCLR‐induced apoptosis. © 2008 Wiley Periodicals, Inc. Environ Toxicol 2008.