[Microcystin-LR induces apoptosis in L-02 cell line].
Nan Fang Yi Ke Da Xue Xue Bao
; 26(4): 386-9, 2006 Apr.
Article
en Zh
| MEDLINE
| ID: mdl-16624733
ABSTRACT
OBJECTIVE:
To investigate the toxicological mechanism of microcystin-LR (MCLR) on L-02 cells.METHODS:
L-02 cells was treated with MCLR at different concentrations and the subsequent changes such as cell proliferation (MTT assay), morphology, lactate dehydrogenase (LDH) leakage, apoptosis rate and apoptosis-related gene expression were examined.RESULTS:
MTT assay showed that MCLR mildly inhibited the cell growth within the initial 24 h of treatment but enhanced the cell viability after that till 60 h in a time- and dose-dependent manner. LDH leakage underwent no marked changes in response to 48-hour MCLR treatment but increased upon prolonged treatment for 60 h, indicating the presence of oxidative damage. After a 48-h treatment with MCLR at 50 microg/ml, obvious apoptosis of L-02 cells occurred as manifested by cell rounding, detachment from the substrate, cell shrinkage and membrane blebbing. The apoptosis rates were rather low (between 22% and 29%) after treatment with MCLR at different concentrations for 36 h, and increased to as much as 80% after a 60-h treatment with 50 microg/ml MCLR. The expressions of p53 and bcl-2 increased in the cells after treatment with high-concentration MCLR, suggesting that MCLR up-regulated the expression levels of the two proteins.CONCLUSION:
MCLR can induce apoptosis and up-regulate p53 and bcl-2 expressions in human normal liver cell line L-02.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Apoptosis
/
Hepatocitos
/
Microcistinas
Límite:
Humans
Idioma:
Zh
Revista:
Nan Fang Yi Ke Da Xue Xue Bao
Año:
2006
Tipo del documento:
Article
País de afiliación:
China