title: [The effects of microcystin-LR on the mRNA expression levels of base excision repair genes and genes related to apoptosis].
abstract: OBJECTIVE
  To explore the effects of microcystin-LR (MCLR) on the expression of base excision repair genes and genes related to apoptosis.
  
  
  METHODS
  The BRL-3A cells were exposed to different concentrations of MCLR for various periods of time and the cell viability was measured by MTT. The mRNA expression was determined with the quantitative real-time polymerase chain reaction (QRT-PCR).
  
  
  RESULTS
  The viability of BRL-3A cells significantly reduced in a concentration- and time-dependent manner. In 30 µg/ml group, the mRNA expression level (1.327 ± 0.028) of p53 increased significantly at 24 h after exposure, as compared with the other groups (1.005 ± 0.117, 0.862 ± 0.154, 1.028 ± 0.056 and 1.015 ± 0.091) (P < 0.05). The mRNA expression levels (5.080 ± 0.729, 5.820 ± 0.373, 6.018 ± 0.359 and 6.183 ± 0.515) of Bax in all exposure groups were significantly higher than that (1.024 ± 0.277) in control group at 24 h after exposure. However, the Bax mRNA expression level (0.604 ± 0.146) in the 30 µg/ml group at 72 h after exposure was significantly lower than those (1.004 ± 0.107, 0.811 ± 0.142, 0.855 ± 0.101 and 0.814 ± 0.056) in other groups (P < 0.05). When compared with control group (1.006 ± 0.132) and 1 µg/ml group (1.034 ± 0.241), the mRNA expression level (0.488 ± 0.147) of PARP1 in 30 µg/ml group at 48 h after exposure decreased significantly (P < 0.05). Furthermore, the mRNA expression levels (0.594 ± 0.180, 0.491 ± 0.015 and 0.305 ± 0.091) of JWA, XRCC1 and PARP1 in 30 µg/ml group at 72 h after exposure decreased significantly, as compared with the other groups (P < 0.05).
  
  
  CONCLUSIONS
  The induction of gene expression is a transient phenomenon that occurred at different times of exposure for different genes. Inhibition of MCLR on the base excision repair gene expression may play important role in the course of MCLR promoting liver tumor.
authors.affiliation: Public Health School, Fujian Medical University, Fuzhou, China.
authors.forename: Zhi-Jian
authors.initials: ZJ
authors.lastname: Hu
authors.forename: Hua
authors.initials: H
authors.lastname: Chen
authors.forename: Zhao-Xia
authors.initials: ZX
authors.lastname: Lai
authors.forename: Xian-E
authors.initials: XE
authors.lastname: Peng
authors.forename: Yuan-She
authors.initials: YS
authors.lastname: Sun
authors.forename: Peng
authors.initials: P
authors.lastname: Lü
mesh_terms: D000818:Animals; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000235:genetics*; D001483:Base Sequence; D002460:Cell Line; D004260:DNA Repair; D015870:Gene Expression; D008387:Marine Toxins; D052998:Microcystins / Q000633:toxicity*; D012333:RNA, Messenger / Q000235:genetics*; D051381:Rats
chemical_list: D051017:Apoptosis Regulatory Proteins; D008387:Marine Toxins; D052998:Microcystins; D012333:RNA, Messenger; C057862:cyanoginosin LR