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目的探讨重金属六价铬[Cr(Ⅵ)]的体外肝毒性。方法 L-02肝细胞经Cr(Ⅵ)0,2,4,8,16和32μmol.L-1分别染毒12,24或36 h后,采用逆转录-荧光定量聚合酶链反应(RT-qPCR)和荧光光度法分别对腺苷酸转运体1(ANT1)mRNA表达水平和活性氧簇(ROS)水平进行检测。结果 Cr(Ⅵ)32μmol.L-1处理细胞12和24 h后,ROS水平明显升高,而处理36 h后,ROS水平明显下降。Cr(Ⅵ)2～32μmol.L-1处理细胞12和24 h后,细胞内ANT1 mRNA呈明显低表达水平,而处理36 h后,细胞内ANT1 mRNA表达水平明显增高,达正常对照组的2倍左右。结论 Cr(Ⅵ)在早期(12,24 h)可使L-02肝细胞内ROS水平升高,发生氧化应激,在后期(36 h)可诱导ANT1 mRNA表达水平升高,发生能量代谢应激,可能是Cr(Ⅵ)诱导细胞线粒体损伤的分子毒性机制之一。
Objective To investigate the in vitro hepatotoxicity of heavy metal hexavalent chromium [Cr (Ⅵ)]. Methods The L-02 hepatocytes were exposed to Cr (Ⅵ) for 0, 2, 4, 8, 16 and 32 μmol·L-1 for 12,24 or 36 h, respectively. Reverse transcription-polymerase chain reaction qPCR and fluorescence spectrophotometry were used to detect the expression of adenylate transporter 1 (ANT1) mRNA and reactive oxygen species (ROS). Results After treated with 32 μmol·L-1 Cr (Ⅵ) for 12 and 24 h, the level of ROS increased significantly, but the ROS level decreased significantly after 36 h treatment. After treatment with Cr (Ⅵ) 2 ~ 32μmol.L-1 for 12 and 24 h, the expression of ANT1 mRNA in cells was significantly decreased, while the expression of ANT1 mRNA in cells treated with Cr (Ⅵ) Times or so. Conclusion Cr (Ⅵ) can induce the ROS level in L-02 hepatocytes at early and late stages (12 and 24 h), and induce oxidative stress. The expression of ANT1 mRNA induced by Cr (Ⅵ) It may be one of the molecular mechanisms of Cr (Ⅵ) -induced mitochondrial damage.