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首页> 外文期刊>African Journal of Biotechnology >Association between VDAC1 mRNA expression and intracellular ATP levels of cultured L-02 hepatocytes during hexavalent chromium toxicity
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Association between VDAC1 mRNA expression and intracellular ATP levels of cultured L-02 hepatocytes during hexavalent chromium toxicity

机译：六价铬中毒期间培养的L-02肝细胞VDAC1 mRNA表达与细胞内ATP水平的关联

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One way in which xenobiotics induce apoptotic cell death is to alter the selective permeability of the intracellular voltage-dependent anion channel (VDAC1) in the mitochondrial membrane. In this study, we explored the association between VDAC1 mRNA expression and mitochondrial function during hexavalent chromium compounds [Cr(VI)] treatment. Cultured L-02 hepatocytes were treated with 2, 4, 8, 16, or 32 μmol/L Cr(VI) for 12, 24, or 36 h. Expression of VDAC1 mRNA was measured by qualitative reverse transcription polymerase chain reaction (RT-PCR), whereas intracellular adenosine triphosphate (ATP) levels were determined by an ATP-specific bioluminescence assay. Over this range of Cr(VI) concentrations, average VDAC1 mRNA expression decreased by 84% after 12 h treatment and by 40% after 24 h of treatment, but it increased 2.33-fold at 36 h when compared with the control cultures. Treatment with Cr(VI) disrupted cellular metabolism as evidenced by changes in ATP levels. Cr(VI) treatment caused ATP levels to increase at 12 h, decrease at 24 h, and increase again at 36 h, resulting in a slant V-shaped curve. Correlation analysis revealed a moderate negative relationship between VDAC1 mRNA expression and intracellular ATP levels during Cr(VI) treatment (r = -0.557, P?< 0.05). The negative association seemed to be more obvious in?32?μmol/LCr(VI) group. Based on these results, heavy metal toxicity may induce over-expression of VDAC1 mRNA, which causes a decrease in ATP levels.
机译：异种生物诱导凋亡细胞死亡的一种方法是改变线粒体膜中细胞内电压依赖性阴离子通道（VDAC1）的选择性通透性。在这项研究中，我们探讨了六价铬化合物[Cr（VI）]处理期间VDAC1 mRNA表达与线粒体功能之间的关系。用2、4、8、16，或32μmol/ L Cr（VI）处理培养的L-02肝细胞12、24或36 h。通过定性逆转录聚合酶链反应（RT-PCR）测量VDAC1 mRNA的表达，而细胞内三磷酸腺苷（ATP）的水平通过ATP特异性生物发光测定法确定。在此Cr（VI）浓度范围内，平均VDAC1 mRNA表达在处理12小时后下降了84％，在处理24小时后下降了40％，但与对照培养物相比，在36 h上升了2.33倍。六价铬的处理破坏了细胞的新陈代谢，ATP水平发生了变化。 Cr（VI）处理导致ATP水平在12小时增加，在24小时减少，然后在36小时再次增加，从而形成倾斜的V形曲线。相关分析显示，Cr（VI）处理期间VDAC1 mRNA表达与细胞内ATP水平呈中等程度的负相关（r = -0.557，P <0.05）。在？32？mol / LCr（VI）组中，负相关似乎更为明显。根据这些结果，重金属毒性可能会诱导VDAC1 mRNA的过表达，从而导致ATP水平降低。

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