Mitochondrial function in microcystin-LR-induced primary mice hepatocytes
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1. Key Laboratory of Gastrointestinal Cancer(Fujian Medical University), Ministry of Education, Fujian Key Laboratory of Tumor Microbiology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China. 2. Center for Experimental Research in Clinical Medicine, Fujian Provincial Hospital, Fuzhou 350001

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    Abstract:

    Objective Microcystin contamination caused by cyanobacteria blooms is a profound global concern. Microcystin-LR (MC-LR) was documented to induce potent hepatotoxicity, but the exact mechanisms have not been fully elucidated. To better understand the mechanisms, we conducted the following investigations. Methods Primary mouse hepatocytes were isolated, purified and exposed to a MC-LR concentration range of 2. 5 ~ 10 nmol / L for 48 h with DMEM treatment as the negative control. Mitochondrial function ( ATP levels and mitochondrial membrane potential), DNA damage (comet assay and 8-OHdG levels) and p53 expression were determined in MC-LR-treated cells and control cells. In addition, experiments were repeated to assess mitochondrial function after pft-α preconditioning. Results MC-LR led to a progressive loss in ATP production and mitochondrial membrane potential in a dose-dependent manner. Furthermore, the comprehensive DNA damage examination and upregulated p53 protein level indicated that MC-LR was associated with DNA damage in primary mouse hepatocytes. However, when p53 was blocked by PFT-α, mitochondrial damage was attenuated after MC-LR treatment. Conclusions Together, these data indicate that MCLR-induced DNA damage promoted p53 production, which was associated with mitochondrial dysfunction.

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History
  • Received:March 31,2021
  • Revised:
  • Adopted:
  • Online: February 17,2022
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