ATP5J and ATP5H Proactive Expression Correlates with Cardiomyocyte Mitochondrial Dysfunction Induced by Fluoride

• DOI: 10.1007/s12011-017-0983-5
• Publication Date: 2017-03-05T21:27:07Z
• Authors: Hong-wei Wang; Wen-peng Zhao; Jing Liu; Pan-pan Tan; Wei-shun Tian; Bian-hua Zhou
• Keywords: Male; 0303 health sciences; Mitochondrial Proton-Translocating ATPases; Gene Expression Regulation, Enzymologic; Mitochondria, Heart; Fluorides; Mice; 03 medical and health sciences; Adenosine Triphosphate; Oxidative Phosphorylation Coupling Factors; Animals; Myocytes, Cardiac; Mitochondrial ADP, ATP Translocases

To investigate the effect of excessive fluoride on the mitochondrial function of cardiomyocytes, 20 healthy male mice were randomly divided into 2 groups of 10, as follows: control group (animals were provided with distilled water) and fluoride group (animals were provided with 150 mg/L F- drinking water). Ultrastructure and pathological morphological changes of myocardial tissue were observed under the transmission electron and light microscopes, respectively. The content of hydrolysis ATP enzyme was observed by ATP enzyme staining. The expression levels of ATP5J and ATP5H were measured by Western blot and quantitative real-time PCR. The morphology and ultrastructure of cardiomyocytes mitochondrial were seriously damaged by fluoride, including the following: concentration of cardiomyocytes and inflammatory infiltration, vague myofilaments, and mitochondrial ridge. The damage of mitochondrial structure was accompanied by the significant decrease in the content of ATP enzyme for ATP hydrolysis in the fluoride group. ATP5J and ATP5H expressions were significantly increased in the fluoride group. Thus, fluoride induced the mitochondrial dysfunction in cardiomyocytes by damaging the structure of mitochondrial and interfering with the synthesis of ATP. The proactive ATP5J and ATP5H expression levels were a good response to the mitochondrial dysfunction in cardiomyocytes.