[Effects of cadmium chloride on mitochondrial function and PGC-1α expression in HK-2 cells].

OBJECTIVE

To observe the effects of cadmium chloride on mitochondrial function and the expression of PGC-1α in HK-2 cells, and explore the possible role of cadmium chloride in the process of mitochondrial oxidative damage of HK-2 cells.

METHODS

HK-2 cells were exposed to 0, 10, 20, 30, 40, 50 and 60 μmol/L of CdCl_2 respectively for 24 h in vitro. MTT assay was used to observe the viability of HK-2 cells. The mitochondrial ROS was detected by Mito SOXTMRed staining. Mitochondrial membrane potential was measured by JC-1 staining flow cytometry. The activity of respiratory chain complex III was determined by Multi-functional microplate reader and PGC-1α expression was detected by Western blot analysis.

RESULTS

Compared with control, CdCl_2 treatment at 20 and 60 μmol/L for 24 h the survival rate of HK-2 cells was decreased from( 77. 60 ± 0. 82) % ( 41. 97 ± 1. 22) %( P < 0. 01). The activity ofrespiratory chain complex III was decreased in a concentration-dependent manner( P <0. 05), while the mitochondrial ROS production was increased at the same time( P <0. 05), the JC-1 monomers positive ratio by the percentage of the treated cells was 1. 51, 1. 58, 1. 71, 2. 41 3. 47 times higher than untreated control( P < 0. 01). In addition, the expression of PGC-1α was decreased at 24 h( P < 0. 05).

CONCLUSION

Cadmium chloride may inhibit the expression of PGC-1α and the activity of respiratory chain complex III, and by inducing the mitochondrial ROS production and reducing mitochondrial membrane potential, leading to the damage of HK-2 cells.