Objective To evaluate effects of tris(2-chloroethyl)phosphate (TCEP) on mitochondrial functions in liver cells.
Methods At 24 and 48 h after L02 and HepG2 cells were treated with 0.00 (solvent control group), 3.12, 12.50, 50.00, 200.00 mg/L TCEP, we detected cell viability, mitochondrial reactive oxygen species (mtROS) levels, mitochondrial DNA copy numbrane, mitochondrial membrane potential, intracellular free Ca2+ levels, and intracellular ATP level.
Results Compared with the control group, TCEP decreased the cell viabilities of L02 cells in the 200 mg/L TCEP group (P < 0.05) and the cell viabilities of HepG2 cells in the ≥ 12.50 mg/L TCEP groups (P < 0.05) at 24 h; decreased the cell viabilities of L02 and HepG2 cells in the 50.00 and 200.00 mg/L TCEP groups at 48 h (P < 0.05); reduced the mitochondrial DNA number of L02 and HepG2 cells in all treatment groups (P < 0.05 or P < 0.01); decreased the mitochondrial membrane potential of L02 or HepG2 cells in all treatment groups at 24 h (P < 0.05 or P < 0.01); increased the intracellular free Ca2+ concentrations of L02 and HepG2 cells only in the 200.00 mg/L TCEP group at 24 h and in the 50.00 and 200.00 mg/L groups at 48 h (P < 0.01); decreased the intracellular ATP levels of L02 cells only in the 200.00 mg/L TCEP group at 24 and 48 h (P < 0.05) and in the 50.00 and 200.00 mg/L TCEP groups of HepG2 cells at 24 and 48 h (P < 0.05 or P < 0.01).
Conclusion A certain concentrations of TCEP could cause mitochondrial damage and abnormal changes in indices reflecting mitochondrial dysfunctions, implying that TCEP could induce mitochondrial toxicity in hepatocytes.
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