[Nickel smelting dust exposures to NIH/3T3 cellular mitochondrial damage and L-ascorbic acid interference effect].

To study the protection of L-ascorbic acid on mouse embryonic fibroblasts (NIH/3T3) from carcinogenic effects caused by nickel smelting smoke subjects.The NIH/3T3 cells were divided into experimental and L-ascorbic acid in the intervention group. Plus exposure group concentration of nickel refining dusts were formulate 0.00, 25.00, 50.00, 100.00 μg/ml suspension, the intervention group on the basis of the added exposure group containing L-ascorbic acid (100 mmol/L) , contacted. Then, the cell viability was detected by MTT assay, we used Calcein-AM fluorescence probe to detect cell mitochondrial permeability transition pore (MPTP) changes, JC-1 staining to observe and detect the cell mitochondrial membrane potential (MMP) change, colorimetric quantitative to study the activity of mitochondrial respiratory chain complex Ⅰ,Ⅱ,Ⅲ,Ⅳ.Upon 24 h incubation, both cell relative inhibition rate, openness of MPTP were increasing enhanced by different concentrations, on the other hand, MMP and the activity of mitochondrial respiratory chain complexⅠ, Ⅱ, Ⅳ were obviously decreased, the differences were statistically significant (P<0.05) .After L-ascorbic acid intervention treatment, the results of the intervention group were lower than that of the exposure group, and the difference was statistically significant (P<0.05) , indicating the protection of L-ascorbic acid on cell mitochondrial from the nickel exposure damage.The damage effects of nickel on NIH/3T3 cell mitochondrial was significantly enhanced with the increasing concentration, and L-ascorbic acid has certain protection on cellular mitochondrial.