[The effect of nickel-smelting fumes on the expression of bcl-2 and bax in NIH/3T3 cells].
OBJECTIVE
To investigate the effect of nickel-smelting fumes on the expression of bcl-2 and bax in mammalian cells.


METHODS
Logarithmic growth NIH/3T3 cells were exposed to venom for 24 h, which sample fumes concentration was respectively 0, 6.25, 12.50, 25.00, 50.00, 100.00 µg/ml. Cell viability was assessed by MTT assay and the level of extracellular LDH activity was detected with Lactate Dehydrogenase (LDH) kit. Morphological changes of apoptotic were observed with Hoechst33342, while Western blot was used to measure the expression of bcl-2 and bax.


RESULTS
In addition to 7 days of 6.25 µg/ml nickel-smelting fumes group, each time point and dose group's cell viability reduced with significant differences compared with the control group (P < 0.05). the extracellular LDH activity increased with increasing dose of nickel-smelting fumes, and the extracellular LDH activity of 6.25, 12.50, 25.00, 50.00, 100.00 µg/ml nickel-smelting fumes group increased as compared with the control group (P < 0.05). Simultaneously, the cells, treated with 100.00 µg/ml nickel-smelting fumes for 24 h, appeared obvious morphological changes of apoptosis, such as chromatin condensation and cell shrinkage. the expression of bcl-2 significantly increased in groups of 6.25, 12.50, 25.00 µg/ml nickel-smelting fumes (0.58 ± 0.01, 0.6 3± 0.01 and 0.57 ± 0.01) and decreased in groups of 50.00, 100.00 µg/m nickel-smelting fume (0.35 ± 0.01 and 0.27 ± 0.01) as compared with that of the control group (P < 0.05). And the expression of bax significantly decreased in group of 6.25 µg/ml nickel-smelting fumes (0.58 ± 0.00) and increased in groups of 50.00, 100.00 µg/m nickel-smelting fumes (0.71 ± 0.01 and 0.78 ± 0.02) as compared with that of the control group (P < 0.05).


CONCLUSIONS
Apoptosis was activated in NIH/3T3 cell after 24 h of exposure to Ni-smelting fumes, which may be induced by oxidative stress.
School of Public Heath, Harbin Medical University, Harbin, 150086, China.
Lin
L
Zhang
School of Public Heath, Harbin Medical University, Harbin, 150086, China.
Yue
Y
Wang
School of Public Heath, Harbin Medical University, Harbin, 150086, China.
Wenhan
W
Ma
School of Public Heath, Harbin Medical University, Harbin, 150086, China.
Yao
Y
Fu
School of Public Heath, Harbin Medical University, Harbin, 150086, China.
Dan
D
Han
School of Public Heath, Harbin Medical University, Harbin, 150086, China. E-mail: wuyonghui777@163.com.
Yonghui
Y
Wu
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D007770:L-Lactate Dehydrogenase; D051379:Mice; D041681:NIH 3T3 Cells / Q000187:drug effects; D009532:Nickel / Q000633:toxicity*; D018384:Oxidative Stress; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D051028:bcl-2-Associated X Protein / Q000378:metabolism*
D000393:Air Pollutants; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D009532:Nickel; D007770:L-Lactate Dehydrogenase