[Oxidative damage and apoptosis in NIT-1 cells induced by ethanol].
OBJECTIVE
To decide whether ethanol induce apoptosis in mouse insulinoma cells (NIT-1) and the potential mechanism involved.


METHODS
After NIT-1 cells were exposed to various concentrations of ethanol, agarose gel electrophoresis was used to detected DNA fragmentation. malondialdehyde (MDA) content, glutathione (GSH) level, superoxide dismutase(SOD) and glutathione peroxidase (GSH-Px) were measured in NIT-1 cells to evaluate the oxidative damage degree. Caspase-3 relative activity was determined by colorimetric assay.


RESULTS
The results showed a "DNA ladder" pattern after treated with ethanol in NIT-1 cells. The MDA content was higher, the SOD activity, GSH-Px activity and GSH content were lower in ethanol group than those of control group. Ethanol increased the caspase-3 activity by a dose and time dependent manner.


CONCLUSIONS
Higher concentration of ethanol induces imbalance of oxidation and antioxidative ability in NIT-1 cells, and oxidative stress further leads to apoptosis which may be related to the increased caspase-3 activity.
Hao
Li-Ping
LP
School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Hu
Xue-Feng
XF
Sun
Xiu-Fa
XF
Ying
Chen-Jiang
CJ
Liu
Liegang
L
Mao
Limei
L
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D045744:Cell Line, Tumor; D000431:Ethanol / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007340:Insulinoma / Q000378:metabolism* / Q000473:pathology*; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D018384:Oxidative Stress / Q000187:drug effects*; D011897:Random Allocation; D013482:Superoxide Dismutase / Q000378:metabolism
D000431:Ethanol; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; C505409:Casp3 protein, mouse; D053148:Caspase 3; D005978:Glutathione