Objective      To investigate the possible effects and changes o

f mammalian target of rapamycin (mTOR) and  its downstream signaling pathway in mouse bone marrow stem cells (mBMSCs) induced by oxidative stress.        Methods      mBMSCs were isolated from bone marrows from 30 healthy Kunming adult male mice

cultured and expanded. An oxidative stress model of mBMSCs was established by different concentrations of H

2

O

2

(100

200

300

400

500

800 and 1 000 μmol/L). Cell viability was detected by MTT assay

and morphological changes of BMSCs were observed by inverted microscopy. The nucleus apotosis were accessed by Hoechst 33342 staining. Western blotting was employed to evaluate the expression of Bcl-2

Bax

mTOR

p70S6K and S6

as well as phosphorylated mTOR

p70S6K and S6.       Results      The mBMSCs had pathophysiologic changes after 100 to 1 000 μmol/L H

2

O

2

treatment in a dose-dependent manner. When H

2

O

2

 was given at concentrations of 100 to 300 μmol/L

the protein expression of mTOR

p70S6K and S6 in mBMSCs tended to be increased in a dose-dependent fashion

while the expression of their phosphorylated forms and anti-apoptosis protein Bcl-2 were significantly increased (P0.01). But

the expression of apoptosis protein Bax was not obviously changed (P0.05). However

when H

2

O

2

was given at concentrations over 400 μmol/L

the expression of Bcl-2

p-mTOR

p-p70S6K and p-S6 proteins were in a dose-dependent decrease in mBMSCs (P0.05

P0.01)

while the expression of mTOR

p70S6K and S6 protein was not visibly altered

whereas the expression of was obviously increased (P0.01).       Conclusion      Oxidative stress to some extent causes reduced survival and increased apoptosis in BMSCs. The underlying mechanisms may be partly due to suppression of mTOR and its downstream signaling

decreased expression of Bcl-2

and enhanced expression of Bax.