Hypothermia enhances bcl-2 expression and protects against oxidative stress-induced cell death in Chinese hamster ovary cells

Oxidative stress is one of the major causes of cellular injury. Various rea ctive oxygen (ROS) and nitrogen (RNS) species such as superoxide, hydroxyl radical, peroxynitrite, and nitric oxide are involved in the manifestations of different types of organ toxicity and the resultant syndromes, symptoms , or diseases. Hypothermic conditions have been reported to reduce the oxid ative stress in various in vitro and in vivo studies. In the present study, we sought to determine the effect of lowered temperatures on oxidative str ess-induced cell death in Chinese hamster ovary (CHO) cells. We also invest igated the oxidative stress-induced alterations in the expression of anti-a poptotic protein, bcl-2, in CHO cells at lowered temperatures. CHO cells we re incubated at four different temperatures of 30, 32, 35, and 37 degreesC (control temperature) from 1 to 4 d. In another set, the cells were incubat ed with 100 muM hydrogen peroxide (H2O2) for 30 min before harvesting at di fferent time points. The cells were harvested at 1, 2, 3, and 4 d. Cell sur vival was significantly higher at 30 degreesC as compared to 37 degreesC ov er 4 d of incubation. In cells incubated with H2O2, significantly higher ce ll viability was observed at lower temperatures as compared to the cells in cubated at 37 degreesC. The activity of glutathione peroxidase (GSH-Px) als o increased significantly at lower temperatures. Lowered temperature also p rovided a significant increase in the expression of anti-apoptotic protein, bcl-2 after 4 d of incubation. These data suggest that hypothermic conditi ons lowers the risk of oxidative stress-induced cellular damage and program med cell death by increasing the activity of GSH-Px and by the induction in the expression of the anti-apoptotic protein, bcl-2. (C) 2001 Elsevier Sci ence Inc.