Brain-derived neurotrophic factor prevents superoxide anion-induced death of PC12h cells stably expressing TrkB receptor via modulation of reactive oxygen species

In our previous report (Satoh et al., 1999. Regulation of reactive oxygen species by nerve growth factor but not by Bcl-2 as a novel mecahnism of protection of PC12 cells from superoxide anion-induced death. J. Biochem. 125, 952-959), we reported that nerve growth factor (NGF) protected PC12 cells from superoxide anion (O-2(-))-induced cell death through a novel regulation of reactive oxygen species (ROS) which increased O-2(-) and decreased hydrogen peroxide (H2O2), indicating that decreasing conversion from O-2(-) to H2O2 is a critical process for the protection by NGF. In the present study, we performed a comparative study on protective mechanisms between NGF and brain-derived neurotrophic factor (BDNF) using TrkB-expressing PC12h cells. When compared with NGF, BDNF induced a weaker but significant protective effect on the cells from O(2)(-)induced death. BDNF did not seem to change the total amount of ROS in the cells treated with xanthine and xanthine oxidase. On the other hand, BDNF increased O-2(-) and decreased H2O2 levels in the same cells, although not so strongly as NGF. These results suggest that decreasing conversion from O-2(-) to H2O2 is also critical for the protection by BDNF, which is considered to play a central role in survival and differentiation of CNS neurons. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.