Bcl-2 inhibition of neural death: decreased generation of reactive oxygen species

TLDR

The proto‑oncogene Bcl‑2 inhibits apoptotic and necrotic neural cell death. Bcl‑2 expression in GT1‑7 neural cells protects against glutathione‑depletion–induced death by reducing reactive oxygen species and lipid peroxidation, and this protective effect also rescues yeast mutants lacking superoxide dismutase, demonstrating that Bcl‑2 prevents cell death by lowering net ROS generation.

Abstract

The proto-oncogene bcl-2 inhibits apoptotic and necrotic neural cell death. Expression of Bcl-2 in the GT1-7 neural cell line prevented death as a result of glutathione depletion. Intracellular reactive oxygen species and lipid peroxides rose rapidly in control cells depleted of glutathione, whereas cells expressing Bcl-2 displayed a blunted increase and complete survival. Modulation of the increase in reactive oxygen species influenced the degree of cell death. Yeast mutants null for superoxide dismutase were partially rescued by expression of Bcl-2. Thus, Bcl-2 prevents cell death by decreasing the net cellular generation of reactive oxygen species.