Abstract
Many studies have demonstrated the protective effects of Bcl-x L against both apoptotic and necrotic cell death, but the mode of action of Bcl-x L remains unclear. This work analyzed effects of Bcl-x L overexpression on cellular levels of reactive oxygen species (ROS), intracellular calcium ([Ca 2+] i), and mitochondrial membrane potential (ΔΨ m) in cultured mouse primary astrocytes after exposure to glucose deprivation (GD) or hydrogen peroxide (H 2O 2). Upon exposure to GD or H 2O 2, uninfected and Lac-Z-expressing astrocytes showed an immediate, rapid increase in ROS accumulation that was slowed and or reduced by Bcl-x L. Changes in ΔΨ m in response to the two insults differed. H 2O 2 induced a decrease in ΔΨ m that was initially greater in Bcl-x L cells, but then held stable. ΔΨ m in control and Lac-Z-expressing cells initially declined more slowly, but after about 20 min showed rapid deterioration. Five hours of GD caused mitochondrial membrane hyperpolarization followed by a decrease in ΔΨ m, which was not observed with Bcl-x L overexpression. Bcl-x L failed to inhibit the calcium dysregulation seen in control cells exposed to 400 μM H 2O 2, but still improved cell survival. There was no increase in [Ca 2+] i with 5 h of GD. These data thus dissociate the effect of Bcl-x L on calcium homeostasis from effects on ROS, ΔΨ m, and for H 2O 2 exposure, cell survival.
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