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Mitochondrial respiratory chain (RC) deficits, resulting in augmented mitochondrial ROS (mROS) generation, underlie pathogenesis of astrocytes. However, mtDNA-depleted cells (  ρ    0 ) lacking RC have been reported to be either sensitive or resistant to apoptosis. In this study, we sought to determine the effects of RC-enhanced mitochondrial stress following oxidative insult. Using noninvasive fluorescence probe-coupled laser scanning imaging microscopy, the ability to resist oxidative stress and levels of mROS formation and mitochondrial calcium (mCa 2+ ) were compared between two different astrocyte cell lines, control and   ρ    0  astrocytes, over time upon oxidative stress. Our results showed that the cytoplasmic membrane becomes permeated with YO-PRO-1 dye at 150 and 130 minutes in RBA-1 and   ρ    0  astrocytes, respectively. In contrast to RBA-1, 30 minutes after 20 mM H 2 O 2  exposure,   ρ    0  astrocytes formed marked plasma membrane blebs, lost the ability to retain Mito-R, and showed condensation of nuclei. Importantly, H 2 O 2 -induced ROS and accompanied mCa 2+  elevation in control showed higher levels than   ρ    0  at early time point but vice versa at late time point. Our findings underscore dual phase of RC-defective cells harboring less mitochondrial stress due to low RC activity during short-term oxidative stress but augmented mROS-mediated mCa 2+  stress during severe oxidative insult.

oxidative medicine and cellular longevity

Dual Phases of Respiration Chain Defect-Augmented mROS-Mediated mCa2+Stress during Oxidative Insult in Normal andρ0RBA1 Astrocytes