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Under low-oxygen conditions, mitochondrial electron transport chain dysfunction and hypoxia-induced activation of oxidases [478] synergistically drive pathological ROS accumulation [479] that overwhelms cellular antioxidant defenses

Oxidative phosphorylation is disrupted at complex I and II in GSH-deficient follicular B cells To determine whether the accumulation of succinate in Gclc -deficient FoB was caused by a dysfunctional ETC, we assessed the respiratory parameters of each ETC complex