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By pumping the accumulated, unbound cytosolic catecholamines backward across the plasma membrane and safely into the extracellular synaptic space, the neuron is able to maintain its free cytoplasmic neurotransmitter levels below toxic thresholds , directly protecting itself from oxidative cell death and preserving neuronal viability (Underhill et al., 2021)

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Decreased glutathione and low catalase activity contribute to oxidative stress in children with alpha-1 antitrypsin deficiency

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