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This review examines the molecular mechanisms underlying ASM-associated oxidative stress in clinical, non-kindled/kindled preclinical, as well as non-epilepsy models, and highlights evidence demonstrating the ability of ascorbic acid to attenuate ROS accumulation, enhance endogenous antioxidant defenses, and modulate redox-sensitive signaling pathways implicated in epileptogenesis and ASM-induced toxicity

Fluorescent sensors that are responsive only in a specific subcellular location have remained elusive

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