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Most experimental evidence supports the role of mitochondria as the main target intracellular organelle for H 2 O 2 toxicity, and excessive ROS accumulation due to oxidative stress is one of the mechanisms leading to apoptosis associated with mitochondrial injury [1,2]

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Increased seizure activity in the brain leads to the activation of NADPH oxidases and lipoxygenases, as well as a rise in the intracellular calcium level, which stimulates the production of ROS and lipid peroxidation (Sun et al., 2022)