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"Deficiencies in inhibitory neurotransmission (e.g., glycine) can result in excessive excitation or reduced inhibition within neural pathways, resulting in seizures and epilepsy disorders."

established a mouse model of ROS overproduction by SOD2 expression knockdown, and in their observations, they reported that a compensatory adaptive metabolic mechanism exists in young mouse oocytes and that this compensatory mechanism is not sufficient to maintain the stability of mtDNA when mitochondrial dysfunction is caused by the accumulation of ROS

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