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A hypothetical model depicting C26:0 injury in oligodendrocytes leading to the depletion of mtGSH. The loss of mtGSH predisposed cells to oxidant injury resulting in increased ROS accumulation, alteration of mitochondria inner membrane potential (∆ψm), and finally cell death. NAC treatment prevented the mitochondrial toxicity of C26:0 by replenishing mtGSH and thus protected cells from additional oxidative stress and death.
