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However, when ROS levels rise beyond the capacity of antioxidants, they can damage cellular macromolecules, disrupt normal cell functions, trigger mitochondria to produce pro-apoptotic proteins, and ultimately lead to the apoptosis of central nervous system neurons (Schieber and Chandel, 2014)

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760 These results together suggest that ACSL4 and LOX-catalyzed lipid peroxidation is involved in cerebral I/R injury, and inhibition of ACSL4 and LOX activity may be therapeutic targets for cerebral I/R injury