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While copper may contribute to intracellular oxidative stress by participating in the Fenton and Haber-Weiss reactions or by interfering with iron homeostasis, either directly or indirectly through the formation of hydroxyl radicals, experimental evidence linking copper deficiency and the formation of SOD1 aggregates to the progression of PD is also discussed in terms of its therapeutic implications (119,120)

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Metabolic parameters including energy expenditure, RER, locomotor activity, and cumulative food intake were continuously recorded and analyzed