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Therapeutics based on mitochondrial dysfunction and oxidative stress, such as mitochondria-targeted antioxidant [10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cyclohexadien-1-yl)decyl]triphenylphosphonium methanesulfonate (MitoQ), modify disease progression by slowing the decline of mitochondrial function and disease progression in the SOD1 G93A mouse model of ALS (Miquel et al., 2014)

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Users should maintain consistent injection timing and technique throughout this assessment period to establish baseline response patterns

5.2 Flavonoid biosynthetic regulation and metabolic stabilization Abiotic stress disrupts metabolic homeostasis not only through excessive ROS accumulation but also by impairing enzyme activity, protein stability, and the coordination of metabolic pathways (Zhao et al., 2025)