Table S2 summarizes the gene knockout mouse models and their phenotypes related to superoxide dismutase (SOD) genes. The SOD family includes SOD1 (Cu/ZnSOD), SOD2 (MnSOD), and extracellular SOD (ecSOD). These enzymes play critical roles in scavenging reactive oxygen species (ROS) and maintaining cellular redox balance. The following studies describe the effects of SOD gene knockouts in mice: - **SOD1 knockout mice** exhibit oxidative stress, impaired neurotransmitter release, neuromuscular junction destabilization, and reduced muscle strength. They also show increased DNA damage and cancer incidence, but no accelerated aging. SOD1 deficiency leads to motor neuron dysfunction and enhanced cell death after axonal injury. - **SOD2 knockout mice** show increased sensitivity to oxygen toxicity, impaired mitochondrial function, and altered apoptosis. Heterozygous SOD2 knockout mice display cardiac mitochondrial dysfunction. - **Extracellular SOD (ecSOD) knockout mice** experience oxidative stress in peripheral nerves, leading to progressive distal motor axonopathy. They also show impaired neuromuscular junction maintenance and increased susceptibility to oxidative stress in the gastric mucosa. - **Manganese SOD (MnSOD) knockout mice** exhibit mitochondrial dysfunction, increased oxidative stress, and hepatocarcinogenesis. Conditional MnSOD knockout in skeletal muscle increases oxidative stress and reduces aerobic exercise capacity. - **SOD1 and SOD2 knockout mice** show various phenotypes, including impaired ovarian function, delayed wound healing, and age-related macular degeneration-like symptoms. Some models show accelerated aging, increased cellular senescence, and reduced exercise capacity. These studies highlight the critical roles of SOD enzymes in maintaining cellular homeostasis and preventing oxidative damage, with significant implications for human diseases such as neurodegeneration, cardiovascular disease, and cancer.Table S2 summarizes the gene knockout mouse models and their phenotypes related to superoxide dismutase (SOD) genes. The SOD family includes SOD1 (Cu/ZnSOD), SOD2 (MnSOD), and extracellular SOD (ecSOD). These enzymes play critical roles in scavenging reactive oxygen species (ROS) and maintaining cellular redox balance. The following studies describe the effects of SOD gene knockouts in mice: - **SOD1 knockout mice** exhibit oxidative stress, impaired neurotransmitter release, neuromuscular junction destabilization, and reduced muscle strength. They also show increased DNA damage and cancer incidence, but no accelerated aging. SOD1 deficiency leads to motor neuron dysfunction and enhanced cell death after axonal injury. - **SOD2 knockout mice** show increased sensitivity to oxygen toxicity, impaired mitochondrial function, and altered apoptosis. Heterozygous SOD2 knockout mice display cardiac mitochondrial dysfunction. - **Extracellular SOD (ecSOD) knockout mice** experience oxidative stress in peripheral nerves, leading to progressive distal motor axonopathy. They also show impaired neuromuscular junction maintenance and increased susceptibility to oxidative stress in the gastric mucosa. - **Manganese SOD (MnSOD) knockout mice** exhibit mitochondrial dysfunction, increased oxidative stress, and hepatocarcinogenesis. Conditional MnSOD knockout in skeletal muscle increases oxidative stress and reduces aerobic exercise capacity. - **SOD1 and SOD2 knockout mice** show various phenotypes, including impaired ovarian function, delayed wound healing, and age-related macular degeneration-like symptoms. Some models show accelerated aging, increased cellular senescence, and reduced exercise capacity. These studies highlight the critical roles of SOD enzymes in maintaining cellular homeostasis and preventing oxidative damage, with significant implications for human diseases such as neurodegeneration, cardiovascular disease, and cancer.