The provided references cover a range of studies on the effects of superoxide dismutase (SOD) gene knockout in mice, focusing on various phenotypes and biological consequences. Key findings include: 1. **Oxygen Toxicity and Sensitivity**: Heterozygous Sod2 mutant mice are more sensitive to oxygen toxicity (Asikainen et al., 2002). 2. **Oxidative Stress and DNA Methylation**: Superoxide dismutase 1 (SOD1) knockdown induces oxidative stress and DNA methylation loss in the prostate (Bhusari et al., 2010). 3. **Hyperoxia Sensitivity**: Mice lacking extracellular SOD are more sensitive to hyperoxia (Carlsson et al., 1995). 4. **Post-Natal Development and Lactation**: Manganese SOD is dispensable for post-natal development and lactation in the murine mammary gland (Case and Domann, 2012). 5. **T Cell Development and Immune Responses**: Elevated mitochondrial superoxide disrupts normal T cell development and impairs adaptive immune responses to influenza (Case et al., 2011). 6. **Hematopoietic Stem Cells**: Manganese SOD depletion in murine hematopoietic stem cells perturbs iron homeostasis, globin switching, and epigenetic control in erythrocyte precursor cells (Case et al., 2013). 7. **Hepatocarcinogenesis**: CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life (Echuru et al., 2005). 8. **Motor Axonopathy**: Absence of SOD1 leads to oxidative stress in peripheral nerve and causes a progressive distal motor axonopathy (Fischer et al., 2012). 9. **Neuromuscular Junctions**: Hindlimb motor neurons require CuZn superoxide dismutase for maintenance of neuromuscular junctions (Flood et al., 1999). 10. **Olfactory Sexual Signaling**: Superoxide dismutase deficiency impairs olfactory sexual signaling and alters bioenergetic function in mice (Garratt et al., 2014). 11. **Acute Lung Damage**: Loss of extracellular SOD leads to acute lung damage in the presence of ambient air, potentially underlying adult respiratory distress syndrome (Gongora et al., 2008). 12. **Dilated Cardiomyopathy**: Genetic modification of prenatal lethality and dilated cardiomyopathy in Mn SOD mutant mice (Huang et al., 2001). 13. **Tissue-Specific Deletion**: Model mice for tissue-specific deletion of the MnThe provided references cover a range of studies on the effects of superoxide dismutase (SOD) gene knockout in mice, focusing on various phenotypes and biological consequences. Key findings include: 1. **Oxygen Toxicity and Sensitivity**: Heterozygous Sod2 mutant mice are more sensitive to oxygen toxicity (Asikainen et al., 2002). 2. **Oxidative Stress and DNA Methylation**: Superoxide dismutase 1 (SOD1) knockdown induces oxidative stress and DNA methylation loss in the prostate (Bhusari et al., 2010). 3. **Hyperoxia Sensitivity**: Mice lacking extracellular SOD are more sensitive to hyperoxia (Carlsson et al., 1995). 4. **Post-Natal Development and Lactation**: Manganese SOD is dispensable for post-natal development and lactation in the murine mammary gland (Case and Domann, 2012). 5. **T Cell Development and Immune Responses**: Elevated mitochondrial superoxide disrupts normal T cell development and impairs adaptive immune responses to influenza (Case et al., 2011). 6. **Hematopoietic Stem Cells**: Manganese SOD depletion in murine hematopoietic stem cells perturbs iron homeostasis, globin switching, and epigenetic control in erythrocyte precursor cells (Case et al., 2013). 7. **Hepatocarcinogenesis**: CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life (Echuru et al., 2005). 8. **Motor Axonopathy**: Absence of SOD1 leads to oxidative stress in peripheral nerve and causes a progressive distal motor axonopathy (Fischer et al., 2012). 9. **Neuromuscular Junctions**: Hindlimb motor neurons require CuZn superoxide dismutase for maintenance of neuromuscular junctions (Flood et al., 1999). 10. **Olfactory Sexual Signaling**: Superoxide dismutase deficiency impairs olfactory sexual signaling and alters bioenergetic function in mice (Garratt et al., 2014). 11. **Acute Lung Damage**: Loss of extracellular SOD leads to acute lung damage in the presence of ambient air, potentially underlying adult respiratory distress syndrome (Gongora et al., 2008). 12. **Dilated Cardiomyopathy**: Genetic modification of prenatal lethality and dilated cardiomyopathy in Mn SOD mutant mice (Huang et al., 2001). 13. **Tissue-Specific Deletion**: Model mice for tissue-specific deletion of the Mn