Table 1.

Summary of Sod2 knockout mouse models and their resulting phenotypes generated to date.

Knockout Target	Phenotype
Homozygous whole animal knockout	Neonatal lethality [4, 5], reduced succinate dehydrogenase and aconitase activities [5], dilated cardiomyopathy [5], impairment of mitochondrial function in organs with high demand for oxidative metabolism including heart, liver, skeletal muscle, and hematopoietic cells [4, 5].
Heterozygous whole animal knockout	Increased superoxide production and mitochondrial injury [46], increased oxidative stress-induced mitochondria-mediated apoptosis [25].
Liver	No gross histological abnormalities [47], spontaneous oxidative damage (i.e. lipid peroxidation) in liver not detected.
Mammary gland	Embryonic knockout: maturation arrest, hyperplastic epithelium [48], Post-natal knockout: no apparent abnormalities associated with loss of Sod2 [10].
Skeletal muscle	Reduced aerobic exercise capacity and decreased mitochondrial enzyme function; damage to glycolytic muscle fibers [49].
Hematopoietic stem cells	Inactivation of metabolic enzymes and iron homeostasis, improper heme formation and impaired erythrocyte development [7].
T-cells	Increase in superoxide and mitochondria-mediated apoptosis, reduced mitochondrial enzyme function [6].