MnSOD (Sod2) is a major antioxidant for the conversion of superoxide produced in the mitochondria during respiration. It has also been shown to be important in protecting the mtiochondria and the cell from irradiation damage. These mice may be useful for studying the role of antioxidants in cellular metabolism aging and in the functioning of the mitochondria.
MnSODtet functions as a knockout allele (abolishes MnSOD expression) in the absence of doxycycline (dox). Both male and female heterozygous (MnSODtet/+) mice are viable and fertile with normal phenotype, regardless of doxycycline treatment. The donating investigator reports that in the absence of dox, homozygous (MnSODtet/tet) newborn mice die within seven days of birth, similar to MnSOD knockout mice. Homozygous mice are smaller than heterozygous or wildtype littermates until weaning, and are similar sized thereafter. At around 5 to 6 weeks of age, homozygotes can be taken off dox and are able to maintain body weight and health for at least one month. The donating investigator also reports that when breeding heterozygotes together, 1 of 10 homozygous pups given dox will survive to weaning. Administration of dox water to nursing dams does not lead to increased survival of homozygous pups; the most effective way to keep homozygous pups alive is by dox injection. Homozygous mice on dox are fertile but have fewer litters.

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MnSODtet functions as a knockout allele (abolishes MnSOD expression) in the absence of doxycycline. MnSODtet mice may be useful for studying the role of antioxidants in cellular metabolism and aging, and in mitochondria function.

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B6N.129S6-Sod2<tm1(rtTA*M2 tetO)Jsg>/J Frozen Embryo