Phenotypes Associated with This Genotype

Genotype
MGI:3639892

• Allelic Composition: Sod2^tm1Cje/Sod2⁺
• Genetic Background: B6.Cg-Sod2^tm1Cje/Mmmh

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

mortality/aging

mortality/aging ( J:87514 )

N • no difference in life span or biochemical and physiological indices of aging are detected

neoplasm

increased tumor incidence ( J:87514 )

• more than 80% have neoplastic lesions by 26-28 months of age compared to 41% of wild-type mice; however the types and severity of lesions are similar to those in wild-type mice

• the incidence of mice with multiple tumor types is increased to 66.6% compared to 18.5% in wild-type mice

increased lymphoma incidence ( J:87514 )

• incidence is increased to 61% compared to 22% in wild-type mice

cellular

abnormal mitochondrial physiology ( J:108637 )

• aconitase and NADH-oxidoreductase (with CoQ as a substrate) activities are reduced by 35% and 45%, respectively, in hearts; however, mitochondrial fumerase and cytosolic aconitase and glutamine synthetase activities are not reduced

• the speed of induction of permeability transition by calcium is significantly increased in heart mitochondria

abnormal respiratory electron transport chain ( J:108637 )

• the respiratory control ratio for complex I and state 3 respiration (with glutamate and malate as substrates) are reduced by 37%; however, state 4 respiration is similar to controls

oxidative stress ( J:87514 , J:108637 )

• significantly higher levels of oxidative DNA damage (measured as 8oxodG) are detected in mitochondrial and nuclear DNA at all ages examined (J:87514)

• treatment with 50 mg paraquat / kg resulted in loss of 30% of heterozygotes within 4 days, unlike wild-type mice which all survived (J:87514)

• increased cardiomyocyte apoptosis after treatment with t-BuOOH to induce oxidative stress compared to controls but less than in homozygous cells (J:108637)