By Douglas C. Wallace (auth.), William C. Copeland (eds.)
Nationwide Institutes of health and wellbeing, learn Triangle Park, NC. positive aspects confirmed equipment for interpreting mitochondrial DNA and the proteins that continue it; remedy of the genetics, biochemistry, and mobile biology of mtDNA; most modern advancements in making use of PCR expertise to the research of mtDNA; and identity of mtDNA mutations.
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Additional resources for Mitochondrial DNA: Methods and Protocols
ANTIOXIDANT THERAPY OF SOD2-DEFICIENT MICE RESCUES CARDIOMYOPATHY THE To confirm that the toxicity of the MnSOD deficiency was caused by the toxicity of mitochondrial O2•–, Sod2tm1Cje –/– mice on the CD1 background were treated by peritoneal injection of the catalytic antioxidant SOD mimetic, MnTBAP [manganese 5,10,15,20-tetrakis (4-benzoic acid) porphyrin]. Peritoneal injection of MnTBAP into Sod2 –/– animals rescued them from their lethal dilated cardiomyopathy, reduced the liver lipid deposition, and extended the mean life-span of the animals to about 16 d of age.
These animals also had increased oxidative damage to their DNA, with the greatest extent and level of base adducts being found in the heart, followed by the brain and then the liver (237). This later observation adds credence to the hypothesis that the primary cause of mtDNA rearrangement mutations in aging and the adPEO patients is oxidative damage to the mtDNA. 3. ANTIOXIDANT THERAPY OF SOD2-DEFICIENT MICE RESCUES CARDIOMYOPATHY THE To confirm that the toxicity of the MnSOD deficiency was caused by the toxicity of mitochondrial O2•–, Sod2tm1Cje –/– mice on the CD1 background were treated by peritoneal injection of the catalytic antioxidant SOD mimetic, MnTBAP [manganese 5,10,15,20-tetrakis (4-benzoic acid) porphyrin].
Still, this latter possibility Animal Models for Mitochondrial Disease 21 does not explain the high levels of rearranged mtDNAs that accumulated in the mouse or the low level of duplicated molecules that were reported. The alternative possibility is that the mouse may be more tolerant of mitochondrial defects than humans. This alternative is supported by the mouse’s greater tolerance of ANT1 deficiency (27) than is seen in human (134). Many different mtDNA mutations will need to be introduced into the mouse before these alternatives can be distinguished.