Conclusion

Aging is a complex multifactorial process that we are only beginning to understand. Although the current evidence strongly suggests that mitochondria play a role in this process, there appears to be a wide range of opinions as to the exact nature of the involvement of mtDNA in aging. Contradictory data make it difficult to reach a consensus on the rates and precise mechanisms of ROS generation with aging. Unavailability of experimental tools that allow for the discrimination of the effects resulting from oxidative damage to mtDNA from the consequences of oxidative damage to other mitochondrial components adds another layer of difficulty. The lack of validated animal models of mitochondrial aging further complicates progress in this area of aging research. However, a recent report on the generation of mice with a mitochondrial mutator phenotype (Trifunovic et al., 2004) may represent an important advance. Clearly, more research must be done to fully elucidate how oxidative damage to mtDNA contributes to the aging process. It is possible that the seemingly contradictory results of different studies will be reconciled or explained through the use of integrative approaches and unified model systems.

D Loop

Chr17-81%

Chr5-86%

Chr5-93%

Chr5-88%

D Loop

Chr17-81%

Chr5-86%

Chr5-93%

Chr5-88%

ChrX-92%

Chr17-82%

Chr1-97%

ChrX-92%

Chr17-82%

Chr1-97%

Chr14-82% Chr17-83% ChrX-83% Chr5-84% Chr17-87% Chr7-83% Chr1-84% Chr9-85% Chr5-93% Chr11-93% Chr7-85% Chr9-85% Chr3-94% Chr17-87% Chr9-84% Chr6-89% Chr7-87% Chr1-83% Chr17-83%

Chr14-93% Chr1-98% Chr2-83% ChrX-92% Chr5-80% Chr17-83% Chr17-96% Chr5-89% Chr3-83%

D Loop

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Figure 41.3 Distribution of regions of nuclear DNA homology over human and mouse mitochondrial genomes. Arrows indicate the orientation of insert, and Chr#A-#B% indicate the site of integration (chromosome #A) and the extent of homology (B%).
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