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- W204961972 startingPage "59" @default.
- W204961972 abstract "Many mutations of the human mitochondrial genome may be the result of mitochondrial oxidative stress (OS), which increases with the age of the individual as well as in correlation with specific diseases. Accumulation of alterations of the mitochondrial DNA (mtDNA) can impair the bioenergetic function of mitochondria in the affected host cells significantly. Because all the proteins encoded by the mtDNA are essential for the execution of normal oxidative phosphorylation, disintegration of the mitochondrial genome would cause severe problems with respect to cellular functions and viability. The increase of mtDNA mutagenesis depends on the capability of repair of damage to mtDNA in the mitochondrium. Several reports have documented repair of some types of mtDNA damage, such as alkylation base damage induced by various agents, cisplatin interstrand cross-links (ICLs), and oxidative lesions induced by hydrogen peroxide. The analysis of human mtDNA is also becoming increasingly important in forensic sciences. This chapter summarizes the recent results and investigations in mitochondrial genetics and maintenance and their application possibilities in pathological and forensic medicine with special regard to mitochondrial mutagenesis in the brain." @default.
- W204961972 created "2016-06-24" @default.
- W204961972 creator A5090723208 @default.
- W204961972 date "2007-01-01" @default.
- W204961972 modified "2023-09-23" @default.
- W204961972 title "Mitochondrial Mutagenesis in the Brain in Forensic and Pathological Research" @default.
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