LEADER 01969nam 2200373 450 001 9910688183903321 005 20230626213347.0 035 $a(CKB)5850000000050203 035 $a(NjHacI)995850000000050203 035 $a(EXLCZ)995850000000050203 100 $a20230626d2022 uy 0 101 0 $aeng 135 $aur||||||||||| 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aMutagenesis and Mitochondrial-Associated Pathologies /$fMichael Fasullo, Angel Catala, editors 210 1$aLondon :$cIntechOpen,$d2022. 215 $a1 online resource (116 pages) 311 $a1-80355-173-9 330 $aReactive oxygen species (ROS) and DNA double-strand breaks can result from mitochondrial defects and external sources, such as ionizing radiation. If not repaired properly, pathogenic mutations are generated. Human diseases resulting from inherited mitochondrial defects manifest in organs that physiologically require a high level of ATP synthesis. These diseases are clinically challenging, but new experimental clinical therapies include gene editing and mitochondrial transplants. Pathogenic ROS-associated cellular damage includes DNA double-strand breaks, and mouse models are now available to study multiple repair pathways. This book discusses the clinical manifestations of mitochondrial diseases in both the eye and the kidney, and presents new insights into double-strand break repair pathways and developmental phenotypes of g-ray-associated ontogenic mutations of Drosophila melanogaste. 606 $aDNA damage 606 $aMutagenicity testing 615 0$aDNA damage. 615 0$aMutagenicity testing. 676 $a616.042 702 $aCatala$b Angel 702 $aFasullo$b Michael 801 0$bNjHacI 801 1$bNjHacl 906 $aBOOK 912 $a9910688183903321 996 $aMutagenesis and Mitochondrial-Associated Pathologies$92903154 997 $aUNINA