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Base excision repair capacity in mitochondria and nuclei: tissue‐specific variations
Author(s) -
Karahalil Bensu,
Hogue Barbara A.,
SouzaPinto Nadja C.,
Bohr Vilhelm A.
Publication year - 2002
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.02-0463com
Subject(s) - dna glycosylase , uracil dna glycosylase , mutyh , mitochondrial dna , biology , dna repair , mitochondrion , ap site , base excision repair , cytochrome c oxidase , nucleotide excision repair , biochemistry , ap endonuclease , xrcc1 , dna damage , microbiology and biotechnology , dna , gene , genotype , single nucleotide polymorphism
Base excision repair is the main pathway for repair of oxidative base lesions in DNA. Mammalian cells must maintain genomic stability in their nuclear and mitochondrial genomes, which have different degrees of vulnerability to DNA damage. This study quantifies DNA glycosylase activity in mitochondria and nucleus from C57/BL 6 mouse tissues including brain, liver, heart, muscle, kidney, and testis. The activities of oxoguanine DNA glycosylase (OGG1), uracil DNA glycosylase, and endonuclease III homologue 1 (NTH1) were measured using oligonucleotide substrates with DNA lesions specific for each glycosylase. Mitochondrial content was normalized to citrate synthase activity and mitochondrial function was assessed by measuring cytochrome c oxidase (COX) activity. In nuclear and mitochondrial extracts, the highest DNA glycosylase activities were in testis. Brain and heart, tissues with the highest oxidative load, did not have higher levels of OGG1 or NTH1 activity than muscle or kidney, which are more glycolytic tissues. In general, mitochondrial extracts have lower DNA glycosylase activity than nuclear extracts. There was no correlation between glycosylase activities in the mitochondrial extracts and COX activity, suggesting that DNA repair enzymes may be regulated by a mechanism different from this mitochondrial enzyme.—Karahalil, B., Hogue, B. A., de Souza‐Pinto, N. C., Bohr, V. A. Base excision repair capacity in mitochondria and nuclei: tissue‐specific variations. FASEB J. 16, 1895–1902 (2002)