LOW EFFICIENCY OF DNA REPAIR SYSTEMS IN MITOCHONDRIA. A REVIEW
A. I. Gaziev, A. Ya. Podlutsky
Institute of Theoretical and Experimental Biophysics RAS, Pushchino;
e-mail: gaziev@venus.iteb.serpukhov.su
Under the action of endogenous reactive oxygen species and exogenous chemical and physical agents, significantly
more lesions occur in mitochondrial DNA (mtDNA) than in nuclear DNA (nDNA). However, the mechanisms of DNA repair
in mitochondria are less efficient that in the nuclei. The mechanisms of nucleotide excision repair capable of
removing UV-induced lesions or other complex adducts induced by chemical compounds are not operative in
mitochondria at all. At the same time, mitochondria of some kinds contain a photoreactivation enzyme providing
monomerization of cyclobutane pyrimidine dimers. Also, the enzyme system for DNA base excision repair (BER) and
O6-alkylguanine-DNA alkyl transferase are functional in mitochondria. However, the rate of
BER-controlled repair of lesions in mtDNA is lower than that in nDNA. The literature data suggest that the
controlling system for the delay of DNA replication till the repair complection (cell cycle checkpoint) cannot be
provided in mitochontria. Besides, it remains unclear whether the mismatch repair mechanisms are operable in
mammalian mitochondria. On the other hand, double-strand breaks in mammalian mtDNA are possibly repaired by
involving the DNA-dependent protein kinase complex, and the process of BER is affected by poly(ADP-ribosyl)ation
of proteins. Possible consequences of induction of the increased level of damage in mtDNA and the low efficiency
of repair systems in mitochondria are discussed in this review.
Key words: mitochondia, mtDNA damage and repair, repair systems, mtDNA mutations and deletions,
aging
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