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Comparative analysis of DNA repair pathways in mammals.
Author(s) -
Podlutsky Andrej,
Podlutskaya Natalia,
Bakri Imad,
Csiszar Anna,
Ungvari Zoltan,
Austad Steven
Publication year - 2008
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/fasebj.22.1_supplement.1239.32
Subject(s) - biology , rodent , marmoset , dna damage , dna repair , primate , comet assay , longevity , dna , microbiology and biotechnology , base excision repair , genetics , ecology
In our study we used three groups of animals: rodents, wild mice and white footed mice; bats, little brown bat and Brazilian free‐tailed bat; primate, marmoset and humans. These groups have different longevity quotient: rodents (0.8 and 1.6); bats (8.1 and 2.7?); primates (4.2 and 2.3) respectively. We hypothesize that DNA repair ability and DNA stability might correlate with species maximum longevity. In order to study different pathways of DNA repair we treated cells with gamma‐radiation (targeting base excision repair, BER) or UV‐C light (targeting nucleotide excision repair, NER). We monitored cell survival as well as DNA‐damage level with comet‐assay. Our results indicate that bat's cells are similar to primate cells following gamma radiation – they survive better and have less damage then rodent's cells. This suggests that bats and primates have superior BER compared with rodents. However, following UV‐C treatment, bat's cells are similar to rodent's cells – they are very sensitive to UV‐type of damage; at same time both primate species show comparable resistance to UV, superior to rodent or bat. These results are indicating that NER pathway is not efficient in repairing DNA in rodents and bats. Study with caspase activation and ROS production are supporting our conclusion ‐ exceptional bat's longevity is not dependant from NER pathway.