Analysis of Mitochondrial DNA Somatic Mutations in OXYS and Wistar Strain Rats

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U. N. Rotskaya¹, I. B. Rogozin¹, E. A. Vasyunina¹, N. G. Kolosova¹, B. A. Malyarchuk², G. A. Nevinsky^1,3, and O. I. Sinitsyna^1*

¹Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Sciences, pr. Lavrent’eva 10, 630090 Novosibirsk, Russia; fax: (383) 333-1278; E-mail: olgasin1@yandex.ru; olgasin@niboch.nsc.ru

²Institute of Biological Problems of the North, Far-Eastern Division of the Russian Academy of Sciences, ul. Portovaya 18, 685000 Magadan, Russia

³Institute of Chemical Biology and Fundamental Medicine, Siberian Division of the Russian Academy of Sciences, pr. Lavrent’eva 8, 630090 Novosibirsk, Russia

^* To whom correspondence should be addressed.

Received February 7, 2008; Revision received March 18, 2008

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Rats of the OXYS strain are sensitive to oxidative stress and serve as a biological model of premature aging. We have compared spectra of somatic mutations in a control region of mtDNA from the liver of the OXYS rat strain and of Wistar rats as a control. The majority of nucleotide substitutions in the mutation spectra were represented by transitions: 94 and 97% in the OXYS and Wistar rats, respectively. It was shown that 40% of somatic mutations in the control region of mtDNA from Wistar rats were significantly consistent with the model of dislocation mutagenesis. No statistical support for this model was found for mutations in the control region of mtDNA from OXYS rats. The mutation frequency in the ETAS section was higher in the OXYS strain rats than in Wistar rats. These results suggest different mechanisms of mutagenesis in the two rat strains under study.

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KEY WORDS: OXYS rats, Wistar rats, somatic mutations, mtDNA, liver

DOI: 10.1134/S0006297909040117

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