Lung cancer increases H2O2 concentration in the exhaled breath condensate, extent of mtDNA damage, and mtDNA copy number in buccal mucosa
Natalya A. Kolbasina,
Artem P. Gureev,
Olga V. Serzhantova,
Andrey A. Mikhailov,
Ivan P. Moshurov,
Anatoly A. Starkov,
Vasily N. Popov
Affiliations
Natalya A. Kolbasina
Department of Genetics, Cytology and Bioengineering, Voronezh State University, Voronezh, Russia
Artem P. Gureev
Department of Genetics, Cytology and Bioengineering, Voronezh State University, Voronezh, Russia
Olga V. Serzhantova
Department of Genetics, Cytology and Bioengineering, Voronezh State University, Voronezh, Russia; Voronezh Regional Clinical Oncological Dispensary, Voronezh, Russia
Andrey A. Mikhailov
Department of Genetics, Cytology and Bioengineering, Voronezh State University, Voronezh, Russia; Voronezh Regional Clinical Oncological Dispensary, Voronezh, Russia
Ivan P. Moshurov
Voronezh Regional Clinical Oncological Dispensary, Voronezh, Russia
Anatoly A. Starkov
Brain and Mind Research Institute, Weill Medical College of Cornell University, New York, NY, USA; Corresponding author.
Vasily N. Popov
Department of Genetics, Cytology and Bioengineering, Voronezh State University, Voronezh, Russia; Voronezh State University of Engineering Technologies, Voronezh, Russia
We have shown that the H2O2 concentration in exhaled breath condensate (EBC) in lung cancer patients increases significantly compared to the EBC of healthy people and revealed the correlation between the H2O2 level in the EBC and amount of mtDNA damage in buccal mucosa cells. The H2O2 hyper-production may trigger mitochondrial biogenesis, thereby resulting in an increase in mtDNA copy number. However, we did not observe a significant difference in the studied parameters between smokers and non-smokers. Overall, our data suggest that H2O2 concentration in the EBC, the extent of mtDNA damage, and mtDNA copy number in buccal mucosa could be potential as an early diagnostic marker of lung cancer.
