Autor: |
Alimova AA; Department of Genetics, Cytology and Bioengineering, Voronezh State University, 394018 Voronezh, Russia., Sitnikov VV; Department of Genetics, Cytology and Bioengineering, Voronezh State University, 394018 Voronezh, Russia.; Laboratory of Metagenomics and Food Biotechnology, Voronezh State University of Engineering Technologies, 394036 Voronezh, Russia., Pogorelov DI; Department of Genetics, Cytology and Bioengineering, Voronezh State University, 394018 Voronezh, Russia., Boyko ON; Department of Genetics, Cytology and Bioengineering, Voronezh State University, 394018 Voronezh, Russia., Vitkalova IY; Department of Genetics, Cytology and Bioengineering, Voronezh State University, 394018 Voronezh, Russia.; Laboratory of Metagenomics and Food Biotechnology, Voronezh State University of Engineering Technologies, 394036 Voronezh, Russia., Gureev AP; Department of Genetics, Cytology and Bioengineering, Voronezh State University, 394018 Voronezh, Russia.; Laboratory of Metagenomics and Food Biotechnology, Voronezh State University of Engineering Technologies, 394036 Voronezh, Russia., Popov VN; Department of Genetics, Cytology and Bioengineering, Voronezh State University, 394018 Voronezh, Russia.; Laboratory of Metagenomics and Food Biotechnology, Voronezh State University of Engineering Technologies, 394036 Voronezh, Russia. |
Abstrakt: |
It is well known that pesticides are toxic for mitochondria of animals. The effect of pesticides on plant mitochondria has not been widely studied. The goal of this research is to study the impact of metribuzin and imidacloprid on the amount of damage in the mtDNA of potato ( Solanum tuberosum L.) in various conditions. We developed a set of primers to estimate mtDNA damage for the fragments in three chromosomes of potato mitogenome. We showed that both metribuzin and imidacloprid considerably damage mtDNA in vitro. Imidacloprid reduces the rate of seed germination, but does not impact the rate of the growth and number of mtDNA damage in the potato shoots. Field experiments show that pesticide exposure does not induce change in aconitate hydratase activity, and can cause a decrease in the rate of H 2 O 2 production. We can assume that the mechanism of pesticide-induced mtDNA damage in vitro is not associated with H 2 O 2 production, and pesticides as electrophilic substances directly interact with mtDNA. The effect of pesticides on the integrity of mtDNA in green parts of plants and in crop tubers is insignificant. In general, plant mtDNA is resistant to pesticide exposure in vivo, probably due to the presence of non-coupled respiratory systems in plant mitochondria. |