High Doses of Pesticides Induce mtDNA Damage in Intact Mitochondria of Potato In Vitro and Do Not Impact on mtDNA Integrity of Mitochondria of Shoots and Tubers under In Vivo Exposure.

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 H2O2 production. We can assume that the mechanism of pesticide-induced mtDNA damage in vitro is not associated with H2O2 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.

The effect of pesticides on the mtDNA integrity and bioenergetic properties of potato mitochondria.

Potato (Solanum tuberosum L.) is one of the most common crops in the world, and it is very susceptible to a wide range of pests such as insects and fungi. The use of pesticides often results in the suppression of seed germination and plant growth, in particular, due to their effect on the respiratory chain of mitochondria. There are numerous studies of the effect of pesticides on animal mitochondria, but their interference with the electron transport in plant mitochondria is not well documented. We present the data showing that a number of pesticides inhibit electron flow, and other pesticides uncouple the respiratory chain. Among the studied pesticides engaging the alternative pathways of electron transport, dithianon led to an increase in the rate of H2O2 production but did not cause a strong increase in the amount of mtDNA damage as compared to other pesticides. In general, the main negative effect of the studied pesticides is manifested in a decrease of membrane potential with the maintenance of the rate of oxygen consumption and a low rate of H2O2 production. The mtDNA damage is caused mainly by pesticides belonging to the pyrethroid class and remains minor as compared to its damage in animals. Our data indicate that the respiratory chain of plant mitochondria is more resistant to pesticides as compared to animal mitochondria due to the presence of the alternative pathways of electron transport.