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.

Alina A Alimova,Vadim V Sitnikov,Olga N Boyko,Vasily N Popov,Inna Y Vitkalova,Artem P Gureev,Daniil I Pogorelov

doi:10.3390/ijms23062970

Abstract

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.

Highlights

Archeological and genetic research indicates that potato domestication (Solanum tuberosum L.) started about 8000 years ago on the border of present-day Peru and Bolivia [1].According to FAOSTAT to 2019, the largest quantities of potatoes are produced in China (91.8 million tons), India (50.2 million tons), Russia (22.1 million tons), Ukraine (20.3 million tons), and the USA (19.2 million tons) [2]
Re3 of 24 cently, we showed that alternative NADH dehydrogenases is a factor responsible for plant resistance to xenobiotics, such as mitochondria-targeted pesticides
We recently showed that plant mitochondria, which oxidized NADH by complex I (not alternative NAD(P)H dehydrogenases), was more prone to pesticide-induced inhibition of the rate of O2 consumption [36] than intact mitochondria, which oxidized of succinate [31]

Summary

Introduction

Archeological and genetic research indicates that potato domestication (Solanum tuberosum L.) started about 8000 years ago on the border of present-day Peru and Bolivia [1].According to FAOSTAT to 2019, the largest quantities of potatoes are produced in China (91.8 million tons), India (50.2 million tons), Russia (22.1 million tons), Ukraine (20.3 million tons), and the USA (19.2 million tons) [2]. The widespread use of pesticides was the main reason for the increase in potato yields [3]. Significant progress in yield protection was halted by the evolution of resistance against pesticides in pest populations. The development of resistance led to the development and wider use of more and more pesticides [4]. The even wider use of pesticides led to environmental consequences. The excessive use of pesticides may lead to the destruction of biodiversity [5]. Pesticides can be toxic, for pests and plant-disease fungi, and for other non-target organisms, including birds [6], fish [7,8], insect pollinators [9,10], and non-target plants [11,12]. The effects of pesticides on humans include headaches and nausea; skin and eye irritation [13]; and chronic problems, such as cancer [14], neurodegenerative diseases, and, especially, Parkinson’s disease [15]

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