Alina Alimova

Ms. Alina Alimova

Voronezh State University, Voronezh, Voronezhskaya Oblast’, Russia
orcid

Research Focus & Metrics

Academic Career Length

5Years (2022-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Journal Article
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AAAlina Alimova
Alina Alimova
VSVadim V. Sitnikov
Vadim V. Sitnikov
DPDaniil I. Pogorelov
Daniil I. Pogorelov
OBOlga N. Boyko
Olga N. Boyko
IBInna Burakova
Inna Burakova
Vasily N. PopovVasily N. Popov
Vasily N. Popov
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.


4 February 2025 in Microorganisms
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MGMaria Gureeva
Maria Gureeva
MKMarina S. Kirillova
Marina S. Kirillova
VTVeronika A. Trandina
Veronika A. Trandina
VKVera A. Kryukova
Vera A. Kryukova
АЕАнна Еремина
Анна Еремина
AGArtem Gureev
Artem Gureev
Heavy metals (HMs) exert a negative impact on physiological processes in plants, which can adversely affect the productivity of agricultural crops. In this experiment, we assessed the potential to mitigate the toxic effects of HMs on soft wheat through the use of rhizospheric microorganisms from the genus Azospirillum. In the initial phase of the experiment, we identified the most resistant Azospirillum strains to Cu (from 1.5 to 15 mg/L), Ni (from 2 to 20 mg/L), and Pb (from 15.9 to 159.4 mg/L). Both Ni and Pb significantly inhibited bacterial growth and induced substantial oxidative stress in the majority of the studied strains. The strain A. picis B-2897T exhibited the highest resistance to all HMs. The cultivation of wheat in soil supplemented with Cu led to an increased growth rate and enhanced wheat productivity. Conversely, Ni and Pb reduced wheat productivity by 65% and 27%, respectively. This was accompanied by chlorophyll depletion and a decrease in the expression of genes NDOR and GST, which are involved in xenobiotic detoxification. Pre-inoculation of seeds with Azospirillum led to a decrease in HM concentration in the plant seedlings; in particular, A. picis B-2897T reduced the level of Ni from 0.005% to a concentration below the detectable level (i.e., below 0.001%), and Pb from 0.014% to 0.008%. The bacteria stimulated the expression of genes responsible for xenobiotic detoxification and contributed to the increased growth and productivity of wheat. Thus, Azospirillum can be utilized as a bioproduct to alleviate the toxic effects of HMs.

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AGArtem P. Gureev
Artem P. Gureev
AAAlina Alimova
Alina Alimova
Denis N. SilachevDenis N. Silachev
Denis N. Silachev
Egor PlotnikovEgor Plotnikov
Egor Plotnikov
Mitochondrial dysfunction contributes to numerous chronic diseases, and mitochondria are targets for various toxins and xenobiotics. Therefore, the development of drugs or therapeutic strategies targeting mitochondria is an important task in modern medicine. It is well known that the primary, although not the sole, function of mitochondria is ATP generation, which is achieved by coupled respiration. However, a high membrane potential can lead to uncontrolled reactive oxygen species (ROS) production and associated dysfunction. For over 50 years, scientists have been studying various synthetic uncouplers, and for more than 30 years, uncoupling proteins that are responsible for uncoupled respiration in mitochondria. Additionally, the proteins of the mitochondrial alternative respiratory pathway exist in plant mitochondria, allowing noncoupled respiration, in which electron flow is not associated with membrane potential formation. Over the past two decades, advances in genetic engineering have facilitated the creation of various cellular and animal models that simulate the effects of uncoupled and noncoupled respiration in different tissues under various disease conditions. In this review, we summarize and discuss the findings obtained from these transgenic models. We focus on the advantages and limitations of transgenic organisms, the observed physiological and biochemical changes, and the therapeutic potential of uncoupled and noncoupled respiration.