4.7 Article

The effect of pesticides on the NADH-supported mitochondrial respiration of permeabilized potato mitochondria

Journal

PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
Volume 183, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.pestbp.2022.105056

Keywords

Solanum Tuberosum L.; NADH; Mitochondria; Pesticides; Inhibitor ETC; Alamethicin

Funding

  1. Russian Science Foundation [20-14-00262]

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Pesticides can negatively impact the respiratory chain of plant mitochondria, resulting in reduced plant growth and yield. Studying the effect of pesticides on bioenergetic parameters of plant mitochondria is a promising method for assessing their toxicity. This study specifically examined the impact of certain pesticides on isolated potato mitochondria, finding that succinate is the preferred substrate for phosphorylating respiration. Some pesticides strongly inhibited mitochondrial respiration, while others had minimal effect. Notably, one pesticide actually increased the respiratory rate of permeabilized potato mitochondria.
Pesticides can seriously affect the respiratory chain of the mitochondria of many crops, reducing the intensity of plant growth and its yield. Studying the effect of pesticides on the bioenergetic parameters of intact plant mitochondria is a promising approach for assessing their toxicity. In this study, we investigated the effect of some pesticides on isolated potato mitochondria, which used exogenous NADH as a substrate for respiration. We showed that succinate is the most preferred substrate for phosphorylating respiration of intact potato tubers mitochondria. Potato mitochondria poorly oxidize exogenous NADH, despite of the presence of external NADH dehydrogenases. Permeabilization of the mitochondrial membrane with alamethicin increased the availability of exogenous NADH to complex I. However, the pathway of electrons through complex I to complex IV makes intact potato mitochondria susceptible to a number of pesticides such as difenoconazole, fenazaquin, pyridaben and tolfenpyrad, which strongly inhibit the rate of mitochondrial respiration. However, these pesticides only slightly inhibited the rate of oxygen consumption during succinate-supported respiration. Dithianon, the inhibitor of Complex II, is the only pesticide which significantly increased the respiratory rate of NADH-supported respiration of permeabilized mitochondria of potato. Thus, it can be assumed that the alternative NADH dehydrogenases for electron flow represent a factor responsible for plant resistance to xenobiotics, such as mitochondria-targeted pesticides.

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