Abstract
Background. The mitochondrial electron transport chain, in particular the respiratory complex I, is one of the main sources of reactive oxygen species (ROS) in living cells. Suppression of the complex I activity in human cells through chemical inhibition or mutations that disrupt the functionality of this complex leads to a significant increase in the content of ROS. The complex I mutants are also known for plants; however, it is still not clear whether the suppression of the activity of this complex leads to an increase in the level of ROS and the development of oxidative stress.
 Purpose. To study the level of superoxide, hydrogen peroxide and sensitivity to prooxidants in Arabidopsis ndufs4 cells with complex I inactivated by insertional mutagenesis.
 Materials and methods. A suspension culture of wild-type Arabidopsis cells and a line with knockout the NDUFS4 complex I subunit was used. The level of hydrogen peroxide in the cells was determined using dichlorofluorescein. The superoxide content was estimated by cell staining in the presence of nitroblue tetrazolium.
 Results. It has been shown that inactivation of the NADH-dehydrogenase complex in Arabidopsis cells due to the absence of one of its subunits leads to a decrease in the content of superoxide and hydrogen peroxide. It was also shown that the level of ROS in cells treated with the menadione and hydrogen peroxide increased several times in wild-type cells, but remained almost unchanged in ndufs4 cells.
 Conclusion. Suppression of the activity of the NADH dehydrogenase complex in plant cells, but not in animal cells, leads to a decrease in the content of both hydrogen peroxide and superoxide. Cells of ndufs4 line have an increased ability to detoxify ROS, possibly associated with the constant mobilization of antioxidant defense systems.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have