Effect of interferon lambda on the generation of active oxygen species in mice under conditions of oxidative stress induced by Mitomycin C

Abstract

This research was aimed at studying the effect of species-specific recombinant bovine interferon lambda (IFN-λ) on the generation of reactive oxygen species (ROS) in mouse liver and bone marrow cells under conditions of mitomycin Cinduced oxidative stress. The experiment included female white laboratory mice. There were formed four groups of 6 animals each: the negative control group (group I); the group of mice that received a three-fold injection of IFN-λ at a dose of 0.1 ml/kg (group II) and mice that, in addition to IFN-λ, were administered a cytotoxic drug that induced free radical oxidation processes - mitomycin C at a dose of 10 mg/kg (group III), as well as the animals receiving only mitomycin C (group IV). We studied the concentration and viability of a cell suspension obtained from the liver of mice, as well as the relative content of intracellular ROS in the liver and bone marrow cells of animals, assessed by the fluorescence intensity of the oxidized form of 2',7'-dichlorodihydrofluorescein diacetate. The concentration and viability of cells in the liver suspension of healthy mice did not change with the introduction of IFN-λ (group II), indicating the absence of a toxic effect of IFN-λ on these cells. An increase in the level of ROS in the studied cells was detected when IFN-λ was administered to mice of group II (an increase in the level of ROS by 1.3 times in liver cells and by 2.9 times in bone marrow cells, relative to the mice of group I) and a decrease in the level of ROS in the mice under conditions of oxidative stress induced by mitomycin C (reduction in the content of intracellular ROS by 1.9 and 7.2 times in liver and bone marrow cells in the animals of group III, relative to the mice of group IV). The presented changes may indicate the normalization of IFN-λ redox balance in the body and, probably, appear in connection with the immunomodulatory activity of IFN-λ.