Influence of lipopolysaccharide and the general adaptation syndrome on the development of oxidative-nitrosative stress in the lacrimal glands of rats

Abstract

The lacrimal glands play a key role in the visual organ functioning due to the production of tear fluid. From a pathogenetic point of view, it is interesting to study the combined effect of the general adaptation syndrome and systemic inflammatory response syndrome (SIRS) on lacrimal glands metabolism. The purpose of this study is to assess changes in the L-arginine-dependent part of nitric oxide cycle, nitric oxide metabolites concentration, and pro- and antioxidant balance in the rat lacrimal glands during modelling of chronic stress and SIRS. The experiments were performed on 18 mature male rats weighing 190-240 g. The animals were divided into 3 groups: I – control, II – water avoidance stress (WAS) group, III – WAS rats injected with lipopolysaccharide (WAS+LPS) group. The NO cycle parameters and markers of oxidative stress were determined in the rat lacrimal glands homogenate. The superoxide anion production and malondialdehyde concentration in the lacrimal glands of WAS+LPS rats increased by 2.48 and 1.86 times, respectively, compared to the control group and by 1.35 and 1.11 times compared to WAS group. The catalase activity in WAS+LPS rats decreased by 1.68 times and superoxide dismutase activity increased by 1.34 times compared to the control group; if compared to WAS group, catalase activity increased by 1.26 times, and superoxide dismutase activity elevated by 6.52 times. The activity of inducible NO-synthase in WAS+LPS rats decreased by 1.29 times compared to the control and increased by 1.23 times compared to WAS group. The concentration of peroxynitrites, nitrites, and nitrosothiols in WAS+LPS rats increased by 2.6, 3.02, and 3.68 times, respectively, compared to the control group and by 1.43, 1.41, and 2 .91 times compared to WAS group. Thus, administration of bacterial LPS to rats under the conditions of stress modeling enhances antioxidant protection and increases nitric oxide production from iNOS; at the same time, such stimulation increases damage to protein and lipid structures.