Investigation of the Effects of Boron on Leucocyte Functions and Formed Free Radical Status in Endotoxin-Mediated Inflammation

Endotoxins are lipopolysaccharides which make up some part of the cell walls of gram negative bacteria. Endotoxemia is one of the most important mechanisms in the generation of inflammation. Inflammation is a powerful physiological response to tissue damage caused by the microorganisms, physical, chemical and other factors. Many cells, especially leukocytes, and the cytokines released from these cells play role at the start of inflammation. The most significant players in inflammation are interleukins (IL) and tumor necrosis factor alpha (TNF-α). The pathogens which cause inflammation are removed through phagocytosis. The oxygen-dependent mechanisms that phagocytic cells use to remove damaging factor include superoxide radical formation and the myeloperoxidase (MPO) system. Boron is an element which has a considerable importance in terms of reserve in our country. Since its areas of use are quite wide the exposure to boron is more in all respects. The boron is thought to have numerous effects on the living organisms. In the light of this information, this study aims to investigate the effect of boron on the functions of leukocyte and the situation of formed free radical in the endotoxin-mediated inflammation. Accordingly, 3 separate experimental groups each of which has 6 rats were created; control, boron+ endotoxin and endotoxin groups. 100 mg / kg boric acid was administered to boron + endotoxin group through gavage for 28 days. On day 28, 4 mg / kg lipopolysaccharide (endotoxin / LPS) were administered to endotoxin group and boron + endotoxin group intraperitoneally. In serums of rats, TNF-α and IL-6 were measured with ELISA as SOD and MPO were measured spectrophotometrically. TNF-α concentration decreased in the boron + endotoxin and endotoxin groups compared to the control group whereas IL-6 concentration did not change between the groups. SOD concentration increased in the Boron + endotoxin group compared to the endotoxin group. SOD value measured in the endotoxin group is lower than the control group. MPO concentration of the boron + endotoxin group is higher than those of the endotoxin and control groups. In conclusion, it is thought that boron has no effect on TNF-α and IL-6 levels. Increase in SOD level due to boron can be attributed to the role of boron as a regulator by affecting the production of free radicals positively. The increase in MPO level suggests that the boron element plays a useful and adaptive role in the destruction of the infectious agent taken by phagocytosis.