Low level, chronic exposure of humans to fluorine compounds (F) in the air, water and food may be atherogenic via the activation of oxidative stress and increased reactive oxygen species (ROS) production. Exposure to lead (Pb) via the same trophic chain may potentiates the intensity of free-radical reactions and changes in lipid metabolism leading to induction and stimulation of the atherosclerosis progression. A long-term exposure can leads also to changes in amount and catalytic properties of many enzymes enhance the inflammatory and proliferation reactions in which a significant role is played by macrophages, cells participating in the formation of atherosclerotic plaques. Early and key changes related to atherogenesis are the implication of low density lipoproteins (LDL) oxidative modification. Macrophages are of the prime importance in this process because of the accumulation of cholesterol originating from LDL and subsequent transformation into foam cells, being the source of locally secreted proinflammatory factors. The abovementioned factors simultaneously with excessive ROS synthesis are the purpose of the inflammatory – proliferative process (atherogenesis) development. Glutathione peroxidase (GPx) by its reducing properties towards wide range of hydroperoxides, influences the activities of the arachidonic acid metabolism key enzymes cyclooxygenases (COX1 and COX2).GPx contributes to hydroperoxides detoxification and eicosanoids synthesis modulation.

The aim of the study was to investigate the influence of simultaneous fluoride and Pb exposure (in concentrations determined in human serum) on the activity of enzymes involved in eicosanoids metabolism: COX1, COX2 (by measuring the products of the enzymes prostaglandine PGE2 and tromboxane TXB2) and GPx1 activity in macrophages obtained from a monocytic line THP-1. THP-1 cells were differentiated into macrophages by administering phorbol myristate acetate (PMA). The THP-1 monocytes were treated with 100 nM PMA for 24 h, and then the adherent macrophages were incubated with combined NaF and lead acetate (PbAc) solution for 48 h at a final concentrations of 1, 3, 6, 10 μM of NaF and 10, 100, 1000 μM of PbAc. Concentration was selected on the basis of results of fluoride and lead level in human serum with environmental exposition.

Simultaneous fluoride and Pb exposure increased the COX-1 and COX-2 activities in macrophages, resulted in pro-inflammatory factors synthesis PGE2 and TXB2 and increased activity of GPx-1 in macrophage. The observed changes of the enzymes activities were probably the compensation mechanism based on protection against excessive ROS generation in chronic exposition to fluoride and Pb. 

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