[ROLE OF MITOCHONDRIAL REACTIVE OXYGEN SPECIES IN LIPOPOLYSACCHARIDE-PROMOTED ACCUMULATION OF INTRACELLULAR LIPID DROPLETS].

It is known that in various cell types bacterial lipopolysaccharide (LPS) causes mitochondrial disfunction and promotes accumulation of triglycerides in intracellular lipid droplets. The precise mechanisms which mediate LPS-induced neutral lipid deposition remain poorly understood. In the present work performed on primary cultured epithelial cells isolated from the frog urinary bladder we studied the possible role of mitochondrial reactive oxygen species (mROS) in LPS-in-duced alteration of lipid metabolism. It was shown that LPS stimulated ROS production, decrea- 705 sed fatty acids oxidation, enhanced intracellular triglyceride deposition and promoted the formation of lipid droplets visualized by Nile red staining. Pretreatment of cells with mitochondrial-tar-geted antioxidant MitoQ at dose 25 nM for 2 h almost completely eliminated all the above effects of LPS. In contrast to MitoQ, a-tocopherol was ineffective. The data obtained indicate that increase of mROS level is a critical factor that mediates LPS-induced intracellular deposition of neutral lipids in epithelial cells.

[EFFECT OF LIPOPOLYSACCHARIDE ON NEUTRAL LIPID METABOLISM AND CELLULAR ENERGETICS IN FROG URINARY BLADDER EPITHELIAL CELLS].

It was shown previously that colonization of the frog urinary bladder by gram-negative bacteria leads to decreased ability of antidiuretic hormone to reabsorb water from the urinary bladder (Fock et al. J. Exp. Zool., 2013, 319A: 487-494). In the present work performed on epithelial cells isolated from the frog urinary bladder the influence of E. coli lipopolysaccharide (LPS) on neutral lipid metabolism and cellular energetics was studied. It was shown that incubation of cells with LPS led to decrease of fatty acids oxidation and to retention of triacylglycerols (TAG) followed by an increase of the cytoplasmic lipid droplets content and cellular amount of TAG. Fatty acid composition of TAG was not changed under LPS. LPS did not alter mitochondrial membrane potential, however, LPS decreased oxygen consumption rate both in basal and uncoupling conditions. Cellular ATP production was also reduced in the presence of LPS. The data obtained indicate that a decreased ability of antidiuretic hormone to reabsorb water from the urinary bladder induced by bacterial pathogens could be related to inhibition of fatty acids oxidation and impaired energy metabolism.