MRI  Vol.1 No.2 , November 2012
Silica inflammation modulates lipoperoxide and thi-obarbituric acid reactive substances levels in liver and glucose concentration in blood of alloxan diabetic rats
Abstract: Inflammatory granulomatous diseases are cha- racterized by a high concentration of granu- lomas in tissue interstitium in which phagocytic cells that produce active oxygen and nitrogen metabolites are accumulated. Because of their high reactivity, free radicals react with unsatu- rated fatty acids that are components of mem- brane phospholipids, activate lipid peroxidation processes (LPP), the products of which have a cytotoxic effect. The role of free radicals in the pathogenesis of diabetes and its complications has been proved. The purpose of the present work was to investigate the activity of lipid peroxidation processes in the liver of rats with silica-induced granulomatous inflammation, allo- xan diabetes and their combination. The expe- riment involved male albino rats divided into four main groups. The first group were rats with silica granulomatous inflammation (SL rats); the second group were alloxan diabetic rats (DB rats); and the third group were alloxan diabetic rats, in which silica granulomatous inflammation was induced 8 days after the disease onset (DB_SL rats), the fourth group were rats that were injected saline physiological solution into the tail vein (control rats). Rats were withdrawn from the experiment within different time pe- riods after the induction of pathological pro- cesses. LPP activity in liver homogenates was determined by the relative concentration of lipo- peroxides in the heptane-isopropanol system and the concentration of products of the reac- tion with 2-thiobarbituric acid-reactive substan- ces (TBARS). The severity of carbohydrate meta- bolism disorders was evaluated through the measurement of the blood level of glucose, daily urine volume and the relative weight of the kindneys. We found that silica administration activated LPP in the liver of SL rats; we ob- served the accumulation of primary products on day 1 after administration and later that of TBA- RS followed by normalization of their concen- tration by day 21 of the experiment. TBARS con- centration was higher in DB rats than in the control at all stages of the experiment indicating the maintenance of high LPP activity in the liver of DB rats. TBARS concentration in the liver of DB_SL rats decreased by 3 times by the end of the experiment compared to DB rats, at the same time, they displayed a decreased blood glucose concentration, reduced diuresis and relative weight of the kidneys caused by hyperglycemia and associated polyuria. We conclude that one of the possible mechanisms of the influence on silica granulomatous inflammation on the cour- se of alloxan diabetes can be 1) a reduced LPO activity in liver cells at the lates stages of gran- ulomagenesis process induced by a single dose of a suspension of silica microparticles and 2) a combined decrease in glucose production in the liver of alloxan diabetics rats.
Cite this paper: Shkurupiy, V., Palchikova, N., Selyatitskaya, V., Makarova, O., Kuznetsova, N. and Kuzminova, O. (2012) Silica inflammation modulates lipoperoxide and thi-obarbituric acid reactive substances levels in liver and glucose concentration in blood of alloxan diabetic rats. Modern Research in Inflammation, 1, 19-25. doi: 10.4236/mri.2012.12003.

[1]   Valko, M., Leibfritz, D., Moncol, J., Cronin, M.T., Mazur, M. and Telser, J. (2007) Free radicals and antioxidants in normal physiological functions and human disease. The International Journal of Biochemistry and Cell Biology, 39, 44-84. Hdoi:10.1016/j.biocel.2006.07.001H

[2]   Shkurupy, V.A., Nadeev, A.P., Karpov, M.A., and Bugrimova, Y.S. (2010) Experimental cytomorphological studies of the reaction of mononuclear phagocyte system in granulomatosis of mixed (silicotic and tuberculous) etiology. Bulletin of Experimental Biology and Medicine, 149, 462-465. Hdoi:10.1007/s10517-010-0971-7H

[3]   Hamilton, R.F. Jr., Thakur, S.A. and Holian, A. (2008) Silica binding and toxicity in alveolar macrophages. Free Radical Biology and Medicine, 44, 1246-1258. Hdoi:10.1016/j.freeradbiomed.2007.12.027H

[4]   Kanta, J., Horsky, J., Kovárová, H., Tilser, I., Korolenko, T.A. and Barto?, F. (1986) Formation of granulomas in liver of silica-treated rats. British Journal of Experimental Pathology, 67, 889-899. H

[5]   Novikova, M.S., Potapova, O.V. and Shkurupy, V.A. (2008) Cytomorphological study of the development of fibrotic complications in chronic SiO2 granulomatosis in the liver during radon treatment. Bulletin of Experimental Biology and Medicine, 146, 279-282. doi:10.1007/s10517-008-0280-6H

[6]   Skurupiy, V.A., Nadeev, A.P. and Karpov, M.A. (2010) Evaluation of destructive and reparative processes in the liver in experimental chronic granulomatosis of mixed (silicotic and tuberculous) etiology. Bulletin of Experi- mental Biology and Medicine, 149, 685-688. Hdoi:10.1007/s10517-010-1024-yH

[7]   Makarova, O.P., Saperova, M.A. and Skurupiy, V.A. (2010) Lipid peroxidation in the liver and lungs in SiO2-induced granulomatosis. Bulletin of Experimental Biology and Medicine, 149, 702-705. doi:10.1007/s10517-010-1029-6H

[8]   Karpov, M.A., Skurupiy, V.A. and Nadeev, A.P. (2010) Analysis of fibrotic depositions in granulomas in chronic silicotuberculosis in mice. Bulletin of Experimental Biol- ogy and Medicine, 149, 659-662. Hdoi:10.1007/s10517-010-1018-9

[9]   Bachan, N., Kovsan, J., Kachko, I., Ovadia, H. and Rudich, A. (2009) Positive and negative regulation of insulin signaling by reactive oxygen and nitrogen species. Physiological Reviews, 89, 27-71. Hdoi:10.1152/physrev.00014.2008

[10]   Shams, M.E., Al-Gayyar, M.M. and Barakat, E.A. (2011) Type 2 diabetes mellitus-induced hyperglycemia in patients with NAFLD and normal LFTs: Relationship to lipid profile, oxidative stress and pro-inflammatory cytokines. Scientia Pharmaceutica, 79, 623-634. Hdoi:10.3797/scipharm.1104-21H

[11]   OsawaH, T. and HKato, Y. H(2005) Protective role of antioxidative food factors in oxidative stress caused by hyperglycemia.H Annals of the New York Academy of SciencesH, 1043, 440-451. Hdoi:10.1196/annals.1333.050

[12]   VessbyH, J., Basu, S., Mohsen, R., Berne, C. and HVessby, B. (2002)H Oxidative stress and antioxidant status in type 1 diabetes mellitus. HJournal of Internal MedicineH, 251, 69-76. Hdoi:10.1046/j.1365-2796.2002.00927

[13]   Jakus, V. (2000) HThe role of free radicals, oxidative stress and antioxidant systems in diabetic vascular disease. HBratislavské Lekárske Listy, 101, 541-551.H H

[14]   Jung, U.J., Lee, M.K., Park, Y.B., Jeon, S.M. and Choi, M.S. (2006) Antihyperglycemic and antioxidant properties of caffeic acid in db/db mice. The Journal of Pharmacology and Experimental Therapeutics, 318, 476-483. Hdoi:10.1124/jpet.106.105163

[15]   Teimouri, F., Amirkabirian, N., Esmaily, H., Mohammadirad, A., Aliahmadi, A. and Abdollahi, M. (2006) Alteration of hepatic cells glucose metabolism as a non-cholinergic detoxication mechanism in counteracting diazinon-induced oxidative stress. Human and Experimental Toxicology, 25, 697-703. Hdoi:10.1177/0960327106075064

[16]   Singh, J. and Kakkar, P. (2009) Antihyperglycemic and antioxidant effect of Berberis aristata root extract and its role in regulating carbohydrate metabolism in diabetic rats. Journal of Ethnopharmacology, 123, 22-26. Hdoi:10.1016/j.jep.2009.02.038

[17]   Selyatitskaya V.G., Cherkasova O.P., Pankina T.V. and Palchikova N.A. (2008) Functional state of adrenocortical system in rats with manifest alloxan-induced diabetes mellitus. Bulletin of Experimental Biology and Medicine, 146, 708-710. Hdoi: 10.1007/s10517-009-0393-6H

[18]   Selyatitskaya, V.G., Palchikova, N.A. and Kuznetsova, N.V. (2012) Adrenocortical system activity in alloxan-resistant and alloxan-susceptible Wistar rats. Journal of Diabetes Mellitus, 2, 165-169. Hdoi: 10.4236/jdm.2012.22026

[19]   Papanas, N., Zissimopoulos, A. and Maltezos, E. (2010) The role of nuclear medicine in the diagnosis of common and specific diabetic infections. Hellenic Journal of Nuclear Medicine, 13, 150-157. H

[20]   Ohkawa, H., Ohishi, N. and Yagi, K. (1979) Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Analytical Biochemistry, 95, 351-358. Hdoi:10.1016/0003-2697(79)90738-3

[21]   Volchegorsky, I.A., Dolgushin, I.I., Kolesnikov, O.L. and Tseilikman, V.E. (2000) Experimental modeling and labo- ratory evaluation of adaptive reactions of the organism. Publishers of the Chelyabinsk State Pedagogical University, Chelyabinsk.

[22]   Glantz S. (1999) Primer of Biostatistics, Practica, Moscow.

[23]   DooleyH, S., HDelvoux, B.,H HLahmeH, B., HMangasser-Stephan, K. andH HGressner, A.M. (2000)H Modulation of transforming growth factor beta response and signaling during transdifferentiation of rat hepatic stellate cells to myofibroblasts. HHepatology, H31, 1094-1106. Hdoi:10.1053/he.2000.6126

[24]   DingH, A., HNathanH, C.F., HGraycarH, J., HDerynckH, R., HStuehrH, D.J. and HSrimal, S. (1990) HMacrophage deactivating factor and transforming growth factors-beta 1-beta 2 and -beta 3 inhibit induction of macrophage nitrogen oxide synthesis by IFN-gamma. Journal of Immunology, 145, 940-944.

[25]   Pernis, B. (2005) Silica and the Immune System. Acta Bio-Medica: Atenei Parmensis, Suppl. 2, 38-44.

[26]   SinghH, S.N., HVatsH, P., HSuriH, S., HShyamH, R., HKumriaH, M.M., HRanganathanH, S. and HSridharan, K. (2001)H Effect of an antidiabetic extract of Catharanthus roseus on enzymic activities in streptozotocin induced diabetic rats. HJournal of EthnopharmacologyH, 76, 269-277. Hdoi:10.1016/S0378-8741(01)00254-9

[27]   SharmaH, N. and HGarg, V. (2009)H Antidiabetic and antioxidant potential of ethanolic extract of Butea monosperma leaves in alloxan-induced diabetic mice. Indian Journal of Biochemistry and Biophysics, 46, 99-105.

[28]   BliugerH, A.F., HDudnikH, L.B., HMa?oreH, A.I., HNozdrunovaH, N.A. and HMieze, I.E. (1985) HIntensity of lipid peroxidation and its relation to changes in the composition and antioxidative properties of lipids in acute viral hepatitis. Voprosy Meditsinskoi Khimii, 31, 35-37.

[29]   Park, N.-Y. and Lim, Y. (2011) Short term supplementation of dietary antioxidants selectively regulates the inflammatory responses during early cutaneous wound healing in diabetic mice. Nutrition and Metabolism, 8, 80-88. Hdoi:10.1186/1743-7075-8-80

[30]   Yagi, H., Matsumoto, M., Suzuki, S., Misaki, R., Suzuki, R., Makino, S. and Harada, M. (1991) Possible mechanism of the preventive effect of BCG against diabetes mellitus in NOD mouse. I. Generation of suppressor macrophages in spleen cells of BCG-vaccinated mice. Cellular Immunology, 138, 130-141. Hdoi:10.1016/0008-8749(91)90138-2

[31]   Yagi, H., Matsumoto, M., Kishimoto, Y., Makino, S. and Harada, M. (1991) Possible mechanism of the preventive effect of BCG against diabetes mellitus in NOD mouse. II. Suppression of pathogenesis by macrophage transfer from BCG-vaccinated mice. Cellular Immunology, 138, 142-149. Hdoi:10.1016/0008-8749(91)90139-3H

[32]   Petrovsky, N., Silva, D. and Schatz, D.A. (2003) Vaccine therapies for the prevention of type 1 diabetes mellitus. Paediatric Drugs, 5, 575-582. Hdoi:10.2165/00148581-200305090-00001