Diabetes-induced impairments in renal cortex of rats: effect of nicotinamide treatment
DOI:
https://doi.org/10.15587/2313-8416.2015.51241Keywords:
renal cortex, diabetes, nephropathy, nicotinamide, NAD, ratio, rats, experiment, model, NAD(P)/NAD(P)H pairsAbstract
There was offered the methods of study of nicotinamide administration modeling effect (invivo) that can be realized by means of NAD and is capable to get combined with renal cortex membranes in a specific way.
The aim of research was to explore is the content of NAD and NADP and free NAD(P)/NAD(P)H pairs ratio in renal cortex changes at diabetes mellitus and nicotinamide effect.
Methods. 50 rats-males of Wistar line weighing 180–210 g. with experimental diabetes mellitus type 1 caused by single intra-abdominal administration of streptozotocin, dose – 60 mg. for 1 kg. of body weight. Animals were separated into 3 groups – the control one (C), the group of rats with diabetes mellitus type 1 (D) and rats with diabetes that underwent administration of Nam (nicotinamide) («Sigma», США), dose – 100 mg\kg of body weight during 14 days. The glucose concentration was defined using glucometer «Accu-chek» (Roshediagnostics, Swizerland).
Results. According to the data received NAD level in renal cortex was reduced to 0,179±0,012 mmol/g at diabetes against 0,259±0,023 mmol/g of tissue, Р<0,05 in the control. The NAD(P)/NAD(P)H free pairs ratio reduced to 202.0±16,1 and 0,008±0,001 in renal cortex at diabetes against 297.0±21,2 and 0.013±0.002 in the control for NAD and NADP respectively. Nicotinamide administration resulted in partial renewal of NAD level in renal cortex and NAD(P)/ NAD(P)H free pairs ratio. The modeling effect invivo of administered nicotinamide can be realized by means of NAD that is capable to get combined in renal cortex membranes in a specific way.
Conclusions. So nicotonamide takes part in regulation of kidney processes that indicates its usefulness for diabetes nephropathy treatment
References
Yang, H., Jin, X., Kei Lam, C. W., Yan, S.-K. (2011). Oxidative stress and diabetes mellitus. Clinical Chemistry and Laboratory Medicine, 49 (11), 1773–1782. doi: 10.1515/cclm.2011.250
Fiorentino, T., Prioletta, A., Zuo, P., Folli, F. (2013). Hyperglycemia-induced Oxidative Stress and its Role in Diabetes Mellitus Related Cardiovascular Diseases. Current Pharmaceutical Design, 19 (32), 5695–5703. doi: 10.2174/1381612811319320005
Popov, D. (2010). Endothelial cell dysfunction in hyperglycemia: Phenotypic change, intracellular signaling modification, ultrastructural alteration, and potential clinical outcomes. International Journal of Diabetes Mellitus, 2 (3), 189–195. doi: 10.1016/j.ijdm.2010.09.002
Dunne, J. L., Overbergh, L., Purcell, A. W., Mathieu, C. (2012). Posttranslational Modifications of Proteins in Type 1 Diabetes: The Next Step in Finding the Cure? Diabetes, 61 (8), 1907–1914. doi: 10.2337/db11-1675
Stanеv, O. І., Zaporozhchenko, O. V., Karpov, L. M. et. al (2006). Vpliv rіznih shtamіv spіrulіni na vmіst laktatu, malatu ta pіruvatu v organah shhurіv za cukrovogo dіabetu. Vіsnik Harkіvs'kogo nacіonal'nogo unіversitetu іmenі V. N. Karazіna, 4 (748), 48–53.
Kuchmerovska, T., Shymanskyy, I., Chlopicki, S., Klimenko, A. (2010). 1-Methylnicotinamide (MNA) in prevention of diabetes-associated brain disorders. Neurochemistry International, 56 (2), 221–228. doi: 10.1016/j.neuint.2009.10.004
Kuchmerovs'ka, T. M., Pentek, Ju. T., Donchenko, G. V., Janіc'ka, L. V., Guzik, M. M., Djakun, K. O. (2013). Okisljuval'nij stres u sercі shhurіv za eksperimental'nogo cukrovogo dіabetu: efekt nіkotinamіdu. Dopovіdі NAN, 8, 176–181.
Guzik, M. M., Djakun, K. O., Janіc'ka, L. V., Kuchmerovs'ka, T. M. (2013). Vpiv іngіbіtorіv polі (ADP-ribozo) polіmerazi na dejakі pokazniki oksidativnogo stresu u lejkocitah krovі shhurіv za eksperimental'nogo cukrovogo dіabetu. UBZh, 85 (1), 62–70.
Bjornstad, P., Cherney, D., Maahs, D. M. (2014). Early diabetic nephropathy in type 1 diabetes. Current Opinion in Endocrinology & Diabetes and Obesity, 21 (4), 279–286. doi: 10.1097/med.0000000000000074
Ivanac-Jancovic R., Lovcic V., Magas S., Sklebar D., Kes P. (2015). The novella about diabetic nephropathy. Acta. Clin. Croat., 54 (1), 83–91.
Bergmeyer, H. U. (Ed.) (1963). MethodsofEnzymaticAnalysis. NewYork: Academic Press Inc., 1064.
Drel, V. R., Pacher, P., Stavniichuk, R., Xu, W., Zhang, J., Kuchmerovska, T. M. et. al. (2011). Poly(ADP-ribose)polymerase inhibition counteracts renal hypertrophy and multiple manifestations of peripheral neuropathy in diabetic Akita mice. International Journal of Molecular Medicine, 28 (4), 629–635. doi: 10.3892/ijmm.2011.709
Mykuliak, T., Kuchmerovska, T. (2013). Defects of energetic processes under diabetes and its complications. Ukranian Food Journal, 2 (3), 52–56.
Belenky, P., Bogan, K. L., Brenner, C. (2007). NAD+ metabolism in health and disease. Trends in Biochemical Sciences, 32 (1), 12–19. doi: 10.1016/j.tibs.2006.11.006
Kuchmerovska, T., Shymanskyy, I., Donchenko, G., Kuchmerovskyy, M., Pakirbaieva, L., Klimenko, A. (2004). Poly (ADP-ribosyl) ation enhancement in brain cell nuclei is associated with diabetic neuropathy. Journal of Diabetes and Its Complications, 18 (4), 198–204. doi: 10.1016/s1056-8727(03)00039-4
Schreiber, V., Dantzer, F., Ame, J.-C., de Murcia, G. (2006). Poly(ADP-ribose): novel functions for an old molecule. Nat Rev Mol Cell Biol, 7 (7), 517–528. doi: 10.1038/nrm1963
Starkov, A. A., Fiskum, G., Chinopoulos, C. et. al (2004). Mitochondrial α-Ketoglutarate Dehydrogenase Complex Generates Reactive Oxygen Species. Journal of Neuroscience, 24 (36), 7779–7788. doi: 10.1523/jneurosci.1899-04.2004
Alano, C. C., Ying, W., Swanson, R. A. (2004). Poly(ADP-ribose) Polymerase-1-mediated Cell Death in Astrocytes Requires NAD+ Depletion and Mitochondrial Permeability Transition. Journal of Biological Chemistry, 279 (18), 18895–18902. doi: 10.1074/jbc.m313329200
Xia, W., Wang, Z., Wang, Q., Han, J., Zhao, C., Hong, Y. et. al (2009). Roles of NAD/NADH and NADP+/NADPH in Cell Death. Current Pharmaceutical Design, 15 (1), 12–19. doi: 10.2174/138161209787185832
Lanaspa, M. A., Ishimoto, T., Cicerchi, C., Tamura, Y., Roncal-Jimenez, C. A., Chen, W. et. al. (2014). Endogenous Fructose Production and Fructokinase Activation Mediate Renal Injury in Diabetic Nephropathy. Journal of the American Society of Nephrology, 25 (11), 2526–2538. doi: 10.1681/asn.2013080901
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