Analysis of glutathione system potential in rats with alimentary obesity

M. I. Marushchak, O. P. Mialiuk, U. P. Hevko, H. H. Habor, T. Ya. Yaroshenko, I. V. Antonyshyn

Abstract


Introduction. Molecular mechanisms of urgent and long-term adaptation to the pathological process are realized with the participation of physiologically active substances, including the glutathione system.

The aim of the study – to investigate the activity of glutathione peroxidase (GP), glutathione reductase (GR), as well as the content of reduced (GSH) and oxidized (GSSG) glutathione in liver, adipose tissue, and blood erythrocytes in experimental alimentary obesity.

Research Methods. The experimental model of alimentary obesity was reproduced in 48 white non-linear male rats by using a food drive inducer-glutamic acid sodium salt in a ratio of 0.6: 100.0 and a high-calorie diet. GSH and GSSG activity were determined by the Elman method, GR activity was measured by the Ramos-Martines method, GP by Mills method. The protein concentration in the supernatants of the homogenate tissues was evaluated by the Lowry method.

Results and Discussion. The obtained data indicates a decrease in the level of GSH after 14 days of the experiment in all the tissues studied. The same trend was observed in the animals of the second experimental group: the GSH index decreased by 36.1 % in the blood and, correspondingly, by 52.8 % and 33.3 % in adipose tissue and liver (p <0.05). The GSSG index changed after 28 days of the experiment, namely increased relative to control. Reduction in the concentration of GSH in rats with alimentary obesity was due to a lack of the studied enzymes of the glutathione system: GP and GR involved in the regeneration of GSH with GSSG.

Conclusions. The data indicate a reduction in overall capacity of glutathione system in rat tissues in case of alimentary obesity, as evidenced by the reduction of glutathione and GSH / GSSG ratio. Significant inhibition of enzymes of glutathione in animals with alimentary obesity (glutathione reductase and glutathione peroxidase) indicates their inability to fully confront the damaging effect of excessive lipid peroxidation products.


Keywords


obesity; glutathione system; experiment.

References


Kornienko, E.A., & Netrebenko, O.K. (2012). Ozhirenie i kishechnaya mikrobiota: sovremennaya kontseptsiya vzaimosvyazi [Obesity and intestinal microbiota: a modern concept of interconnection]. Pediatriya – Pediatrics, 2, 110-122 [in Ukrainian].

Bradshaw, T., & Mairs, Н. (2014). Obesity and serious mental ill health: a critical review of the literature. Healthcare, 2, 166-182.

Sharma, A.M., & Kushner, R.F. (2009). A proposed clinical staging system for obesity. Int. J. Obesity, 33, 289-295.

Obesity. Situation and trends. (2012). Geneva: World Health Organization.

Pankrushina, A.N., & Tolstykh, K.Yu. (2008). Leptin: novye perspektivy i podkhody k korrektsii ozhyreniya [Leptin: New approaches and prospects for correction obesity]. Vestnik TvGU. Seriya «Biologiya i ekologiya» – Journal TvHU. Series "Biology and Ecology", 10, 91-97 [in Russian].

Reducing Obesity and Improving Diet. (2013).

Prevention of weight gain and obesity in adults: a systematic review. Calgary: Canadian Task Force on Preventive Health Care. (2006).

Prystupa, L.N., & Dudchenko, I.O. (2013). Vplyv polimorfizmu heniv β1–adrenoretseptoriv ta α–subodynytsi g–bilka na ryzyk rozvytku alimentarnoho ozhyrinnya (ohlyad literatury) [Effect of polymorphisms of genes β1-adrenoceptor and α-subunit g-protein nutritional risk for obesity (literature review)]. Zhurnal klinichnykh ta eksperymentalnykh medychnykh doslidzhen – Journal of Clinical and Experimental Medical Research,1 (3), 285-291 [in Ukrainian].

Maruschak, M.I., Antonуshуn, I.V., Mіalіuk, O.P., Orel, Yu.M., Krуnуtska, I.Ya. Sposіb modeliuvannia alіmentarnoho ozhуrіnnia [The method of modeling of alimentary obesity]. Patent Ukraina, № u 2013 12044, 2014 [in Ukrainian].

Jeyakumar, S.M., Vajreswari, А., & Giridharan, N.V. (2006). Chronic dietary vitamin A supplementation regulates obesity in an obese mutant WNIN/Ob rat model. Obesity, 14, 52-59.

Ellman, G.L. (1959). Tissue sulfhydryl groups. Arch. Biochem. Biophys, 82 (1), 70-77.

Ramos–Martines, I.L., & Torres, А.М. (1985). Glutathione reductase of mantle tissue from sea mussel medulis. Рurification and characterization two seasonal enzymatic forms. Biochem. Physiological, 80 (213), 355-360.

Mills, G.C. (1959). The purification and properties of glutathione peroxidase of erythrocytes. J. Biol. Chem, 234 (3), 502-506.

Lowry, О.М., Rosebrough, N.J., Farr, A.L., & Randall, R.J. (1951). Protein measurement with the Folin phenol reagent. J. Biol. Chem, 193 (1), 265-275.

Dalton, T.P., Shertzer, H.G., & Puga, А. (1999). Regulation of gene expression by reactive oxygen. Annu. Rev. Pharmacol. Toxicol, 39, 67-101.

Forman, H.J., Fukuto, J. M., & Torres, М. (2004). Redox signaling: thiol chemistry defines which reactive oxygen and nitrogen species can act second messengers. Am. J. Physiol. Cell. Physiol, 287 (2), 246-256.




DOI: http://dx.doi.org/10.11603/mcch.2410-681X.2017.v0.i2.7972

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