A comparative study of adrenalin and fluocinolon induced oxidative stress in male wistar rats
DOI:
https://doi.org/10.24193/subbbiol.2020.2.01Keywords:
stress, thymus, adrenal, free radicals.Abstract
Hormone secretion by the hypothalamic-pituitary-adrenocortical (HPA) axis is modulated by multiple factors which include the circadian rhythm, various types of stressors and glucocorticoids. Treatment with synthetic glucocorticoids as e.g. dexamethasone or dermocorticosteroids and repeated immobilization stress, decreases the total body weight gain of animals by disturbing the HPA axis function and accelerating the catabolism of the organism. Synthetic glucocorticoids are widely used as anti-inflammatory and anti-allergic drugs. Neverteheless, their administration may cause side effects in the normal functioning of several organs. Starting from the above findings and from the important physiological roles of the glucocorticoids in the metabolism, we investigated the reactions of the adrenal and thymus, the evolution of the body and organ weight and the level of the free radicals after adrenaline- and fluocinolon stress. In this study, we used electron paramagnetic resonance spectroscopy for the direct detection of free radical content in the organs of stressed Wistar rats. We followed the changes of the blood glucose level, body weight, structural modification and whole redox state of the rats during adrenaline and Fluocinolon-acetonid N treatment, as endogenous and exogenous sources of elevated glucocoticoid levels. We found a relationship between changes of the redox state and modified homeostasis of the organism, as an effect of elevated glucocorticoid levels. The oxidative stress induced by adrenalin treatment seemed to be an inducer rather than the result of the tissue damage.
Article history: Received 12 August 2020; Revised 2 November 2020; Accepted 15 November 2020; Available online 20 December 2020.
References
Adcock, I.M., & Mumby, S. (2017). Glucocorticoids, Handb. Exp. Pharmacol., 237: 171-196. doi:10.1007/164_2016_98.
Barnes, P.J. (2017). Glucoccorticosteroids, Handb. Exp. Pharmacol., 237: 93-115. doi: 10.1007/164_2016_62.
Costa Rosa, L. F., Curi, R., Murphy, C., & Newsholme, P. (1995). Effect of adrenalin and phorbol myristate acetate or bacterial lipopolysaccharide on stimulation of pathways of macrophage glucose, glutamine and O2 metabolism. Evidence for cyclic AMP-dependent protein kinase mediated inhibition of glucose-6-phosphate dehydrogenase and activation of NADP+dependent 'malic' enzyme, Biochem. J., 310, 709-714.
Crăciun, C., Madar, I., Tarba, C., Frăţilă, S., Ardelean, A., Crăciun, V., & Ilyes, I. (1998). Correlation betwen ultrastructural thymus modification, thymolisis, thymus and blood-serum lipids in response to epicutaneously applied dermacorticosteroids in pubertal rats, In: Current Problems in Cellular and Molecular Biology, Crăciun, C., Ardelean, A. (eds.), Risoprint, pp. 218-235.
Crăciun, C., Ardelean, A., Madar, I., Tarba, C., Şildan, N., Crăciun, V., & Fărcaş,T. (1997). Ultrastructural studies of the secondary effets induced at the level of thymus by topic application of Fluocinolon-acetonid-N in prepubertal rats, In: Current Problems and Techniques in Cellular and Molecular Biology, Crăciun, C., Ardelean, A. (eds.), Mirton, pp.176-186.
Daley-Yates, P.T. (2015). Inhaled corticosteroids: potency, dose equivalence and therapeutic index, Br. J. Clin. Pharmacol., 80(3): 372-380.
Deng, S., Dai, G., Chen, S., Nie, Z., Zhou, J., Fang, H., & Peng, H. (2019). Dexamethasone induces osteoblast apoptosis through ROS-PI3K/AKT/GSK3β signaling pathway, Biomed. Pharmacother., 110, 602-608.
Gavan, N., Popa, R., Orasan, R., & Maibach, H. (1997). Effect of pericutaneous absorbtion of fluocinolon acetonide on the activity of superoxide dismutase and total antioxidant status in patients with psoriasis, Skin Pharmacol., 10, 178-82.
Gounarides, J.S., Korach-André, M., Killary, K., Argentieri, G., Turner, O., & Laurent, D. (2008). Effect of dexamethasone on glucose tolerance and fat metabolism in a dietinduced obesity mouse model, Endocrinol., 149 (2), 758-766.
Ivy, J.R., Oosthuyzen, W., Peltz, T.S., Howarth, A.R., Hunter, R.W., Dhaun, N., Al-Dujaili, E.A.S., Webb, D.J., Dear, J.W., Flatman, P., & Bailey, A.M. (2016). Glucocorticoids induce nondipping blood pressure by activating the thiazide-sensitive cotransporter, Hypertension, 67, 1029-1037.
Kis, E. (2012). Glucocorticoid excess and fetal development in white Wistar rats. Annals of Romanian Society for Cell Biology, 17 (2), 82-85
Kis, E., & András, P. (2017). Has the Fluocinolon-acetonid N ointment any effect on the kidneys and the thyroid gland structure and function? Studia UBB Biologia, 62(2), 41-52..
Kis, E., & Crăciun, C. (2006). Efecte secundare ale unor glucocoticoizi topici, Ed. Risoprint, Cluj-Napoca.
Kis, E., Crăciun, C., Paşca, C., Sandu, V. D., Crăciun, V., & Madar, I. (2001). Comparative studies of the ulrastructure of somatotrope, gonadotrope and corticotrope cells in mature rats treated with topical dermocorticoids, Studia UBB Biologia, 46(1), 99-110.
Landfield, P.W., & Eldridge I.C. (1994). The glucocorticoid hyphotesis of age-related hippocampal neurodegeneration: role of dysregulated neuronal calcium, Ann. N. Y. Acad. Sci., 746, 308-321.
Liu, W., Zhao, Z., Na, Y., Meng, C., Wang, J., & Bai, R. (2018). Dexamethasone-induced production of reactive oxygen species promotes apoptosis via endoplasmic reticulum stress and autophagy in MC3T3-E1 cells, Internat. J. Molec. Medicin, 41(4), 2028-2036.
Lundgren, M., Burén, J., Ruge, T., Myrnäs, T., & Eriksson, J.W. (2004). glucocorticoids downregulate glucose uptake capacity and insulin-signaling proteins in omental but not subcutaneous human adipocytes, J. Clin. Endocrinol. Metab., 89 (6), 2989-2999.
Madar, I., Şildan, N., & Frecuş, G. (1993). Studiul comparativ al efectului stresului şi tratamentului cu fluocinolon-acetonid asupra unor parametri endocrino-metabolici la şobolani Wistar tineri, Stiinte şi cercetări biologice, Seria Biol. Anim., t. 45(1), 53-59.
Mann, C.L., Hughes, F.M., & Cidlowski, J.A. (2000). Delineation of the signalling pathway involved in glucocorticoid-induced and spontaneous apoptosis of rat thymocytes, Endocrynol., 141:528-538.
Mureşan, E., Gaboreanu, M., Bogdan, A.T., & Baba, A.I. (1974). Tehnici de histologie normală şi patologică, Ed. Ceres, Bucureşti, 482pp.
Nittoh, T., Fujimoti, H., Kozumi, Y., Ishihara, K., Mue, S., & Ohuchi, K. (1998). Effects of glucocorticoids on apoptosis of infiltrated eosinophils and neutrophils in rats, Euro. J. Pharmacol., 354, 73-81.
Orzechowski, A J., Grizard, M., Jank, B., Gajkowska, M., Lokociejewska, M., & Godlewskia, M. (2000a). Dexamethasone-mediated regulation of death and differentiation of muscle cells. Is hydrogen peroxide involved in the process? Reprod. Nutrit. Develop., 42,197-216.
Orzechowski, A.P., Ostaszewski, J., Wilczak, M., Jank, B., Balasinska, P., & Wareski, J.F. (2000b). Rats with a glucocorticoid-induced catabolic state, show symptoms of oxidative stress and spleen atrophy: the effect of age and recovery, J. Vet. Med., 49, 256-263.
Paragliola, R.M., Papi, G., Pontecorvi, A., & Corsello, S.M. (2017). Treatment with synthetic glucocorticoids and the hypothalamus-pituitary-adrenal axis. Internat. J. Mol. Sci., 18(10), 2201.
Pereira, B., Costa-Rosa, L.F.B.P., Bechara, E.J.H. , Newsholme, P., & Curi, R. (1998). Changes in TBARs content and superoxid dismutase, catalase and glutathione peroxidase activities in the lymphoid organs and skeletal muscles of adrenodemedullated rats, Braz. J. Med. Biol. Res., 31, 827-833.
Pereira, B., Costa Rica, L.F.B.P., Safi, D.A., Bechara, E.J.H., & Curi, R. (1995). Hormonal regulation of superoxid dismutase, catalase, and glutathione peroxidase activities in rat macrophages, Biochem. Pharmacol., 50 (12): 2093-2098.
Pereira, B., Bechara, E.J.H., Mendoca, J.R., & Curi, R. (1999). Superoxid dismutase, catalase and glutathione peroxidase activities in teh lymphoid organs and skeletal muscles of rats treated with dexamethasone, Cell Biochem., Funct., 17, 15-19.
Sapolsky, R. M. (1999). Glucocorticoids, stress, and their adverse neurological effects: relevance to aging, Exper. Gerontol., 34, 721-732.
Sapolsky, R.M., Romero, L.M., & Munck, A.U. (2000). How do glucocorticoids influence Stress Responses? Integraing, Permissive, Supressive, Stimulatory and Preparative Actions, Endocr. Rev., 21(1), 55-89.
Schafer, Q.F., & Buettner, R.G. (2001). Redox environment of the cell as viewed trought the redox state of the glutathione disulfide/glutathione couple, Free Radic. Biol. Med., 30(11), 1191-1212.
Seiji, M., Yasuaki, N., Eisuke, F., Sato, K.Y., Masanobu, M., & Masayasu, I. (1997). Cold stress induces thymocyte apoptosis in the rat, Pathophys., 213-219.
Tietze, F. (1969). Enzymic method for quantitative determination of nanogram amounts of total and oxidized glutathione: Applications to mammalian blood and other tissues, Ann. Biochem., 27, 502-522,1969.
Waldron, N.H., Jones, C.A., Gan, T.J., Allen, T.K., & Habib, A.S. (2013). Impact of perioperative dexamethasone on postoperative analgesia and side-effects: systematic review and meta-analysis, Br. J. Anaesth., 110, 191-200.
Yan, H., Arturo, C., Erdal, G, Philip, A., & Mohammed, K. (2000). Anti-stress effects of dehydroepiandrosterone, Biochem. Pharmacol., 59, 753-762.
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