STUDY OF ENERGY PROCESS ACTIVITY IN RATS UNDER TOBACCO-NITRITE INTOXICATION AFTER CARBOLINE APPLICATION

Authors

  • P. H. Lykhatskyi I. HORBACHEVSKY TERNOPIL NATIONAL MEDICAL UNIVERSITY
  • L. S. Fira I. HORBACHEVSKY TERNOPIL NATIONAL MEDICAL UNIVERSITY
  • D. B. Fira I. HORBACHEVSKY TERNOPIL NATIONAL MEDICAL UNIVERSITY
  • K. O. Aleksevych I. HORBACHEVSKY TERNOPIL NATIONAL MEDICAL UNIVERSITY

DOI:

https://doi.org/10.11603/mcch.2410-681X.2021.i3.12557

Keywords:

sodium nitrite, tobacco smoke, methemoglobin, carboxyhemoglobin, energy enzymes, carboline

Abstract

Introduction. A significant role in the development of pathology is played by bad habits – smoking, abuse of alcohol and drugs. A significant ecological and medico-biological problem is the combined effect of inorganic nitro compounds on the human and animal b, accompanied by cases of nitrate-nitrite intoxication. A pathological process can arise as a result of the summation of environmental risk factors in which all organs and tissues are involved. This indicates the advisability of studying the mechanisms of the combined action of nitrites and tobacco smoke on the body.

The aim of the study – to analyze the activity of energy supply processes in rats with tobacco-nitrite intoxication and to learn the effectiveness of the use of the enterosorbent carboline in this pathology.

Research Methods. The studies were carried out on male white rats, which were divided into three age groups: immature, mature and old rats. The tobacco smoke generated from the combustion of 6 cigarettes containing 0.6 mg of nicotine and 8 mg of tar through the holes in the sealed chamber was fed into it, where 6 animals were simultaneously kept for 6 minutes. Animals received sodium nitrite once intragastrically at a dose of 45 mg/kg of body weight. The animals were removed from the experiment on day 45 of tobacco intoxication (and after 24 and 72 hours of sodium nitrite poisoning) by euthanasia under thiopental anesthesia. In blood neutrophils, the content of active forms of oxygen was determined, in the blood – met- and carboxyhemoglobin, in the lungs and heart – succinate dehydrogenase and cytochrome oxidase activity. All experiments were carried out in accordance with the provisions of the European Convention for the Protection of Vertebrate Animals.

Results and Discussion. It was found that on day 45 of nitrite-tobacco toxicosis in the blood of rats, the content of active forms of oxygen, meth- and carboxyhemoglobin probably increased. The most pronounced changes were observed in the blood of immature animals. By the end of the study, succinate dehydrogenase activity in the lungs of immature rats decreased 2.1 times, in mature rats – 1.9 times, and in old rats – 1.7 times relative to the control level. The most pronounced changes in the activity of these enzymes were noted in the myocardium of old rats. The use of carboline led to a likely increase in succinate dehydrogenase activity in the lungs of animals of all research groups, in the myocardium there was a tendency to an increase in this indicator. In immature and old rats, cytochrome oxidase activity in the lungs decreased by 60 % after injury, in mature rats by 50 %. The myocardium of old rats turned out to be more sensitive in relation to this indicator. The use of carboline led to a partial resumption of the activity of energy supply enzymes.

Conclusions. In the blood of immature rats under conditions of nitrite-tobacco toxicosis, the most pronounced increase in the content of active forms of oxygen was noted, which decreased after the use of the enterosorbent carboline. Carboline caused a likely decrease in blood methemoglobin in rats of all ages. In the study of the content of carboxyhemoglobin after the application of the sorbent, a tendency to its decrease was observed. In the myocardium and lungs of rats affected by toxicants, a probable decrease in the activity of energy enzymes was noted, which was probable in immature and old animals. The use of carboline led to a slight increase in succinate dehydrogenase and cytochrome oxidase activity both in the lungs and in the myocardium of rats of all ages.

References

Kvasha, Ye.A. (2010). Meditsinskiye aspekty tabakokureniya [Medical aspects of tobacco smoking]. Zdorovia Ukrainy – Health of Ukraine, 20 (249), 40-41. [in Ukrainian].

Pikas, O.B. (2015). Pro stan kurinnia tsyharok u suchasnykh umovakh, yoho vplyv na vynyknennya za­khvoriuvan v orhanizmi liudyny [On the state of cigarette smoking in modern conditions, its impact on the occur­rence of diseases in the human body]. Bukovynskyi medychnyi visnyk – Bukovynian Medical Bulletin, 6 (4), 227-230.[in Ukrainian].

Krasovskyy, K.S. (2009). Naslidky hlobalnoi tiutiunovoi epidemii [Consequences of the global tobacco epidemic]. Profilaktychna medytsyna – Preventive Medicine, 4, 72-74 [in Ukrainian].

Ballweg, K., Mutze, K., & Königshoff, M., Eickelberg, O., Meiners, S. (2014). Cigarette smoke extract affects mitochondrial function in alveolar epithelial cells. Am. J. Physiol. Lung Cell Mol. Physiol., 307 (11), 895-907.

Oliynyk, S.A., & Kozerenko, O.L. (2010). Okysnyi stres za hipoksychnykh staniv [Oxidative stress in hypoxic conditions]. Visnyk problem biolohiyi i medytsyny – Bulletin of Problems of Biology and Medicine, 1, 15-21 [in Ukrainian].

Bikkad, M.D., Ghuge, S.H., & Somwanshi, S.D., & Ingle, S.B. (2014). Evaluation of Lipid Peroxide and Antioxidants in Smokers. International Journal of Basic and Applied Medical Sciences, 4 (1), 1-6.

Churg, A., & Wright, J. (2010). Animal models of cigarette smoke-induced chronic obstructive pulmonary disease. Expert Rev. Respir. Med., 4 (6), 723-34.

Smolyar, V.I., Tsyhanenko, O.I., & Petrashenko H.I. (2007). Nitraty, nitryty ta nitrozaminy u kharchovykh produktakh i ratsioni [Nitrates, nitrites and nitrosamines in food and diet]. Problemy kharchuvannia – Problems of Nutrition, 3, 7-8 [in Ukrainian].

Andreychyn, S.M., Lototska, S.V., & Meretskyy, V.M. (2015). Zminy pokaznykiv tsytokinovoi lanky imunitetu u khvorykh na KHOZL pry zastosuvanni enterosorbtsiyi [Changes in the indicators of the cytokine level of immunity in patients with COPD with the use of enterosorption]. Infektsiini khvoroby – Infectious Diseases, 3, 44-47 [in Ukrainian].

Rybolovlev, Yu.R., & Rybolovlev, R.S. (1979). Dozirovaniye veshchestv dlya mlekopitayushchikh po konstante biologicheskoy aktivnosti [Dosing of substances for mammals according to the constant of biological activity]. Zhurnal AMN SSSR – Journal of the USSR Academy of Medical Sciences, 247 (6), 1513-1516. [in Russian].

Looney, M.R. (2009). Neutrophil sandwiches injure. Nat. Med., 15 (4), 364-366.

Gladwin, M., Grubina, R., & Doyle, M. (2009). The new chemical biology of nitrite reactions with hemoglobin: R-state catalysis, oxidative denitrosylation, and nitrite reductase/anhydrase. Accounts of Chemical Research, 42 (1), 157-167.

Vlizlo, V.V., Fedoruk, R.S., & Ratych I.B. (2012). Laboratorni metody doslidzhenʹ u biolohiyi, tvarynnytstvi ta veterynarnii medytsyni [Laboratory research methods in biology, animal husbandry and veterinary medicine]. Lviv: Spolom [in Ukrainian].

Gross, D., & Tolba, R.H. (2015). Ethics in animal-based research. Eur. Surg. Res., 55 (1-2), 43-57.

Jannot, A.S., Agoritsas, T., & Gayet-Ageron, A. (2013). Citation bias favoring statistically significant studies was present in medical research. J. Clin. Epide­miol., 66 (3), 296-301.

Ansari, F.A., & Mahmood, R. (2016). Sodium nitrite enhances generation of reactive oxygen species that decrease antioxidant power and inhibit plasma membrane redox system of human erythrocytes. Cell Biol Int., 40 (8), 887-894.

Malinska, D., Szymański, J., & Patalas-Kra­wczyk, P., Michalska, B., Wojtala, A., & Prill, M. (2018). Assessment of mitochondrial function following short- and long-term exposure of human bronchial epithelial cells to total particulate matter from a candidate modified-risk tobacco product and reference cigarettes. Food and Chemical Toxicology, 115, 1-12.

Dikalov, S.I., Li, W., & Doughan, A.K., Blanco, R.R., Zafari, A.M. (2012). Mitochondrial reactive oxygen spe­cies and calcium uptake regulate activation of phagocytic NADPH oxidase. Am. J. Physiol. Regul. Interg. Comp. Physiol., 302 (10), 1134-1142.

Solaini, G., Baracca, A., & Lenaz, G., & Sgarbi, G. (2010). Hypoxia and mitochondrial oxidative metabolism. Biochimica et Biophysica Acta (BBA) - Bioenergetics.,1797 (6-7), 1171-1177.

Yang, Z., Harrison, C.M., & Chuang, G.C., Ballinger, S.W. (2007). The role of tobacco smoke induced mitochondrial damage in vascular dysfunction and atherosclerosis. Mutat Res., 621 (1-2), 61-74.

Published

2021-12-14

How to Cite

Lykhatskyi, P. H., Fira, L. S., Fira, D. B., & Aleksevych, K. O. (2021). STUDY OF ENERGY PROCESS ACTIVITY IN RATS UNDER TOBACCO-NITRITE INTOXICATION AFTER CARBOLINE APPLICATION. Medical and Clinical Chemistry, (3), 10–18. https://doi.org/10.11603/mcch.2410-681X.2021.i3.12557

Issue

Section

ORIGINAL INVESTIGATIONS