Dynamics of superoxide dismutase-1 gene expression in different types of drug correction of toxic disorders in the liver
- Авторлар: Karimov D.O.1, Mukhammadiyeva G.F.1, Bakirov A.B.1, Ziatdinova M.M.1, Valova Y.V.1, Kudoyarov E.R.1, Khusnutdinova N.Y.1, Yakupova T.G.1
-
Мекемелер:
- Ufa Research Institute of Occupational Health and Human Ecology
- Шығарылым: Том 101, № 1 (2022)
- Беттер: 83-86
- Бөлім: PREVENTIVE TOXICOLOGY AND HYGIENIC STANDARTIZATION
- ##submission.datePublished##: 10.02.2022
- URL: https://medjrf.com/0016-9900/article/view/639555
- DOI: https://doi.org/10.47470/0016-9900-2022-101-1-83-86
- ID: 639555
Дәйексөз келтіру
Толық мәтін
Аннотация
Introduction. Drugs are needed to counteract oxidative stress to prevent toxic liver damage. Relevant and promising is the use of analysis of changes in gene expression under the influence of drugs to assess the effectiveness of their use and identify the molecular genetic mechanisms of the development of hepatotoxicity.
The purpose of this study was to examine the effect of the drugs “Heptor”, “Mexidol”, and “Oxymethyluracil” (OMU) on the level of expression of the Sod1 gene in the liver of rats with carbon tetrachloride lesion of the liver.
Material and methods. The experiment was performed on 70 male outbred white rats. The control group received olive oil subcutaneously; first experimental group — subcutaneous carbon tetrachloride (CTC); second experimental group — CTC and intraperitoneal “Heptor”; third experimental — CTC and subcutaneous “Mexidol”; fourth experimental — CTC and oral OMU. The material was collected at two-time intervals, 24 and 72 hours. To analyze the expression of the studied gene, quantitative RT-PCR in real-time mode was carried.
Results. The use of all three drugs after 72 h resulted in a decrease in the Sod1 gene expression level under oxidative stress induced by CTC. OMU exerted the most significant influence on the transcriptional activity of the Sod1 gene.
Limitations. The limitations of the study are due to the methodology of the analysis: since expression was evaluated by quantitative RT-PCR in real time, we evaluated the transcriptional activity of the gene without taking into account further post-transcriptional regulation of expression.
Conclusion. The study results indicate the ability of the studied hepatoprotectors to suppress the expression of the Sod1 gene in rat liver when exposed to CTC. It can be assumed that the studied drugs, through a change in the expression of the Sod1 gene, can participate in the regulation of free radical processes in liver damage.
Contribution:
Karimov D.O., Mukhammadiyeva G.F. — research concept and design, writing the text.
Bakirov A.B. — research concept and design, editing.
Ziatdinova M.M., Kudoyarov E.R., Khusnutdinova N.Yu., Yakupova T.G. — collection and processing of material.
Valova Ya.V. — statistical data processing.
All co-authors — approval of the final version of the article, responsibility for the integrity of all parts of the article.
Acknowledgements. The study had no sponsorship.
Conflict of interest. The authors declare no conflict of interest.
Received: September 1, 2021 / Accepted: November 25, 2021 / Published: February 09, 2022
Негізгі сөздер
Авторлар туралы
Denis Karimov
Ufa Research Institute of Occupational Health and Human Ecology
Хат алмасуға жауапты Автор.
Email: karimovdo@gmail.com
ORCID iD: 0000-0003-0039-6757
MD, PhD, Head of the Department for Toxicology and Genetics with The Experimental Clinics for Laboratory Animals, Ufa Research Institute of Occupational Health and Human Ecology, Ufa, 450106, Russian Federation.
e-mail: karimovdo@gmail.com
РесейGuzel Mukhammadiyeva
Ufa Research Institute of Occupational Health and Human Ecology
Email: noemail@neicon.ru
ORCID iD: 0000-0002-7456-4787
Ресей
Akhat Bakirov
Ufa Research Institute of Occupational Health and Human Ecology
Email: noemail@neicon.ru
ORCID iD: 0000-0003-3510-2595
Ресей
Munira Ziatdinova
Ufa Research Institute of Occupational Health and Human Ecology
Email: noemail@neicon.ru
ORCID iD: 0000-0002-1848-7959
Ресей
Yana Valova
Ufa Research Institute of Occupational Health and Human Ecology
Email: noemail@neicon.ru
ORCID iD: 0000-0001-6605-9994
Ресей
Eldar Kudoyarov
Ufa Research Institute of Occupational Health and Human Ecology
Email: noemail@neicon.ru
ORCID iD: 0000-0002-2092-1021
Ресей
Nadezhda Khusnutdinova
Ufa Research Institute of Occupational Health and Human Ecology
Email: noemail@neicon.ru
ORCID iD: 0000-0001-5596-8180
Ресей
Tatyana Yakupova
Ufa Research Institute of Occupational Health and Human Ecology
Email: noemail@neicon.ru
ORCID iD: 0000-0002-1236-8246
Ресей
Әдебиет тізімі
- Koroleva M.V. Exogenous-toxic hepatitis. Modern view on the etiology, pathogenesis, clinical course. Lekarstvennyy vestnik. 2015; 9(2): 18–22. (in Russian)
- Avdeeva M.G., Kulbuzheva M.I., Kolod’ko E.I., Chernikova N.V., Zapashnyaya O.V. Problems of treatment of toxic hepatitis on the background of chronic viral lesion of HCV-etiology. Klinicheskiy primer uspeshnoy terapii. Epidemiologiya i infektsionnye bolezni. 2018; 23(1): 50–6. https://doi.org/10.18821/1560-9529-2018-23-1-50-56 (in Russian)
- Li S., Tan H.Y., Wang N., Zhang Z.J., Lao L., Wong C.W., et al. The role of oxidative stress and antioxidants in liver diseases. Int. J. Mol. Sci. 2015; 16(11): 26087–124. https://doi.org/10.3390/ijms161125942
- Ingawale D.K., Mandlik S.K., Naik S.R. Models of hepatotoxicity and the underlying cellular, biochemical and immunological mechanism(s): a critical discussion. Environ. Toxicol. Pharmacol. 2014; 37(1): 118–33. https://doi.org/10.1016/j.etap.2013.08.015
- Nada S.A., Omara E.A., Abdel-Salam O.M., Zahran H.G. Mushroom insoluble polysaccharides prevent carbon tetrachloride-induced hepatotoxicity in rat. Food Chem. Toxicol. 2010; 48(11): 3184–8. https://doi.org/10.1016/j.fct.2010.08.019
- Debnath S., Ghosh S., Hazra B. Inhibitory effect of Nymphaea pubescens Willd. flower extract on carrageenan-induced inflammation and CCl4-induced hepatotoxicity in rats. Food Chem Toxicol. 2013; 59: 485–91. https://doi.org/10.1016/j.fct.2013.06.036
- Okado-Matsumoto A., Fridovich I. Subcellular distribution of superoxide dismutases (SOD) in rat liver: Cu,Zn-SOD in mitochondria. J. Biol. Chem. 2001; 276(42): 38388–93. https://doi.org/10.1074/jbc.M105395200
- Szymonik-Lesiuk S., Czechowska G., Stryjecka-Zimmer M., Słomka M., Madro A., Celiński K., et al. Catalase, superoxide dismutase, and glutathione peroxidase activities in various rat tissues after carbon tetrachloride intoxication. J. Hepatobiliary Pancreat. Surg. 2003; 10(4): 309–15. https://doi.org/10.1007/s00534-002-0824-5
- Aggarwal B.B., Harikumar K.B. Potential therapeutic effects of curcumin, the anti-inflammatory agent, against neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseases. Int. J. Biochem. Cell Biol. 2009; 41(1): 40–59. https://doi.org/10.1016/j.biocel.2008.06.010
- Manubolu M., Goodla L., Ravilla S., Thanasekaran J., Dutta P., Malmlöf K., et al. Protective effect of Actiniopteris radiata (Sw.) Link. against CCl₄ induced oxidative stress in albino rats. J. Ethnopharmacol. 2014; 153(3): 744–52. https://doi.org/10.1016/j.jep.2014.03.040
- Goodla L., Manubolu M., Pathakoti K., Jayakumar T., Sheu J.R., Fraker M., et al. Protective effects of Ammannia baccifera against CCl4-induced oxidative stress in rats. Int. J. Environ. Res. Public Health. 2019; 16(8): 1440. https://doi.org/10.3390/ijerph16081440
- Lee J., Koo N., Min D.B. Reactive oxygen species, aging, and antioxidative nutraceuticals. Compr. Rev. Food Sci. F. 2004; 3(1): 21–33. https://doi.org/10.1111/j.1541-4337.2004.tb00058.x
- Rahal A., Kumar A., Singh V., Yadav B., Tiwari R., Chakraborty S., et al. Oxidative stress, prooxidants, and antioxidants: the interplay. Biomed. Res. Int. 2014; 2014: 761264. https://doi.org/10.1155/2014/761264
- Myshkin V.A., Enikeev D.A., Srubilin D.V., Gimadieva A.R. Experimental evaluation of pyrimidine derivatives using models of the toxically damaged liver: a review. Nauchnoe obozrenie. Meditsinskie nauki. 2016; (3): 88–98. (in Russian)
Қосымша файлдар
