ТНЕ RELATIONSHIP BETWEEN A MALIGNANT TUMOR GROWTH AND PECULIARITIES OF BEHAVIOR OF LABORATORY ANIMALS

2021 ◽  
Vol 2 (1) ◽  
pp. 44-47
Author(s):  
Zhukova E.S. ◽  
Shcherbatyuk T.G. ◽  
Pozdniakova M.A.
Keyword(s):  
Free Radical ◽  
Tumor Growth ◽  
Renal Carcinoma ◽  
Carcinoma Cell ◽  
Laboratory Animals ◽  
Behavioral Characteristics ◽  
Laboratory Rats ◽  
Condi Tions ◽  
Radical Processes ◽  
Model Tumor

Laboratory rats' basic behavioral characteristics were studied in the experimental "Open field" test. A rat renal carcinoma cell line RA was used to model tumor growth. Free radical processes were assessed in normal condi-tions of organism and with tumor progression. Correla-tions were revealed between the levels of behavioral ac-tivity, the intensity of tumor growth, and free radical pro-cesses. The obtained data will serve as the basis for the development of risk management systems for the oncology and development of oncopathology in the population.

Study of photobiomodulation effects with violet-blue and red light in experimental oncogenesis

2020 ◽  
Vol 60 (9) ◽  
pp. 618-623
Author(s):  
Evgeniya S. Zhukova ◽  
Tatiana G. Shcherbatyuk ◽  
Arseniy L. Potapov ◽  
Irina A. Chernigina ◽  
Vladimir V. Chernov ◽  
...  
Keyword(s):  
Free Radical ◽  
Tumor Growth ◽  
Electromagnetic Radiation ◽  
Electromagnetic Waves ◽  
Biological Effects ◽  
Red Light ◽  
Free Radical Processes ◽  
Low Intensity ◽  
Radical Processes

Introduction. There is still an open question about the limits of medical use of low-intensity electromagnetic radiation of the optical range in tumor growth due to the risk of increased proliferation of tumor cells. The conditions under which the tumor process is stimulated, as well as the mechanisms of photobiomodulation in oncological pathology, remain unclear. The aim of the study - in vitro evaluation and comparison of the effect of low-intensity electromagnetic radiation with wavelengths of 400, 460 and 660 nm on the activity of free-radical processes in tumor tissue and blood in normal and growing experimental neoplasia. Materials and methods. The study was conducted on biological material obtained from white non-linear rats intact and with subcutaneously transplanted cholangiocellular cancer MS-1. The sources of low-intensity radiation with wavelengths of 400, 460 and 660 nm were led generators. The content of hemoglobin, the activity of superoxide dismutase and catalase, changes in the overall level of free radical processes and antioxidant activity by induced chemiluminescence, and DNA damage by the method of DNA comets were studied. Data analysis was performed using nonparametric statistics methods. Results. The multidirectional effect of radiation with wavelengths of 400, 460 and 660 nm on free-radical homeostasis indicators at the early and late stages of tumor growth, as well as the dependence of biological effects on the wavelength of radiation, was found. Conclusions. The results obtained allow making a number of assumptions about the mechanisms of action of the optical electromagnetic waves on tumor growth, modulating free radical processes in the tumor-bearing organism.

EFFECT OF INSULIN SHOCK ON OXIDATIVE MODIFICATION OF PROTEINS IN THE NERVOUS TISSUE OF THE BRAIN OF LABORATORY RATS

2020 ◽  
Vol 6(72) (1) ◽  
pp. 110-124
Author(s):  
V. A. Nikolskaya ◽  
I. V. Cheretaev
Keyword(s):  
Free Radical ◽  
Nervous Tissue ◽  
Study Groups ◽  
Oxidative Modification ◽  
Laboratory Animals ◽  
Intact Group ◽  
Laboratory Rats ◽  
Insulin Shock ◽  
Protein Molecules ◽  
Carbonyl Products

The rationale for the study of the formation of products of oxidative modification of proteins (OMP) in the nervous tissue in an experimental study of the effects of insulin shock was the literature data indicating that, oxidative destruction of proteins is one of the early indicators of tissue damage. The OMP considered as a factor in the pathogenesis of nervous tissue in many diseases. In some studies, there is information about the effect of experimental GP on oxidative processes in blood serum, red blood cells, adrenal glands and some other tissues, but the effect of this pathology on the processes of free radical oxygenation in the nervous tissue not studied. The purpose of this article was to evaluate changes in the level of OMP in the nervous tissue of laboratory rats under the influence of insulin shock. The experiment was performed on 32 sexually mature mongrel male rats weighing 380–400 g (age 6 months), divided into 4 groups of 8 individuals: control (intact) group, group 1-laboratory animals exposed to a single insulin shock (1 time per day, 1 day); group 2 – laboratory rats exposed to a double insulin shock (1 time per day, 2 days); group 3 – laboratory rats exposed to triple exposure to insulin shock (1 time per day, 3 days). Rats of the experimental groups insulin (3.5 Units) subcutaneously were injected. The presence of hypoglycemic coma determined by the appearance of convulsions. Animals that are intact at this time remained in their cells. Experimental animals slaughtered by decapitation on a guillotine. The material for research was a homogenate of nervous tissue obtained by the method Of Kutlubaev M. A. and co-authors. The study of the level of OMB in nervous tissue was performed using the Dubinina E. E. method, based on the reaction of oxidized amino acid residues of protein with 2,4-dinitrophenylhydrazine (2,4 – DNFG) with the formation of anhydrous 2,4 – DNFG. Measurements of supernatant extinction at wavelengths (λ) of 356, 370, 430 and 530 nm performed using a 5400-UV spectrophotometer (Ekros-Analytica, Russia). Statistical processing of the experiment results performed using the student’s parametric t-test, since the experimental data obeyed the law of normal distribution. It was found, that insulin shock and experimental hyperinsulinemia (HI) contributed to a decrease in free radical protein oxidation in rat nervous tissue homogenate, reducing the total level of OMP carbonyl products in all the study groups exposed to insulin shock: in the 1st group – by 37.6 % (n=8; p≤0.01), in the 2nd group – by 40.4 % (n=8; p≤0.01), in the 3rd group – by 40.8 % (n=8; p≤0.01). Experimental HI causes significant changes in the level of OMP products in the nervous tissue of laboratory animals, which expressed in a decrease in aldehyde and ketone derivatives of both the main and neutral characters in comparison with the indicators of the intact group. In all three groups with experimental HI, compared with the intact group, there was a significant decrease in primary and secondary carbonyl products of OMP, which indicates that free radical oxidation processes associated with both fragmentation of protein molecules and their aggregation suppressed under conditions of insulin shock. At one- and three-time exposure to HI, primary markers of oxidative stress, formed mainly due to fragmentation of protein molecules, prevailed among the carbonyl products of OMP in the nervous tissue. The content of primary and secondary carbonyl products was almost equal when the HI applied twice, which indicates that the processes of fragmentation and aggregation of protein molecules were almost the same under these conditions. In all three experimental groups, compared with the intact group, there was a significant decrease in carbonyl products of both neutral and basic nature due to a decrease in free radical damage to neutral and basic amino acids of protein molecules. In all the study groups, including the intact group, the level of OMPo was significantly lower than the level of OMPn. The most pronounced differences between the level of carbonyl products of OMP and OMPo were observed with three-fold HI, and the least pronounced-with a single one. With increasing duration of insulin shock, the spectrum of carbonyl products of OMP shifted towards increasing the content of the main products, as the role of the main amino acids as targets for damage to protein molecules by free radicals increased.

Effect of 1,3,6-trimethyl-5-hydroxyuracil succinate on the antioxidant system and free-radical processes in the liver of adult and old rats treated with carbon tetrachloride

2018 ◽  
pp. 55-59
Author(s):  
И.Д. Габдрахманова ◽  
В.А. Мышкин ◽  
Д.А. Еникеев ◽  
А.Р. Гимадиева
Keyword(s):  
Superoxide Dismutase ◽  
Free Radical ◽  
Carbon Tetrachloride ◽  
Antioxidant System ◽  
Complex Compound ◽  
Antiradical Activity ◽  
Conjugated Dienes ◽  
Experimental Animals ◽  
Old Rats ◽  
Radical Processes

Цель исследования: изучение влияния сукцината 1,3,6-триметил-5-гидроксиурацила на антиоксидантную систему и свободнорадикальные процессы в печени взрослых и старых крыс при воздействии тетрахлорметана. Методика. В эксперименте использованы половозрелые животные 12-месячного возраста со средней массой 250 г и старые животные 24-месячного возраста, средней массой 395 г по 30 особей в каждой возрастной группе. Токсическое поражение печени вызывали подкожным введением 50%-ного масляного раствора тетрахлорметана (ТХМ, 2 г/кг) в течение 4 сут. Одновременно с токсикантом опытным животным внутрибрюшинно вводили водный раствор коплексного соединения сукцинат-1,3,6-триметил-5-гидроксиурацила (2,5 мг/100 г) 3 раза в сут. в течение первых 4 сут. и в течение последующих 3 сут. 1 раз в сут. Контролем служили опытные животные, которым вводили физиологический раствор в том же объеме. Изучали окислительную модификацию белков, перекисное окисление липидов (по содержанию ТБК-реагирующих продуктов, уровню гидроперекисей липидов и содержанию диеновых конъюгатов). Состояние антиоксидантной системы оценивали по активности ферментов супероксиддисмутазы, каталазы и глутатионпероксидазы, определяемых биохимическими методами. Антирадикальную активность комплексного соединения и его составляющих субстанций исследовали в модельной системе «этилбензол-ледяная уксусная кислота» с вычислением константы К - скорости взаимодействия перекисных радикалов с молекулами изучаемого соединения в сравнении с эталонным антиоксидантом-ионолом с витамином Е. Результаты. Сукцинат + 1,3,6-триметил-5-гидрокси-урацила существенно снижает токсическое действие ТХМ на печень взрослых и старых крыс, устраняет дисбаланс в системах свободнорадикального окисления белков у старых крыс, статистически значимо улучшает показатели свободнорадикального окисления (СРО) липидов в печени взрослых и старых крыс: снижает уровень продуктов ПОЛ - гидроперекисей, диеновых конъюгатов, ТБК-реагирующих продуктов, а также улучшает работу антиоксидантной системы (АОС), повышая активность каталазы, супероксиддисмутазы и глутатионпероксидазы. Установлена высокая антирадикальная активность изучаемого препарата сопоставимая с активностью эталонного антиоксиданта ионола. Заключение. Сукцинат и его производные способны выступать как индивидуальные вещества с непосредственным антирадикальным механизмом действия, а не только как стимуляторы ферментативных систем антиоксидантной защиты. Aim. To study the effect of a complex compound, 1,3,6-trimethyl-5-hydroxyuracil succinate, on the antioxidant system and free radical processes induced by carbon tetrachloride in the liver of adult and old rats. Methods. The study used sexually mature animals aged 12 months and weighing 250 g and old animals aged 24 months weighing 395 g (total n= 60, 30 rats in each age group). Toxic damage of liver was induced by subcutaneous injections of a 50% oil solution of carbon tetrachloride (CTC) at 2 g/kg for 4 days. Together with the toxicant, experimental animals were injected with a water solution of a complex compound, succinate 1,3,6-trimethyl-5-hydroxyuracil, at a dose of 2.5 mg/100 g, i.p., 3 times per day for the first 4 days and once daily for the following 3 days. Experimental animals were used as controls, which were administered saline in the same volume. Oxidative modifications of proteins, lipid peroxidation (by levels of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides, and conjugated dienes) were studied. Condition of the antioxidant system was evaluated by activities of superoxide dismutase, catalase, and glutathione peroxidase using biochemical methods. Antiradical activity of the complex compound and its components was studied in a model system of ethylbenzene-glacial acetic acid; the K7 constant of the rate of peroxide radical interaction with molecules of the studied compound was compared with the reference antioxidant ionol with vitamin E. Results. Succinate +1.3.6-trimethyl-5-hydroxyuracil, considerably reduced TXM hepatotoxicity in adult and old rats; removed the disbalance in free radical systems of protein oxidation in old rats; significantly improved indexes of free-radical oxidation (FRO) of hepatic lipids in adult and old rats; decreased levels of LP products, hydroperoxides, conjugated dienes, and TBARS, and enhanced performance of the antioxidant system (AOS) by increasing activities of catalase, superoxide dismutase, and glutathione peroxidase. The study demonstrated a high antiradical activity of the study drug comparable with the activity of the reference antioxidant, ionol. Сonclusion. Succinate and its derivatives can perform as individual substances with a direct antiradical mechanism of action rather than as stimulators of enzymic systems of antioxidant defence.

Adaptogenic correction of free radical brain damage in subchronic exposure to sodium fl uoride

2020 ◽  
pp. 381-386
Author(s):  
A. G. Zhukova ◽  
L. G. Gorokhova ◽  
A. S. Kazitskaya ◽  
T. K. Yadykina ◽  
N. N. Mikhailova ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Free Radical ◽  
Brain Tissue ◽  
Free Radical Oxidation ◽  
Radical Oxidation ◽  
Free Radical Processes ◽  
Subchronic Exposure ◽  
Antioxidant Defense Enzymes ◽  
Radical Processes ◽  
Complex Drug

Introduction. Fluorine compounds in small doses, but with prolonged exposure, cause various disorders in organs at the cellular and molecular levels. Activation of free-radical processes plays an important role in the damaging eff ect of fl uorides. Th erefore, one of the most eff ective ways to limit fl uorine-induced damage is to directly aff ect free-radical processes using herbal preparations with antioxidant properties.The aim of the study is to study the eff ect of a dihydroquercetin-based drug on the activity of free radical processes in brain tissue under subchronic exposure to sodium fl uoride (NaF).Materials and methods. Th e work was performed on white male laboratory rats weighing 200-250 g. Th e rats were divided into 3 groups: 1 — control; 2 — rats with chronic exposure to sodium fl uoride (NaF) for 9 weeks; 3 — rats receiving a NAF solution with simultaneous administration of a complex drug based on dihydroquercetin at a dose of 3 mg/kg in 1% starch gel for 3, 6 and 9 weeks. The activity of free radical oxidation and antioxidant defense enzymes — superoxide dismutase (SOD) and catalase-was determined in the cerebral cortex. Th e level of expression of hypoxia-induced transcription factor HIF — 1A and inducible forms of proteins HSP72 and HSP32 were determined in the cytosolic fraction of brain tissue.Results. In the early stages of subchronic fl uoride exposure (1-3 weeks), the expression of protective proteins HIF-1α, HSP72, HSP32 and catalase was shown in the rat cortex, as a result of which the activity of free-radical processes was maintained at the control level. An increase in the timing of fl uoride intake to 9 weeks led to a decrease in antioxidant protection and signifi cant activation of free radical oxidation in brain tissue. Daily administration of a complex drug with dihydroquercetin for 3, 6 and 9 weeks to rats with subchronic fl uoride exposure led to a decrease in the severity of pro- and antioxidant balance disorders in the cerebral cortex. At the same time, the greatest protective eff ect of dihydroquercetin with fl uoride exposure was manifested by the 9th week of its administration.Conclusions. When subchronic intake of fl uorides in the body, the drug based on dihydroquercetin has a neuroprotective eff ect, which is manifested by an increase in the activity of antioxidant enzymes of fr ee radical oxidation and catalase and the resistance of the cortex to induced fr ee radical oxidation.

scholarly journals LncRNA-SNHG6 promotes the progression of hepatocellular carcinoma by targeting miR-6509-5p and HIF1A

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaoxi Fan ◽  
Zhongwei Zhao ◽  
Jingjing Song ◽  
Dengke Zhang ◽  
Fazong Wu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Growth ◽  
Bioinformatics Analysis ◽  
Carcinoma Cell ◽  
Noncoding Rnas ◽  
Migration And Invasion ◽  
Carcinoma Cell Lines ◽  
Huh7 Cells ◽  
Hepatocellular Carcinoma Cell

Abstract Background Accumulating evidences have been reported that long noncoding RNAs play crucial roles in the progression of hepatocellular carcinoma (HCC). SnoRNA host gene 6 (SNHG6) is believed to be involved in several human cancers, but the specific molecular mechanism of SNHG6 in HCC is not well studied. Methods In this study, we experimentally down-regulated the SNHG6 in two hepatocellular carcinoma cell lines in vitro, and then measured the proliferation, migration and invasion abilities and the apoptotic levels. Also, we performed the xenograft assay to investigate the function of SNHG6 during the tumor growth in vivo. Results We found SNHG6 was highly expressed in HCC tissues. Next, using Hep3B and Huh7 cells, we confirmed knockdown of SNHG6 reduced the proliferation, migration and invasion abilities in vitro. Also, by bioinformatics analysis, further molecular and cellular experiments, we found miR-6509-5p bound to SNHG6 directly, and the expression level of HIF1A was regulated through SNHG6/miR-6509-5p axis. Finally, we found that down-regulation of SNHG6 dramatically reduced the tumor growth ability of Huh7 cells in vivo. Conclusions We concluded that SNHG6/miR-6509-5p/HIF1A axis functioned in the progression of hepatocellular carcinoma, and could be the promising therapeutic targets during the development of hepatocellular carcinoma drugs.

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