O. Kachur, L. Fira, P. H. Lykhatskyі, I. Bekus, ,. M. V. Kyryliv
Colorectal cancer is one of the leading causes of mortality in the world. The search for new methods of therapy for this disease that could correct the state of oxidative stress during the development of neoplasms is up to date. The aim of this work was to study the level of reduced glutathione and the activity of glutathione-dependent enzymes in the development of 1,2 dimethylhydrazine-induced colon cancer in rats while treated with vincristine and the use of enterosorbent. To induce carcinogenesis, dimethylhydrazine was administered to male rats subcutaneously for 30 weeks at a dose of 7.2 mg/kg of body weight. The rats with induced colon cancer received entorosorbent per os at a dose of 0.2 g per 100 g of body weight daily for 21 days. After detoxification therapy, the rats were administered cytostatic vincristine daily at a dose of 0.23 mg/kg for 14 days. A decrease in the content of reduced glutathione, the activity of glutathione reductase and glutathione peroxidase in the blood and liver tissue of rats with colorectal cancer was established. The use of enterosorbent AUT-M was shown to be effective in stabilizing the indicators of the glutathione system in rats with induced colon cancer. Cytostatic vincristine did not significantly affect the change of the studied indicators, confirming the effectiveness of previous sorption measures. Keywords: blood, colorectal cancer, entorosorbent, glutathione, glutathione peroxidase, glutathione reductase, liver, vincristine
{"title":"AUT-M enterosorbent stabilizes glutathione system in vincristine-treated rats with dimethylhydrazine-induced colon cancer","authors":"O. Kachur, L. Fira, P. H. Lykhatskyі, I. Bekus, ,. M. V. Kyryliv","doi":"10.15407/ubj95.06.064","DOIUrl":"https://doi.org/10.15407/ubj95.06.064","url":null,"abstract":"Colorectal cancer is one of the leading causes of mortality in the world. The search for new methods of therapy for this disease that could correct the state of oxidative stress during the development of neoplasms is up to date. The aim of this work was to study the level of reduced glutathione and the activity of glutathione-dependent enzymes in the development of 1,2 dimethylhydrazine-induced colon cancer in rats while treated with vincristine and the use of enterosorbent. To induce carcinogenesis, dimethylhydrazine was administered to male rats subcutaneously for 30 weeks at a dose of 7.2 mg/kg of body weight. The rats with induced colon cancer received entorosorbent per os at a dose of 0.2 g per 100 g of body weight daily for 21 days. After detoxification therapy, the rats were administered cytostatic vincristine daily at a dose of 0.23 mg/kg for 14 days. A decrease in the content of reduced glutathione, the activity of glutathione reductase and glutathione peroxidase in the blood and liver tissue of rats with colorectal cancer was established. The use of enterosorbent AUT-M was shown to be effective in stabilizing the indicators of the glutathione system in rats with induced colon cancer. Cytostatic vincristine did not significantly affect the change of the studied indicators, confirming the effectiveness of previous sorption measures. Keywords: blood, colorectal cancer, entorosorbent, glutathione, glutathione peroxidase, glutathione reductase, liver, vincristine","PeriodicalId":23007,"journal":{"name":"The Ukrainian Biochemical Journal","volume":"15 12","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139003047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Т. О. Veklich, R. Rodik, О. V. Tsymbalyuk, О. V. Shkrabak, O. V. Maliuk, S. Karakhim, S. Vyshnevskyi, V. І. Kalchenko, S. Kosterin
The enzymatic and kinetic analyses were used to demonstrate that 5,11,17,23-tetra(trifluoro)methyl(phenylsulfonylimino)methylamino-25,27-dihexyloxy-26,28-dihydroxythiacalix[4]arene С-1087 effectively inhibited the Са2+,Mg2+-АТРase activity of the rat myometrium cells plasma membrane (І0.5 = 9.4 ± 0.6 µM) with no effect on the relative activity of other membrane ATPases. With the use of confocal microscopy and Ca2+-sensitive fluorescent probe fluo-4, it was shown that the application of thiacalix[4]arene С-1087 to the immobilized uterus myocytes increased the cytosolic concentration of Ca2+. Tenzometric studies of rat uterus smooth muscles with the subsequent mechanokinetic analysis revealed that thiacalix[4]arene С-1087 considerably decreased the maximal velocity of the relaxation of both spontaneous contractile response and contraction induced by hyperpotassium solution. Keywords: contraction-relaxation mechanokinetics, cytosolic Ca(2+), myometrium, plasma membrane Са(2+)‚Mg(2+)-АТРase, smooth muscle cell, thiacalix[4]arene
{"title":"Thiacalix[4]arene С-1087 is the selective inhibitor of the calcium pump of smooth muscle cells plasma membrane","authors":"Т. О. Veklich, R. Rodik, О. V. Tsymbalyuk, О. V. Shkrabak, O. V. Maliuk, S. Karakhim, S. Vyshnevskyi, V. І. Kalchenko, S. Kosterin","doi":"10.15407/ubj95.06.005","DOIUrl":"https://doi.org/10.15407/ubj95.06.005","url":null,"abstract":"The enzymatic and kinetic analyses were used to demonstrate that 5,11,17,23-tetra(trifluoro)methyl(phenylsulfonylimino)methylamino-25,27-dihexyloxy-26,28-dihydroxythiacalix[4]arene С-1087 effectively inhibited the Са2+,Mg2+-АТРase activity of the rat myometrium cells plasma membrane (І0.5 = 9.4 ± 0.6 µM) with no effect on the relative activity of other membrane ATPases. With the use of confocal microscopy and Ca2+-sensitive fluorescent probe fluo-4, it was shown that the application of thiacalix[4]arene С-1087 to the immobilized uterus myocytes increased the cytosolic concentration of Ca2+. Tenzometric studies of rat uterus smooth muscles with the subsequent mechanokinetic analysis revealed that thiacalix[4]arene С-1087 considerably decreased the maximal velocity of the relaxation of both spontaneous contractile response and contraction induced by hyperpotassium solution. Keywords: contraction-relaxation mechanokinetics, cytosolic Ca(2+), myometrium, plasma membrane Са(2+)‚Mg(2+)-АТРase, smooth muscle cell, thiacalix[4]arene","PeriodicalId":23007,"journal":{"name":"The Ukrainian Biochemical Journal","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138973304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P. Virych, V. Chumachenko, V. Pavlenko, N. Kutsevol
The toxicity of drugs for chemotherapy and cell resistance to their action are the main obstacles in anticancer therapy. Advances in nanotechnology may offer an alternative to traditional methods of anticancer therapy and overcoming drug resistance. The study was carried out on doxorubicin-resistant MCF-7/Dox breast cancer cells and BALB/3T3 clone A31 as a model of normal fibroblasts with the use of Dextran-graft-polyacrylamide/zinc oxide (D-PAA/ZnO) nanoparticles. Cytomorphological analysis was carried out after cells staining with acridine orange. Immunocytochemical study of Ki-67, p53, Bcl-2, Bax, E-cadherin, N-cadherin, СD44 expression was done. Cytotoxicity of D-PAA/ZnO nanoparticles (EC50 = 2.2 mM) against MCF-7/Dox cancer cells but not against normal fibroblasts was demonstrated. The increased expression of proapoptotic proteins, E-cadherin, CD44 and decreased expression of proliferation-associated marker Ki-67 in cancer cells treated with D-PAA/ZnO was revealed. Cytotoxicity of D-PAA/ZnO NPs against MCF-7/Dox cancer cells can be potentially used for elaboration of new approaches to cancer treatment. Keywords: breast cancer cells, cytotoxicity, dextran-graft-polyacrylamide, doxorubicin-resistance, fibroblasts, zinc oxide nanoparticles
{"title":"Cytotoxicity of dextran-graft-polyacrylamide/zinc oxide nanoparticles against doxorubicin-resistant breast cancer cells","authors":"P. Virych, V. Chumachenko, V. Pavlenko, N. Kutsevol","doi":"10.15407/ubj95.06.073","DOIUrl":"https://doi.org/10.15407/ubj95.06.073","url":null,"abstract":"The toxicity of drugs for chemotherapy and cell resistance to their action are the main obstacles in anticancer therapy. Advances in nanotechnology may offer an alternative to traditional methods of anticancer therapy and overcoming drug resistance. The study was carried out on doxorubicin-resistant MCF-7/Dox breast cancer cells and BALB/3T3 clone A31 as a model of normal fibroblasts with the use of Dextran-graft-polyacrylamide/zinc oxide (D-PAA/ZnO) nanoparticles. Cytomorphological analysis was carried out after cells staining with acridine orange. Immunocytochemical study of Ki-67, p53, Bcl-2, Bax, E-cadherin, N-cadherin, СD44 expression was done. Cytotoxicity of D-PAA/ZnO nanoparticles (EC50 = 2.2 mM) against MCF-7/Dox cancer cells but not against normal fibroblasts was demonstrated. The increased expression of proapoptotic proteins, E-cadherin, CD44 and decreased expression of proliferation-associated marker Ki-67 in cancer cells treated with D-PAA/ZnO was revealed. Cytotoxicity of D-PAA/ZnO NPs against MCF-7/Dox cancer cells can be potentially used for elaboration of new approaches to cancer treatment. Keywords: breast cancer cells, cytotoxicity, dextran-graft-polyacrylamide, doxorubicin-resistance, fibroblasts, zinc oxide nanoparticles","PeriodicalId":23007,"journal":{"name":"The Ukrainian Biochemical Journal","volume":"306 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138974210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ziziphus Spina-Christi (L.) (ZSC) is a traditional Arabian medicinal plant used to treat inflammatory symptoms, swellings and pain since long. Triple negative breast cancer (TNBC) is a form of cancer with a poor prognosis owing to the paucity of therapy alternatives. Two of the most critical pathways of TNBC development are Wnt/β-catenin signaling and autophagy. In the present study, we intended to identify the possible mechanisms of the cytotoxic effects mediated by ZSC extract on MDA-MB-231 breast cancer cells and to improve the efficacy of DOX in combination with ZSC. The MTT test was used to estimate cell viability and IC50 values. Apoptosis was detected using AnnexinV-FITC detection kit. ELISA was used to measure caspase-3 levels. Cell cycle and the level of autophagosome marker LC3-II were analysed using flow cytometry. Acidic vesicular organelle (AVOs) formation was observed by fluorescence microscopy. Real-time PCR was used to monitor changes in gene expression of β-catenin and autophagic adapter NBR1. It was shown that ZSC treatment dose-dependently inhibited MDA-MB-231 cell viability and induced apoptosis with accompanying elevation of caspase-3 level. Besides ZSC caused a significant elevation in LC3II level and downregulation of NBR1 gene expression with subsequent downregulation of β-catenin gene expression, indicating the inhibition of the oncogenic Wnt pathway. ZSC and DOX combination had synergistic cytotoxic effect by more effective suppression of Wnt pathway and induction of apoptosis and autosis. Keywords: apoptosis, autophagic adapter NBR1, autophagosome marker LC3-II, breast cancer cells, DOX, Wnt/β-catenin signaling, Ziziphus Spina-Christi
{"title":"Cytotoxic effect of Ziziphus Spina-Christi extract alone and in combination with doxorubicin on breast cancer cells","authors":"E. El-Shafey, E. Elsherbiny","doi":"10.15407/ubj95.06.050","DOIUrl":"https://doi.org/10.15407/ubj95.06.050","url":null,"abstract":"Ziziphus Spina-Christi (L.) (ZSC) is a traditional Arabian medicinal plant used to treat inflammatory symptoms, swellings and pain since long. Triple negative breast cancer (TNBC) is a form of cancer with a poor prognosis owing to the paucity of therapy alternatives. Two of the most critical pathways of TNBC development are Wnt/β-catenin signaling and autophagy. In the present study, we intended to identify the possible mechanisms of the cytotoxic effects mediated by ZSC extract on MDA-MB-231 breast cancer cells and to improve the efficacy of DOX in combination with ZSC. The MTT test was used to estimate cell viability and IC50 values. Apoptosis was detected using AnnexinV-FITC detection kit. ELISA was used to measure caspase-3 levels. Cell cycle and the level of autophagosome marker LC3-II were analysed using flow cytometry. Acidic vesicular organelle (AVOs) formation was observed by fluorescence microscopy. Real-time PCR was used to monitor changes in gene expression of β-catenin and autophagic adapter NBR1. It was shown that ZSC treatment dose-dependently inhibited MDA-MB-231 cell viability and induced apoptosis with accompanying elevation of caspase-3 level. Besides ZSC caused a significant elevation in LC3II level and downregulation of NBR1 gene expression with subsequent downregulation of β-catenin gene expression, indicating the inhibition of the oncogenic Wnt pathway. ZSC and DOX combination had synergistic cytotoxic effect by more effective suppression of Wnt pathway and induction of apoptosis and autosis. Keywords: apoptosis, autophagic adapter NBR1, autophagosome marker LC3-II, breast cancer cells, DOX, Wnt/β-catenin signaling, Ziziphus Spina-Christi","PeriodicalId":23007,"journal":{"name":"The Ukrainian Biochemical Journal","volume":"2013 18","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139001869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The aim of this work was to analyze the process of oxidative phosphorylation and ATP synthesis in a cell using a mathematical model. The scenario of occurrence of the autoperiodic and chaotic modes depending on the ATP dissipation values was determined. The invariant measure of the strange attractor was calculated, and histograms of its projections on the phase plane were plotted. Some recommendations were made on how to eliminate biochemically the chaotic mode and restore the stability of the self-organization of the cell biosystem. Keywords: ATP, Feigenbaum scenario, invariant measure, Krebs cycle, mathematical model, oxidative phosphorylation, self-organization, strange attractor
这项工作的目的是利用数学模型分析细胞中氧化磷酸化和 ATP 合成的过程。根据 ATP 的耗散值，确定了自周期和混沌模式的发生情况。计算了奇异吸引子的不变量，并绘制了其在相平面上的投影直方图。就如何从生化角度消除混沌模式并恢复细胞生物系统自组织的稳定性提出了一些建议。关键词ATP、费根鲍姆情景、不变量、克雷布斯循环、数学模型、氧化磷酸化、自组织、奇异吸引子
{"title":"Instability and invariant measure in the mathematical model for oxidative phosphorylation and ATP synthesis in the cell","authors":"V. Grytsay","doi":"10.15407/ubj95.06.105","DOIUrl":"https://doi.org/10.15407/ubj95.06.105","url":null,"abstract":"The aim of this work was to analyze the process of oxidative phosphorylation and ATP synthesis in a cell using a mathematical model. The scenario of occurrence of the autoperiodic and chaotic modes depending on the ATP dissipation values was determined. The invariant measure of the strange attractor was calculated, and histograms of its projections on the phase plane were plotted. Some recommendations were made on how to eliminate biochemically the chaotic mode and restore the stability of the self-organization of the cell biosystem. Keywords: ATP, Feigenbaum scenario, invariant measure, Krebs cycle, mathematical model, oxidative phosphorylation, self-organization, strange attractor","PeriodicalId":23007,"journal":{"name":"The Ukrainian Biochemical Journal","volume":"24 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138973308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. V. Ziablitsev, D. Zhupan, A. O. Tykhomyrov, O. Dyadyk
One of the primary mechanisms of retinal neurodegeneration in diabetes mellitus is gamma-aminobutyric acid (GABA) deficiency that makes the use of GABA-benzodiazepine receptor modulators a promising option for the correction of this diabetic complication. The aim of this study was to determine the effect of the benzodiazepine receptor agonist carbacetam on the expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1α (HIF-1α) in retina of rats with hyperglycemia. Experimental diabetes was modeled by a single administration of streptozotocin (50 mg/kg) to three-month-old male Wistar rats. Immunoblotting and immunohistochemical studies were performed using monoclonal antibodies against VEGF and HIF-1α. It was shown that the development of diabetic retinopathy (DR) at the early stages was accompanied by a progressive multifold increase in the retina content of VEGF on 7-28 days and HIF-1α on 28th day. Insulin and insulin+carbacetam treatment significantly alleviated diabetes-induced overexpression of both HIF-1α and VEGF. Carbacetam was shown to block the diabetogenic increase in VEGF content in retina. The introduction of insulin with carbacetam significantly reduced the expression of VEGF and the development of specific morphological manifestations of DR. Thus, restoration of GABA-ergic signaling can be used as a promising therapeutic option for the correction of DR disorders. Keywords: carbacetam, GABA-benzodiazepine receptors, HIF-1α hyperglycemia, retinopathy, streptozotocin-induced diabetes, VEGF
{"title":"Benzodiazepine receptor agonist carbacetam modulates the level of vascular endothelial growth factor in the retina of rats with streptozotocin-induced diabetes","authors":"S. V. Ziablitsev, D. Zhupan, A. O. Tykhomyrov, O. Dyadyk","doi":"10.15407/ubj95.06.021","DOIUrl":"https://doi.org/10.15407/ubj95.06.021","url":null,"abstract":"One of the primary mechanisms of retinal neurodegeneration in diabetes mellitus is gamma-aminobutyric acid (GABA) deficiency that makes the use of GABA-benzodiazepine receptor modulators a promising option for the correction of this diabetic complication. The aim of this study was to determine the effect of the benzodiazepine receptor agonist carbacetam on the expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1α (HIF-1α) in retina of rats with hyperglycemia. Experimental diabetes was modeled by a single administration of streptozotocin (50 mg/kg) to three-month-old male Wistar rats. Immunoblotting and immunohistochemical studies were performed using monoclonal antibodies against VEGF and HIF-1α. It was shown that the development of diabetic retinopathy (DR) at the early stages was accompanied by a progressive multifold increase in the retina content of VEGF on 7-28 days and HIF-1α on 28th day. Insulin and insulin+carbacetam treatment significantly alleviated diabetes-induced overexpression of both HIF-1α and VEGF. Carbacetam was shown to block the diabetogenic increase in VEGF content in retina. The introduction of insulin with carbacetam significantly reduced the expression of VEGF and the development of specific morphological manifestations of DR. Thus, restoration of GABA-ergic signaling can be used as a promising therapeutic option for the correction of DR disorders. Keywords: carbacetam, GABA-benzodiazepine receptors, HIF-1α hyperglycemia, retinopathy, streptozotocin-induced diabetes, VEGF","PeriodicalId":23007,"journal":{"name":"The Ukrainian Biochemical Journal","volume":"28 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139003095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
O. P. Matyshevska, V. M. Danilova, M. Grigorieva, S. Komisarenko
Leland Hartwell, Paul Nurse and Timothy Hunt in 2001 were awarded the Nobel Prize for their discovery of molecular and genetic mechanisms of the cell cycle. The review analyzes the features of the objects chosen by scientists, a wide range of methods from conventional light microscopy to recombinant DNA technology and complementation test, used for research, and covers a history of the discoveries made. Thanks to the work of these scientists, a modern understanding of the cell cycle checkpoints, the complexes formed by cyclin and cyclin-dependent kinases at different phases of the cell cycle, as well as the mechanism of periodic cyclin degradation and the universality of the cyclin mechanism of cellular division in all living organisms was gained. Keywords: cdc mutants, cdc2/cdc28, cdk protein kinase, cdk/cyclin complex, cell cycle, cyclin, Saccharomyces cerevisiae, Schizosaccharomyces pombe
2001 年，利兰-哈特威尔、保罗-诺斯和蒂莫西-亨特因发现细胞周期的分子和遗传机制而获得诺贝尔奖。这篇综述分析了科学家们所选择对象的特点、从传统的光学显微镜到重组 DNA 技术和互补试验等多种研究方法，并介绍了所取得发现的历史。得益于这些科学家的工作，人们对细胞周期检查点、细胞周期蛋白和细胞周期蛋白依赖性激酶在细胞周期不同阶段形成的复合物，以及周期性细胞周期蛋白降解机制和所有生物体细胞分裂的细胞周期蛋白机制的普遍性有了现代认识。关键词：CDC突变体；CDC2/CDC28；CDK蛋白激酶；CDK/细胞周期蛋白复合物；细胞周期；细胞周期蛋白；酿酒酵母；酿酒酵母小鼠
{"title":"Discovery of molecular and genetic mechanisms of cell cycle regulation: 2001 Nobel laureates leland Hartwell, Timothy Hunt and Paul Nurse","authors":"O. P. Matyshevska, V. M. Danilova, M. Grigorieva, S. Komisarenko","doi":"10.15407/ubj95.06.112","DOIUrl":"https://doi.org/10.15407/ubj95.06.112","url":null,"abstract":"Leland Hartwell, Paul Nurse and Timothy Hunt in 2001 were awarded the Nobel Prize for their discovery of molecular and genetic mechanisms of the cell cycle. The review analyzes the features of the objects chosen by scientists, a wide range of methods from conventional light microscopy to recombinant DNA technology and complementation test, used for research, and covers a history of the discoveries made. Thanks to the work of these scientists, a modern understanding of the cell cycle checkpoints, the complexes formed by cyclin and cyclin-dependent kinases at different phases of the cell cycle, as well as the mechanism of periodic cyclin degradation and the universality of the cyclin mechanism of cellular division in all living organisms was gained. Keywords: cdc mutants, cdc2/cdc28, cdk protein kinase, cdk/cyclin complex, cell cycle, cyclin, Saccharomyces cerevisiae, Schizosaccharomyces pombe","PeriodicalId":23007,"journal":{"name":"The Ukrainian Biochemical Journal","volume":"2010 15","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139002021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Vari, O. Shevchuk, A. Boychuk, S. Kramar, Z. Nebesna, Y. Yakymchuk, L. Kobylinska, V. Chernyshenko, D. Korolova, A. Gaspar-Suranyi, T. Altorjay, R. Gáspár
COVID-19 infection, preeclampsia and gestational diabetes mellitus in pregnancy cause similar changes in the placenta and influence development of the fetus between conception and birth in gestation. Proper uterine and placental vascularization is essential for normal fetal development. The transplacental exchange is regulated and maintained by the placental endothelium. During placental implantation, the trophoblast differentiates into two distinct layers, the inner cytotrophoblast and outer syncytiotrophoblast, which are key elements of the human placental barrier. Proinflammatory cytokines exacerbate ischemic events and create an upward spiral of an inflammatory reaction in the placenta. Placental pathology in gestational COVID-19 shows desquamation and damage of trophoblast and chronic histiocytic intervillositis. Similar lesions also occur in gestational diabetes mellitus and preeclampsia. The systemic inflammatory response of the mother, the increased inflammation in the placenta and cytokine production by placental trophoblasts should be monitored throughout pregnancy. Placental angiogenesis can be evaluated by serum vascular endothelial growth factor, Annexin A2, placental growth factor or sclerostin. Tissue damage can be assessed by measuring levels of serum lactate dehydrogenase and myeloperoxidase. Blood flow can be monitored with three-dimensional Doppler and pathological changes can be documented with paraffin-embedded tissue sections stained with hematoxylin and eosin, and electron microscope images as well as immunohistochemistry tests for vascular endothelial growth factor, placental growth factor, sclerostin and Annexin A2. The damage of maternal and fetal vascular perfusion (villitis and fibrin deposition) is a common mechanism of gestational diseases. The placenta lesions liberate anti-endothelial factors that lead to anti-angiogenic conditions and are the common mechanism of maternal placental vascular malperfusion in gestational diseases. Keywords: dysfunction, inflammation, pathology, placenta, pregnancy, vascularization
{"title":"Common mechanisms of placental dysfunction in preeclampsia, gestational diabetes, and COVID-19 in pregnant women","authors":"S. Vari, O. Shevchuk, A. Boychuk, S. Kramar, Z. Nebesna, Y. Yakymchuk, L. Kobylinska, V. Chernyshenko, D. Korolova, A. Gaspar-Suranyi, T. Altorjay, R. Gáspár","doi":"10.15407/ubj95.03.005","DOIUrl":"https://doi.org/10.15407/ubj95.03.005","url":null,"abstract":"COVID-19 infection, preeclampsia and gestational diabetes mellitus in pregnancy cause similar changes in the placenta and influence development of the fetus between conception and birth in gestation. Proper uterine and placental vascularization is essential for normal fetal development. The transplacental exchange is regulated and maintained by the placental endothelium. During placental implantation, the trophoblast differentiates into two distinct layers, the inner cytotrophoblast and outer syncytiotrophoblast, which are key elements of the human placental barrier. Proinflammatory cytokines exacerbate ischemic events and create an upward spiral of an inflammatory reaction in the placenta. Placental pathology in gestational COVID-19 shows desquamation and damage of trophoblast and chronic histiocytic intervillositis. Similar lesions also occur in gestational diabetes mellitus and preeclampsia. The systemic inflammatory response of the mother, the increased inflammation in the placenta and cytokine production by placental trophoblasts should be monitored throughout pregnancy. Placental angiogenesis can be evaluated by serum vascular endothelial growth factor, Annexin A2, placental growth factor or sclerostin. Tissue damage can be assessed by measuring levels of serum lactate dehydrogenase and myeloperoxidase. Blood flow can be monitored with three-dimensional Doppler and pathological changes can be documented with paraffin-embedded tissue sections stained with hematoxylin and eosin, and electron microscope images as well as immunohistochemistry tests for vascular endothelial growth factor, placental growth factor, sclerostin and Annexin A2. The damage of maternal and fetal vascular perfusion (villitis and fibrin deposition) is a common mechanism of gestational diseases. The placenta lesions liberate anti-endothelial factors that lead to anti-angiogenic conditions and are the common mechanism of maternal placental vascular malperfusion in gestational diseases. Keywords: dysfunction, inflammation, pathology, placenta, pregnancy, vascularization","PeriodicalId":23007,"journal":{"name":"The Ukrainian Biochemical Journal","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75525302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D. Korolova, A. Pavlenko, Á. Altorjay, S. I. Zhuk, I. Us, Y. Tsaryk, A. Surányi, V. Chernyshenko
Thrombotic events are among the most dangerous complications of pregnancy. Therefore, selection of appropriate tests and standardization of techniques used for accurate diagnostics of blood coagulation system state is of great importance. In this present study, we monitored several molecular markers of the dangers of intravascular thrombus formation and estimated the platelet function in pregnant women during gestation. We performed independent measurements using the same methodology for different cohorts of patients recruited in Kyiv (Ukraine) and in Szeged (Hungary). D-dimer and soluble fibrin were measured using ELISA. Protein C (PC) level was estimated using chromogenic substrate assay. Fibrinogen concentration was measured by spectrophotometry using thrombin-like enzyme. Platelet function was estimated by aggregometry. Statistical data analysis was performed using the Kruskal-Wallis test. Statistically significant increases of fibrinogen concentration from first to third gestational trimester was shown for both studied cohorts of patients (5-6 mg/ml at third trimester on average). Applied methods allowed us to detect the same tendencies of decreases in PC level as well as the appearance of moderate amounts of D-dimer (up to 300 ng/ml) and SF (up to 10-15 ug/ml). Platelet function was increased on the first trimester of pregnancy and decreased during following trimesters slightly. Results indicated the changes in the blood coagulation system of pregnant women during gestation with the same effectiveness independently of the selected cohorts, time and place of measurements. The application of the proposed diagnostics algorithm may allow estimating the risk of thrombotic complications during pregnancy. Keywords: D-dimer, fibrinogen, platelets, pregnancy, soluble fibrin, thrombosis
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