H. B. Opanasenko, L. V. Bratus, B. L. Havenauskas, O. Honchar, I. M. Man'kovs'ka, V. Nosar, S. B. Frantsuzova
Influence of prolonged immobilization (6 h strict horizontal position of rats in the tight containers daily for 2 weeks) on oxygen tension, oxygen consumption, pro-/antioxidant balance, and energetic metabolism of soft and hard periodontal tissues has been investigated. It was established that prolonged immobilization stress resulted in marked decrease in the gum tissue PO2 (36%) and in the bone tissue oxygen consumption rate (46%) compared to control. It was also determined that prolonged stress led to a reduction in the gum mitochondrial respiration rate. The latter was more expressed in case of the NAD-dependent substrate oxidation than of the FAD- dependent one. It was determined that the prolonged stress results in intensification of peroxide processes and depletion of antioxidant protection of soft tissues of periodontum. It was found that Thiotriazolin and Actovegin have modified and diminished stress-induced disorders in the soft and hard periodontal tissues oxygen homeostasis under prolonged immobilization stress.
{"title":"[Disturbances of oxygen-dependent processes in periodontal tissues under prolonged immobilization stress and ways of their pharmacological correction].","authors":"H. B. Opanasenko, L. V. Bratus, B. L. Havenauskas, O. Honchar, I. M. Man'kovs'ka, V. Nosar, S. B. Frantsuzova","doi":"10.15407/FZ59.01.017","DOIUrl":"https://doi.org/10.15407/FZ59.01.017","url":null,"abstract":"Influence of prolonged immobilization (6 h strict horizontal position of rats in the tight containers daily for 2 weeks) on oxygen tension, oxygen consumption, pro-/antioxidant balance, and energetic metabolism of soft and hard periodontal tissues has been investigated. It was established that prolonged immobilization stress resulted in marked decrease in the gum tissue PO2 (36%) and in the bone tissue oxygen consumption rate (46%) compared to control. It was also determined that prolonged stress led to a reduction in the gum mitochondrial respiration rate. The latter was more expressed in case of the NAD-dependent substrate oxidation than of the FAD- dependent one. It was determined that the prolonged stress results in intensification of peroxide processes and depletion of antioxidant protection of soft tissues of periodontum. It was found that Thiotriazolin and Actovegin have modified and diminished stress-induced disorders in the soft and hard periodontal tissues oxygen homeostasis under prolonged immobilization stress.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"20 1","pages":"17-24"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75490703","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}
R. B. Strutyns'kyĭ, R. A. Rovenets, N. A. Strutyns'ka, O. P. Neshcheret, O. Moibenko
In experiments on the anaesthetized dogs the influence of a new fluorine-containing opener of ATP-sensitive potassium (K(ATP)) channels flocalin on the cardiohemodynamic of great animals in vivo was studied. Flocalin introduced intravenously in doses 0.01 - 1.5 mgs/kg. It is shown that it reduces in dose-dependent manner a system arterial pressure, perfusion pressure in coronary artery and general peripheral resistance of vessels with maximal effects on 56.8 +/- 2.7, 22.4 +/- 4.7 and 47.2% +/- 6.5% accordingly at most dose 1.5 mgs/kg. Flocalin causes development of cardiodepressive reactions in heart, that is exhibited in dose-dependent the decrease of pressure in the left ventricle, speed of growth (dP/dt(max)) and reduction (dP/dt(min)) in it's of pressure with maximal effects on 37.1 +/- 5.1, 51.2 +/- 9.4 and 55.6% +/- 6.9% accordingly at introduction of most dose of flocalin. Diminish of the cardiac out put and heart rate with a maximal effects on 23.1% +/-12.7% and 19.2% +/- 1.7% accordingly at a dose 1.0 mgs/kg was shown. It should be noted that considerable reduction of heart rate and general peripheral resistance of vessels takes place only at the large doses of flocalin - 1 and 1.5 mgs/kg. Thus, it is shown that activation of K(ATP) channels by flocalin causes the dose-dependent decrease of pressure in the system of circulation of blood and contraction activity of myocardium.
{"title":"[The influence of activation of the ATP-sensitive potassium channels by flocalin on the function of the cardiovascular system].","authors":"R. B. Strutyns'kyĭ, R. A. Rovenets, N. A. Strutyns'ka, O. P. Neshcheret, O. Moibenko","doi":"10.15407/FZ59.01.011","DOIUrl":"https://doi.org/10.15407/FZ59.01.011","url":null,"abstract":"In experiments on the anaesthetized dogs the influence of a new fluorine-containing opener of ATP-sensitive potassium (K(ATP)) channels flocalin on the cardiohemodynamic of great animals in vivo was studied. Flocalin introduced intravenously in doses 0.01 - 1.5 mgs/kg. It is shown that it reduces in dose-dependent manner a system arterial pressure, perfusion pressure in coronary artery and general peripheral resistance of vessels with maximal effects on 56.8 +/- 2.7, 22.4 +/- 4.7 and 47.2% +/- 6.5% accordingly at most dose 1.5 mgs/kg. Flocalin causes development of cardiodepressive reactions in heart, that is exhibited in dose-dependent the decrease of pressure in the left ventricle, speed of growth (dP/dt(max)) and reduction (dP/dt(min)) in it's of pressure with maximal effects on 37.1 +/- 5.1, 51.2 +/- 9.4 and 55.6% +/- 6.9% accordingly at introduction of most dose of flocalin. Diminish of the cardiac out put and heart rate with a maximal effects on 23.1% +/-12.7% and 19.2% +/- 1.7% accordingly at a dose 1.0 mgs/kg was shown. It should be noted that considerable reduction of heart rate and general peripheral resistance of vessels takes place only at the large doses of flocalin - 1 and 1.5 mgs/kg. Thus, it is shown that activation of K(ATP) channels by flocalin causes the dose-dependent decrease of pressure in the system of circulation of blood and contraction activity of myocardium.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"6 1","pages":"11-6"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74353522","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}
Pub Date : 2013-01-01DOI: 10.1615/INTJPHYSPATHOPHYS.V5.I1.80
M. Spivak, L. Lazarenko, T. Falalieieva, O. Virchenko, K. Neporada
It was investigated the effect of probiotic strains Bifidobacterium animalis VKL and VKB and their mixture on erosive and ulcerative lesions in the gastric mucosa (GM) of rats induced by water immersion restraint stress. It was found that separate prophylactic introduction for 14 days of Bifidobacterium animalis VKL or Bifidobacterium animalis VKB didn't protect the GM from erosive and ulcerative lesions induced by stress. Contrary prophylactic introduction of Bifidobacterium animalis VKL and VKB mixture has been effective in protecting the GM from the lesions. One of the mechanisms of the gastroprotection of these probiotic strains is prevention of mucus barrier from degradation, which was evident in decrease of free fucose and hexuronic acids content. These results confirm the expediency ofprobiotics use for the prevention of stress-induced lesions in the GM.
{"title":"[Prophylactic effect of probiotic strains Bifidobacterium animalis VKL and VKB on stress-induced lesions in the gastric mucosa of rats].","authors":"M. Spivak, L. Lazarenko, T. Falalieieva, O. Virchenko, K. Neporada","doi":"10.1615/INTJPHYSPATHOPHYS.V5.I1.80","DOIUrl":"https://doi.org/10.1615/INTJPHYSPATHOPHYS.V5.I1.80","url":null,"abstract":"It was investigated the effect of probiotic strains Bifidobacterium animalis VKL and VKB and their mixture on erosive and ulcerative lesions in the gastric mucosa (GM) of rats induced by water immersion restraint stress. It was found that separate prophylactic introduction for 14 days of Bifidobacterium animalis VKL or Bifidobacterium animalis VKB didn't protect the GM from erosive and ulcerative lesions induced by stress. Contrary prophylactic introduction of Bifidobacterium animalis VKL and VKB mixture has been effective in protecting the GM from the lesions. One of the mechanisms of the gastroprotection of these probiotic strains is prevention of mucus barrier from degradation, which was evident in decrease of free fucose and hexuronic acids content. These results confirm the expediency ofprobiotics use for the prevention of stress-induced lesions in the GM.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"20 1","pages":"23-30"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84461301","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}
In this work we investigated changes in the cytochrome P450 2E1 (CYP2E1) expression level in the liver of mice that have been exposed to psycho-emotional stress (PES). It was shown twofold relative to control reduction of the enzyme, which does not normalize after termination of the stressor. The changes in level of Cyp2e1 mRNA is not observed at any time point of the experiment. At the same time it was found a significant decrease in the expression level of hsp90--one of the factors determines of the level of CYP2E1 degradation in the cell. Also it was shown, the oxidative stress develops in the liver of experimental animals, and this is indicated by a 3-fold increase in the malondialdehyde level on the background of a 5-fold decrease in catalase activity. A decrease in the level of expression of cytochrome P450 2E1 in the liver of mice that have been exposed to psycho-emotional stress is due to the intensification of the peroxide process and the development of oxidative stress. Reduction of protein content of CYP2E1 is apparently not related to the hsp90-dependent processes of its degradation in the cell.
{"title":"[Stress-induced changes in the content of cytochrome P450 2E1 in the liver of mice with chronic psychoemotional overexertion].","authors":"Maksymchuk Ov, Chashchyn Mo","doi":"10.15407/FZ59.04.067","DOIUrl":"https://doi.org/10.15407/FZ59.04.067","url":null,"abstract":"In this work we investigated changes in the cytochrome P450 2E1 (CYP2E1) expression level in the liver of mice that have been exposed to psycho-emotional stress (PES). It was shown twofold relative to control reduction of the enzyme, which does not normalize after termination of the stressor. The changes in level of Cyp2e1 mRNA is not observed at any time point of the experiment. At the same time it was found a significant decrease in the expression level of hsp90--one of the factors determines of the level of CYP2E1 degradation in the cell. Also it was shown, the oxidative stress develops in the liver of experimental animals, and this is indicated by a 3-fold increase in the malondialdehyde level on the background of a 5-fold decrease in catalase activity. A decrease in the level of expression of cytochrome P450 2E1 in the liver of mice that have been exposed to psycho-emotional stress is due to the intensification of the peroxide process and the development of oxidative stress. Reduction of protein content of CYP2E1 is apparently not related to the hsp90-dependent processes of its degradation in the cell.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"11 1","pages":"67-73"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89134804","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}
Pub Date : 2013-01-01DOI: 10.1615/INTJPHYSPATHOPHYS.V5.I3.20
O. V. Lun'ko, O. Fedorenko, S. Marchenko
Previously we have found the large conductance cation channels (LCCC) in the nuclear membranes, where inositol-1,4,5-triphosphate receptors (IP3Rs) were also observed. Probably IP3Rs and LCCC are functionally connected: LCCC may provide the counterflow of K+, which prevent the formation of the negative potential in the lumen of the nuclear envelope and in such way may prolong the Ca2+ releasing by IP3Rs. LCCC are poorly studied and their molecular nature is still unknown. We investigated the effect of Ca2+ on properties of these channels. Our results demonstrated the main biophysical properties of LCCC changed significantly neither in Ca(2+)-free solution, nor with high concentrations of Ca2+ in the nuclear lumen. So, the level of Ca2+ repletion of the store does not influence the activity of LCCC.
{"title":"[The effect of Ca2+ on the properties of the large conductance cation channels of the nuclear envelope of the cerebellar neurons].","authors":"O. V. Lun'ko, O. Fedorenko, S. Marchenko","doi":"10.1615/INTJPHYSPATHOPHYS.V5.I3.20","DOIUrl":"https://doi.org/10.1615/INTJPHYSPATHOPHYS.V5.I3.20","url":null,"abstract":"Previously we have found the large conductance cation channels (LCCC) in the nuclear membranes, where inositol-1,4,5-triphosphate receptors (IP3Rs) were also observed. Probably IP3Rs and LCCC are functionally connected: LCCC may provide the counterflow of K+, which prevent the formation of the negative potential in the lumen of the nuclear envelope and in such way may prolong the Ca2+ releasing by IP3Rs. LCCC are poorly studied and their molecular nature is still unknown. We investigated the effect of Ca2+ on properties of these channels. Our results demonstrated the main biophysical properties of LCCC changed significantly neither in Ca(2+)-free solution, nor with high concentrations of Ca2+ in the nuclear lumen. So, the level of Ca2+ repletion of the store does not influence the activity of LCCC.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"98 1","pages":"28-32"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86950651","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. Minchenko, K. Kubaichuk, O. V. Hubenia, I. V. Kryvdiuk, I. Khomenko, R. M. Herasymenko, R. Sulik, N. Murashko, O. Minchenko
The endoplasmic reticulum is a dynamic intracellular organelle with exquisite sensitivity to alterations in homeostasis, and provides stringent quality control systems to ensure that the only correctly folded proteins transit to the Golgi and unfolded or misfolded proteins are retained and ultimately degraded. The endoplasmic reticulum stress represents the unfolded protein response to cope with the accumulation of unfolded or misfolded proteins and is required to maintain the functional integrity of the endoplasmic reticulum. The endoplasmic reticulum stress is a fundamental phenomenon which provides a secure protection of the cells from different factors. This stress provides a wide spectrum of physiological roles in diverse developmental and metabolic processes, especially for professional secretory cells with high-level secretory protein synthesis, such as pancreatic beta cells, hepatocytes and osteoblasts and is required throughout the entire life. The endoplasmic reticulum stress and hypoxia are the obligate components of malignant tumor growth, are interconnected and activate angiogenesis via growth and metabolism control. The endoplasmic reticulum stress is mediated by three by three sensor and signaling pathways (PERK, ATF6 and ERN1), besides that blockade one (ERN1) leads to a decrease of tumor growth through suppression of angiogenesis and proliferation. The data concerning the interaction of signaling enzyme ERN1 and pro- and anti-angiogenic gene expressions is analyzed.
{"title":"[Endoplasmic reticulum stress and angiogenesis].","authors":"D. Minchenko, K. Kubaichuk, O. V. Hubenia, I. V. Kryvdiuk, I. Khomenko, R. M. Herasymenko, R. Sulik, N. Murashko, O. Minchenko","doi":"10.15407/FZ59.04.093","DOIUrl":"https://doi.org/10.15407/FZ59.04.093","url":null,"abstract":"The endoplasmic reticulum is a dynamic intracellular organelle with exquisite sensitivity to alterations in homeostasis, and provides stringent quality control systems to ensure that the only correctly folded proteins transit to the Golgi and unfolded or misfolded proteins are retained and ultimately degraded. The endoplasmic reticulum stress represents the unfolded protein response to cope with the accumulation of unfolded or misfolded proteins and is required to maintain the functional integrity of the endoplasmic reticulum. The endoplasmic reticulum stress is a fundamental phenomenon which provides a secure protection of the cells from different factors. This stress provides a wide spectrum of physiological roles in diverse developmental and metabolic processes, especially for professional secretory cells with high-level secretory protein synthesis, such as pancreatic beta cells, hepatocytes and osteoblasts and is required throughout the entire life. The endoplasmic reticulum stress and hypoxia are the obligate components of malignant tumor growth, are interconnected and activate angiogenesis via growth and metabolism control. The endoplasmic reticulum stress is mediated by three by three sensor and signaling pathways (PERK, ATF6 and ERN1), besides that blockade one (ERN1) leads to a decrease of tumor growth through suppression of angiogenesis and proliferation. The data concerning the interaction of signaling enzyme ERN1 and pro- and anti-angiogenic gene expressions is analyzed.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"1 1","pages":"93-106"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89649930","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}
M. B. Baskakov, A. Zheludeva, S. Gusakova, L. Smaglii, A. Aleinik, P. I. Ianchuk, M. Medvedev, S. Orlov
Carbon monoxide (CO) is one of a family of gas transmitters. In this article we present the results of mechanographic investigations of the mechanisms of CO action on a rat thoracic aorta segments. We found that relaxing effect of CO donor CORM-2 on vascular smooth muscles is mediated mainly by opening of voltage-dependent potassium channels in smooth muscle cells: 4-aminopyridine, blocking these channels, almost completely eliminated the CO-induced vasorelaxation of the segments precontracted by depolarization of the smooth muscle cells membranes with high potassium (30 mM KCl) solution or by phenylephrine (10 microM). For the first time we documented that CORM-2 reduces the nicardipine-sensitive input of 45Ca2+ in freshly isolated aorta cells. There are reasons to suggest that the L-type voltage-dependent calcium channels of vascular smooth muscle cells are another target for CO, which is implemented in the relaxing effect of this gas transmitter. Additional research is needed to determine the influence of ruthenium complexes (Ru(II)) on phenomenology of carbon monoxide effects.
一氧化碳(CO)是气体变送器家族中的一员。在这篇文章中，我们介绍了CO作用于大鼠胸主动脉段的机制的力学研究结果。我们发现CO供体CORM-2对血管平滑肌的松弛作用主要是通过打开平滑肌细胞中电压依赖性钾通道介导的:4-氨基吡啶阻断这些通道，几乎完全消除了CO诱导的平滑肌细胞膜去极化预收缩节段的血管松弛，高钾(30 mM KCl)溶液或苯肾上腺素(10微米)。我们首次证明，CORM-2减少了新鲜分离的主动脉细胞中对尼卡地平敏感的45Ca2+输入。有理由认为，血管平滑肌细胞的l型电压依赖性钙通道是CO的另一个靶点，这是通过这种气体递质的放松作用来实现的。需要进一步的研究来确定钌配合物(Ru(II))对一氧化碳效应现象学的影响。
{"title":"[Ionic mechanisms of carbon monoxide action on the contractile properties of smooth muscles of the blood vessels].","authors":"M. B. Baskakov, A. Zheludeva, S. Gusakova, L. Smaglii, A. Aleinik, P. I. Ianchuk, M. Medvedev, S. Orlov","doi":"10.15407/FZ59.03.018","DOIUrl":"https://doi.org/10.15407/FZ59.03.018","url":null,"abstract":"Carbon monoxide (CO) is one of a family of gas transmitters. In this article we present the results of mechanographic investigations of the mechanisms of CO action on a rat thoracic aorta segments. We found that relaxing effect of CO donor CORM-2 on vascular smooth muscles is mediated mainly by opening of voltage-dependent potassium channels in smooth muscle cells: 4-aminopyridine, blocking these channels, almost completely eliminated the CO-induced vasorelaxation of the segments precontracted by depolarization of the smooth muscle cells membranes with high potassium (30 mM KCl) solution or by phenylephrine (10 microM). For the first time we documented that CORM-2 reduces the nicardipine-sensitive input of 45Ca2+ in freshly isolated aorta cells. There are reasons to suggest that the L-type voltage-dependent calcium channels of vascular smooth muscle cells are another target for CO, which is implemented in the relaxing effect of this gas transmitter. Additional research is needed to determine the influence of ruthenium complexes (Ru(II)) on phenomenology of carbon monoxide effects.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"74 1","pages":"18-24"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86798783","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}
Strutyns'ka Na, Dorofeieva No, Vavilova Hl, Sahach Vf
In experiments in vivo and in vitro on the mitochondria isolated from the control and spontaneously hypertensive rats (SHR) hearts, we studied the effects of a donor of hydrogen sulfide (H2S), NaHS, and H2S biosynthesis substrate, L-cysteine, on the sensitivity of the mitochondrial permeability transition pore (mPTP) opening to its natural inductor, Ca2+. We found that NaHS (10(-4), 10(-5) and 5 10(-5) mol/l) influenced the mitochondrial swelling in a concentration-dependent manner in control and spontaneously hypertensive rats. The H2S donor NaHS used in physiological concentrations (10(-6), 10(-5) and 5 10(-5) mol/l) exerted the inhibiting effect on the Ca(2+)-induced mPTP opening in control hearts (corresponding values of such effect were 31, 76, and 100%, respectively), while in spontaneously hypertensive rats hearts the protector effect of NaHS was observed only at its concentration of 10(-5) - 10(-4) mol/l. In experiments in vivo, single intraperitoneal injections of L-cysteine (10(-3) mol/kg) resulted in a decrease in the sensitivity of mPTP to it's inductor Ca2+ in control rats and SHR. In experiments in vivo in which we used a specific blocker of cystathionine-gamma-lyase, propargylglycine (10(-4) mol/kg), with the further injections of L-cysteine we observed a decrease in the threshold Ca2+ concentration (that induce the mitochondrial swelling) by three orders of magnitude in SHR, but in control rats did not effect of L-cysteine. Thus, both endogenous and exogenous hydrogen sulfide inhibits Ca(2+)-induced mitochondrial permeability transition pore opening, indicating its protective effect on pore formation in spontaneously hypertensive rats hearts. Therefore, our studies are indicative of the involvement of H2S in modulation of changes in the permeability of mitochondrial membranes, which can be an important regulatory factor in the development of cardiovascular diseases.
{"title":"[Hydrogen sulfide inhibits Ca(2+)-induced mitochondrial permeability transition pore opening in spontaneously hypertensive rats].","authors":"Strutyns'ka Na, Dorofeieva No, Vavilova Hl, Sahach Vf","doi":"10.15407/FZ59.01.003","DOIUrl":"https://doi.org/10.15407/FZ59.01.003","url":null,"abstract":"In experiments in vivo and in vitro on the mitochondria isolated from the control and spontaneously hypertensive rats (SHR) hearts, we studied the effects of a donor of hydrogen sulfide (H2S), NaHS, and H2S biosynthesis substrate, L-cysteine, on the sensitivity of the mitochondrial permeability transition pore (mPTP) opening to its natural inductor, Ca2+. We found that NaHS (10(-4), 10(-5) and 5 10(-5) mol/l) influenced the mitochondrial swelling in a concentration-dependent manner in control and spontaneously hypertensive rats. The H2S donor NaHS used in physiological concentrations (10(-6), 10(-5) and 5 10(-5) mol/l) exerted the inhibiting effect on the Ca(2+)-induced mPTP opening in control hearts (corresponding values of such effect were 31, 76, and 100%, respectively), while in spontaneously hypertensive rats hearts the protector effect of NaHS was observed only at its concentration of 10(-5) - 10(-4) mol/l. In experiments in vivo, single intraperitoneal injections of L-cysteine (10(-3) mol/kg) resulted in a decrease in the sensitivity of mPTP to it's inductor Ca2+ in control rats and SHR. In experiments in vivo in which we used a specific blocker of cystathionine-gamma-lyase, propargylglycine (10(-4) mol/kg), with the further injections of L-cysteine we observed a decrease in the threshold Ca2+ concentration (that induce the mitochondrial swelling) by three orders of magnitude in SHR, but in control rats did not effect of L-cysteine. Thus, both endogenous and exogenous hydrogen sulfide inhibits Ca(2+)-induced mitochondrial permeability transition pore opening, indicating its protective effect on pore formation in spontaneously hypertensive rats hearts. Therefore, our studies are indicative of the involvement of H2S in modulation of changes in the permeability of mitochondrial membranes, which can be an important regulatory factor in the development of cardiovascular diseases.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"84 1","pages":"3-10"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75948859","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}
NADPH-oxidase (NOX) is a novel transmembrane enzyme that appears to have pivotal role in the control of platelet signal pathways. The NOX activity in platelets is controlled by agonist receptors activation, which, in turn are modulated by NOX. This review focuses on participation of NOX in autocrine and paracrine regulation of platelet activation, aggregation secretion, protein synthesis and cell recruitment processes during thrombus formation. Possible involving of NOX in the cell-to-cell communication and coordination in response to trombogenic stimulus is discussed.
{"title":"[The role of NADPH-oxidase in paracrine and autocrine regulation of platelet functional activity].","authors":"S. A. Talanov, T. I. Liashenko, I. I. Patalakh","doi":"10.15407/FZ59.05.085","DOIUrl":"https://doi.org/10.15407/FZ59.05.085","url":null,"abstract":"NADPH-oxidase (NOX) is a novel transmembrane enzyme that appears to have pivotal role in the control of platelet signal pathways. The NOX activity in platelets is controlled by agonist receptors activation, which, in turn are modulated by NOX. This review focuses on participation of NOX in autocrine and paracrine regulation of platelet activation, aggregation secretion, protein synthesis and cell recruitment processes during thrombus formation. Possible involving of NOX in the cell-to-cell communication and coordination in response to trombogenic stimulus is discussed.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"18 1","pages":"85-94"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81504345","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. M. Semenykhina, N. A. Strutyns'ka, A. I. Bud'ko, H. L. Vavilova, V. F. Sahach
In experiments on mitochondria isolated from the heart tissue of adult rats we studied the effects of a donor of hydrogen sulfide, NaHS, on the respiratory chain of the organelles. We found that NaHS (10(-9)-10(-6) mol/l) caused a dose-dependent decrease in the rate of oxygen consumption in the presence of succinate and ADP (state 3 to Chance), and in the absence of ADP (state 4). The decrease in the rate of oxygen consumption in a concentration NaHS 10(-9) mol/l and 10(-8) mol/l associated with an increased conjugation of oxidation and phosphorylation, as evidenced by the increase in the respiratory control, the efficiency of oxidative phosphorylation (ADP/O) is not changed. Our studies suggest a protective effect of hydrogen sulfide donor on the functional state of the mitochondria. To elucidate of other the mechanisms of the protective action H2S we also investigated the effect of hydrogen sulfide donor on the mitochondrial swelling. It was found that NaHS in the range of concentration 10(-12) - 10(-4) mol/l influences the level of mitochondria swelling of the rats heart in the dose-dependent manner. It was also shown that when the concentration of Ca2+ 1 nmol/mg protein in the medium, under the action of hydrogen sulfide in the donor concentration range 10(-12) - 10(-8) mol/l, there was a moderate swelling of rats heart mitochondria. Under the action of NaHS at a concentration of 10(-9) mol/l it was observed swelling of the mitochondria, the maximum change in the level of which was 11%. Inhibitor of mitochondrial ATP-sensitive K+ channels (K(ATP) channels) 5-hydroxydecanoate (10(-4) mol/l) partially reduced the mitochondrial swelling in the presence of NaHS (10(-9) mol/l), which may indicate the activation of K(ATP) channels. Our studies point for possible involvement of mitochondrial K(ATP) channels in implementation of the mechanisms of H2S.
{"title":"[Effect of hydrogen sulfide donor NaHs on the functional state of the respiratory chain of the rat heart mitochondria].","authors":"O. M. Semenykhina, N. A. Strutyns'ka, A. I. Bud'ko, H. L. Vavilova, V. F. Sahach","doi":"10.15407/FZ59.02.009","DOIUrl":"https://doi.org/10.15407/FZ59.02.009","url":null,"abstract":"In experiments on mitochondria isolated from the heart tissue of adult rats we studied the effects of a donor of hydrogen sulfide, NaHS, on the respiratory chain of the organelles. We found that NaHS (10(-9)-10(-6) mol/l) caused a dose-dependent decrease in the rate of oxygen consumption in the presence of succinate and ADP (state 3 to Chance), and in the absence of ADP (state 4). The decrease in the rate of oxygen consumption in a concentration NaHS 10(-9) mol/l and 10(-8) mol/l associated with an increased conjugation of oxidation and phosphorylation, as evidenced by the increase in the respiratory control, the efficiency of oxidative phosphorylation (ADP/O) is not changed. Our studies suggest a protective effect of hydrogen sulfide donor on the functional state of the mitochondria. To elucidate of other the mechanisms of the protective action H2S we also investigated the effect of hydrogen sulfide donor on the mitochondrial swelling. It was found that NaHS in the range of concentration 10(-12) - 10(-4) mol/l influences the level of mitochondria swelling of the rats heart in the dose-dependent manner. It was also shown that when the concentration of Ca2+ 1 nmol/mg protein in the medium, under the action of hydrogen sulfide in the donor concentration range 10(-12) - 10(-8) mol/l, there was a moderate swelling of rats heart mitochondria. Under the action of NaHS at a concentration of 10(-9) mol/l it was observed swelling of the mitochondria, the maximum change in the level of which was 11%. Inhibitor of mitochondrial ATP-sensitive K+ channels (K(ATP) channels) 5-hydroxydecanoate (10(-4) mol/l) partially reduced the mitochondrial swelling in the presence of NaHS (10(-9) mol/l), which may indicate the activation of K(ATP) channels. Our studies point for possible involvement of mitochondrial K(ATP) channels in implementation of the mechanisms of H2S.","PeriodicalId":12306,"journal":{"name":"Fiziolohichnyi zhurnal","volume":"12 1","pages":"9-17"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87872225","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}
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