Adenosine 3',5'-cyclic monophosphate (cAMP) participates in the regulation of numerous cellular functions, including the $Na^+-K^+$-ATPase (sodium pump). Ouabain, used in the treatment of several heart diseases, is known to increase cAMP levels but its effects on the atrium are not understood. The aim of the present study was to examine the effect of ouabain on the regulation of atrial cAMP production and its roles in atrial endothelin-1 (ET-1) secretion in isolated perfused beating rabbit atria. Our results showed that ouabain ($3.0{\mu}mol/L$) significantly increased atrial dynamics and cAMP levels during recovery period. The ouabain-increased atrial dynamics was blocked by KB-R7943 ($3.0{\mu}mol/L$), an inhibitor for reverse mode of $Na^+-Ca^{2+}$ exchangers (NCX), but did not by L-type $Ca^{2+}$ channel blocker nifedipine ($1.0{\mu}mol/L$) or protein kinase A (PKA) selective inhibitor H-89 ($3.0{\mu}mol/L$). Ouabain also enhanced atrial intracellular cAMP production in response to forskolin and theophyline ($100.0{\mu}mol/L$), an inhibitor of phosphodiesterase, potentiated the ouabain-induced increase in cAMP. Ouabain and 8-Bromo-cAMP ($0.5{\mu}mol/L$) markedly increased atrial ET-1 secretion, which was blocked by H-89 and by PD98059 ($30{\mu}mol/L$), an inhibitor of extracellular-signal-regulated kinase (ERK) without changing ouabain-induced atrial dynamics. Our results demonstrated that ouabain increases atrial cAMP levels and promotes atrial ET-1 secretion via the mitogen-activated protein kinase (MAPK)/ERK signaling pathway. These findings may explain the development of cardiac hypertrophy in response to digitalis-like compounds.
There have been many studies on patients who suffer from anxiety disorders. However, there is been not enough attention on the difference in the level of between the two populations with and without anxiety disorders. This study was performed to investigate the difference in the ANS responses induced by fear in children. Experimental procedures were as follow: All subjects were in upper grade levels in elementary school. ANX(anxiety) scales of PIC(Personality Inventory for Children) were used to measure fear anxiety. Audio-visual clips were used as stimulus to provoke fear emotion. Baseline of physiological signals, ECG, PPG, EDA, and SKT, were measured for 30 seconds before the fear stimulus. Physiological signals were then recorded for 2 minutes while fear is evoked. Psychological and physiological responses were analyzed. All the children reacted to the fear stimulus with high intensity of fear. Physiological responses showed that SKT, SCR, NSCR, HR, RSA, RESP, HF were increased, while R-R was significantly decreased, respectively, during the period of fear induction. Analysis of the level of anxiety and the physiological responses produced by the experience of fear revealed a statistically significant positive correlation in SKT, HR, and RSA. In other words, the higher the level of anxiety, the higher the levels of SKT, HR, and RSA when children experienced fear in conclusion, it is confirmed through this research that physiological responses to fear is associated with the level of anxiety each individual.
In order to observe the distribution of mast cell on the stages of the mammary carcinogenesis, the numerical changes of mast cells in the mammary tumor development in rats treated with DMBA and compound 48/80 have been investigated by the light microscope. The results observed were summarized as follows: The appearance of tumor were not observed during the whole experimental period in the rats of the control group received injection of sterile saline, but tumors appeared in 100% of the animals, the tumor induction time that represented the number of days elapsing between the 3rd DMBA administration until a first tumor became $10{\times}10mm$ in diameter was $42.5{\pm}4.7$ days and the mean number of tumor masses per rat was $3.4{\pm}1.2$ in the DMBA treated group. And the majority of the DMBA-induced mammary neoplasms were appeared cervical mammary gland and thoracic mammary gland. The histological findings of mammary carcinoma were recognized adenocarcinoma in the DMBA treated group. Mast cells were distributed within the adipose tissues and the interglandular connective tissue in the control, but found to be randomly dispersed within the tumor cell masses, in the connective tissues adjacent to the periphery of the tumor, the adipose tissues and the subcutaneous tissues contiguous to the region of tumor development in the DMBA treated group. Numerical alterations of mast cells were observed in the mammary tumors that separated into three major classes of tumors: hyperplasia, atypical hyperplasia and carcinoma. The number of mast cells were distributed in the connective tissues adjacent to the mammary gland was $45.3{\pm}3.4$ cells in the control group, but was $50.2{\pm}4.9$ cells, $126.7{\pm}10.5$ cells and $340.3{\pm}19.2$ cells according to each stages of mammary tumorigenesis in the DMBA treated group.
Melatonin, known as a powerful wide-spectrum antioxidant, is consumed as a food supplement in some countries, but its applicability as an antioxidant additive was not yet studied. Therefore, we evaluated the antioxidant activity of melatonin by DPPH, ABTS, FRAP and ORAC assays as well as its ability to inhibit perilla oil oxidation. The activities of four other related indoles were also compared. Melatonin showed the highest antioxidant activity (mmol trolox equivalent per mol indole, mmol TE) in ORAC (2,159) assay, but a low antioxidant activity in DPPH (0.63), ABTS (91), and FRAP (764) assays, whereas serotonin showed an opposite result. Addition of 1% (w/w) melatonin to perilla oil extended the induction period of oxidation up to about 2 times ($2.93{\pm}0.47h$) compared to that of control ($1.43{\pm}0.26h$) in the Rancimat assay, corresponding to almost 50% of the ability of butylated hydroxyl toluene (BHT). Tryptamine was the most effective indole that inhibited perilla oil oxidation ($9.53{\pm}1.43h$).
Objectives : To evaluate the effects on the formation of benzidine-hemoglobin, and benzidine metabolite-hemoglobin adducts, caused by pretreatment with the known xenobiotic metabolism effectors, ethanol and phenobarbital, in rats administered Direct Black 38 dye. Methods : The experimental rats were divided into three groups: a control group, an ethanol group and a phenobarbital group. Rats were pretreated with ethanol (1g/kg) or phenobarbital (80mg/kg) 24 hours prior to the oral administration of Direct Black 38 (0.5mmol/kg), with the control group being administered the same amount of distilled water. Blood samples were obtained from the vena cava of 5 rats from each group prior to, and at 30 min, 3h, 5h, 9h, 12h, 24h, 48h, 72h, 96h, and 144h following the oral administration of Direct Black 38. Directly after sampling the blood was separated into hemoglobin and plasma, with the adducts being converted into aromatic amines by basic hydrolysis. Hydrolyzed benzidiene, monoacetylbenzidine and 4-aminobiphenyl were analyzed by reverse-phase liquid chromatography with an electrochemical detector, The quantitative amount of the metabolites was expressed by the hemoglobin binding index (HBI). Results : In the ethanol group, benzidine-, monoacetylbenzidine-, and 4-aminobiphenyl-HBI were increased to a greater extent than those in the control group. These results were attributed to the ethanol inducing N-hydrgxylation, which is related to the formation of the hemoglobin adduct, In the phenobarbital group, all the HBIs, with the exception of the benzidine-HBI, were increased to a greater extent than those of the control group. These results were attributed to the phenobarbital inducing N-hydroxylation related to the formation of the hemoglobin adduct. The N-acetylation ratio was only increased with the phenobarbital pretreatment due to the lower benzidine-HBI of the phenobarbital group compared to these of the control and ethanol groups. The N-acetylation ratios for all groups were higher than f for the duration of the experimental period. Although the azo reduction was unaffected by the ethanol, it was inhibited by the phenobarbital, The ratio of the benzidine-HBI in the phenobarbital group was lower than those of the ethanol the control groups for the entire experiment. Conclusion : Our results indicate that both ethanol and phenobarbital increase the formation of adducts by the induction of N-hydroxylation, but also induced N-acetylation. Phenobarbital decreased the formation of benzidine-HBI due to the decrease of the azo reduction. These results suggest that the effects or ethanol and phenobarbital need to be considered in the biochemical monitoring of Direct Black 38.
Oxidants in environment or cigarette smoke are known to be implicated in the oxidative damages of pulmonary system. Such cellular damages are prevented by the presence of adequate levels of antioxidants in the tissue. In the present study, we investigated the influences of smoking duration and concentration of smoke on lung antioxidant defense in rats. Subchronic exposure of rats to smoke generated from 6 cigarettes per day for 90 days caused the activities of catalase and superoxide dismutase (SOD) to increase. However, glutathione peroxidase (GP-Xase) was not significantly changed. Total sulfhydryl compounds (Total-SH) in the lung homogenates from the rats inhaled with cigarette smoke for 15 days was decreased by 44% , thereafter it was returned to the level of normal rats. On the contrary, when rats were daily exposed to a different concentration of smoke generated from 1 to 20 cigarettes per day for 15 days, the activity of catalase was increased gradually with dose, but total SOD activity was increased only in the rats of low dose groups less than 5 cigarettes. Three types of SOD (one Cu, Zn-SOD with pI 4.9, and two Zn-SOD with pI 4.7 and 7.9)were detected in the lung homogenates and Zn-SOD with pI 4.7 was the major and cigarette-smoke inducible form. These results indicate that the protection of lung against oxidants from cigarette smoke seems to be accomplished by the induction of catalase and SOD, especially a cyanide resistant Zn-SOD with pI 4.f, following the consumption of antioxidants such as GSH in the beginning of inhalation period.
Bacteria in the viable but nonculturable (VBNC) state fail to produce colonies on routine bacteriological media, but are still alive in the state of very low metabolic activity. The aim of the present study was to induce the VBNC state of the Edwardsiella tarda using sea water microcosm under starvation conditions at $10^{\circ}C$ and to investigate resuscitation of the VBNC cells in temperatures changed from 10 to $25^{\circ}C$, with and without additives. E. tarda entered into the VBNC state within about 42-84 days of incubation in the microcosm. Throughout this period, the total cell counts as determined using acridine orange direct counting remained near the original inoculum level of ${\sim}10^8cells/ml$. The live cell counts measured with direct viable counting, on the other hands, declined to ${\sim}10^4cells/ml$. When the VBNC cells were incubated with addition of yeast extract, fish muscle extract or serum at $25^{\circ}C$, the ratios of resuscitated samples were 37%, 23%, and 37%, respectively. The characteristics of resuscitated E. tarda were consistent with those of the original E. tarda. When the resuscitated E. tarda were intraperitoneally injected into olive flounders, all fishes died within 5 days, indicating that the VBNC E. tarda might retain its pathogenic potential. Therefore, E. tarda under starvation conditions in the winter enter into the VBNC state and the VBNC E. tarda cells resuscitated at summer and autumn seawater temperature are considered to be pathogen continuously to olive flounder on the southern coast of Korea.
The Journal of the Korean Society for Microbiology
/
v.21
no.4
/
pp.423-434
/
1986
The role of macrophages in the resistance of ICR mice to Candida albicans and Salmonella typhimurium was assessed using silica, agent which selectively inactivates macrophages or poly-2-vinylpyridine-N-oxide(PVNO), a lysosomal stabilizing agent. In addition, effect of silica on humoral and cellular immune responses to sheep red blood cells(SRBC) or polyvinylpyroridone(PVP) was examind. Colonyforming units(CFU) of C. albicans or S. typhimurium in the spleen, livers and kidneys of silica-treated or diluent-treated mice were enumerated at various times after infection. Silica was given i. v. to mice at 4 days or 1 day before infection. Although there was no apparent differences in the number of CFU of C. albicans cultured from the spleens or livers of silica-treated and control mice at every assay period, significant differences in the number of CFU of C. albicans in the kidneys of silica-treated and control mice. Namely, silica given to mice 1 day before infection significantly increased the number of CFU of C. albicans in the kidneys at 2, 4 and 6 days after infection, but did not change the number of CFU at 8 days after infection. Silica given to mice at 4 days before infection significantly increased the number CFU in the kidneys at 2 and 4 days after infection, but rather decreased the number of CFU at 8 days after infection. The number of CFU of C. albians cultured from the kidneys of splenectomized which were experimentally infected mice was similar to the number recovered from sham-operated mice at 4 and 8 days postinfection irrespective of time of infection relative to operation. The pretreatment of mice with PVNO appeared to abrogate the silica-induced susceptibility of mice to C. albicans. PVNO alone showed somewhat protective effect against challenge with C. albicans. In contrast, silica treatment did not alter the number of CFU of S. typhimurium recovered from the spleens and kidneys of mice. The administration of silica to mice at 4 days or 1 day before SRBC immunization significantly suppressed delayed-type hypersensitivity(DTH) reactions to SRBC and antibody production to SRBC, a thymus-dependent antigen and PVP, a thymus-independent antigen. These results provide evidence that macrophages play an important role in susceptibility to Candida infection and strongly demonstrated that macrophages play an essential role in the induction of immune responses in mice.
The inhibitory effects of red-ginseng saponin hydrolyzates (prosapogenin, panaxadiol and panaxatriol) on lipoperoxide formation in vitro and in vivo were investigated and correlated with anti-aging. Saponin hydrolyzates showed the electron-donating ability (EDA) of 12.88 - 19.76% to DPPH in vitro, and the ability was distinctively decreased in order of prosapogenin, panaxatriol and panaxadiol. The induction period of saponin hydrolyzates, which was measured by the method of peroxide value (POV), was much longer than red-ginseng saponin and decreased in order of prosapogenin, panaxatriol and panaxadiol. The inhibitory effect of saponin, hydrolyzates in vivo was remarkably greater than control. In contrast to red-ginseng saponin, almost similar inhibitory effect in rat liver and kidney was observed, whereas they were much more effective than red-ginseng saponin in blood. The superoxide dismutase (SOD) activity of saponin hydrolyzates in vitro was also measured, and the inhibitory effect of saponin hydrolyzates was found to be 24.2-36.4% and 2-3 times greater than that of red-ginseng saponin (12.1%). Saponin hydrolyzates showed the inhibitory effects of 11.2-21.6% and 12.9-22.2% in oral and intraperitioneal administrations, respectively. It was also found from the measurement of peroxidase activity that the inhibitory effects of saponin hydrolyzates were 111.4-139.6% in oral administration and 129.0-188.6% in intraperitoneal administration.
Park, Bock-Hee;Cho, Hee-Sook;Kim, Kyung-Hee;Kim, Sun-Sook;Kim, Hyun-A
Korean journal of food and cookery science
/
v.24
no.4
/
pp.452-459
/
2008
The purpose of this study was to investigate the antioxidative effects of Sea tangle powder(STP) solvent extracts as well as Maejakgwa made with STP. The STP solvent extracts were added to soybean oil at a quantity of 0.05%. The solvents used for extraction were methanol, ethanol, ethyl acetate, and petroleum ether. Soybean oil without added STP was used as a negative control, and soybean oil samples containing 0.02% butylated hydroxy toluene(BHT) and $\alpha$-tocopherol were used as positive control, respectively. Each sample was stored at $50^{\circ}C$ for 30 days. The oxidation levels of these samples were determined by measuring their acid values, peroxide values, and thiobarbituric acid(TBA) values. The soybean oil samples containing the STP extracts had lower oxidation levels than both the negative control and $\alpha$-tocopherol positive control, and the sample containing the 0.05% methanol extracts had the lowest oxidation. According to the Rancimat method, the methanol extract(320 min) and ethanol extract(316 min) demonstrated longer induction periods as, compared to the control(253 min), $\alpha$-tocopherol(255 min), and BHT(309 min) samples. For the Maejakgwa, acid values increased over the storage period, however, the samples made with STP had lower values than the control group. Peroxide values increased rapidly for 30 days and then decreased. The TBA values of the Maejakgwa samples made with 3% and 9% STP were lower than those of the 15% STP sample and the control. In conclusion, the oxidative stability of soybean oil containing solvent extracts of STP and Maejakgwa made with STP were increased.
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