• Tuberculosis and Respiratory Diseases
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• v.42 no.6
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• pp.862-870
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• 1995

Background: Oxygen free radicals have generally been considered as cytotoxic agents. On the other hand, recent results suggest that small nontoxic amounts of these radicals may act a role in intracellular signal transduction pathway and many efforts to reveal the role of these radicals as secondary messengers have been made. It is evident that the oxygen radicals are released by various cell types in response to extracellular stimuli including LPS, TNF, IL-1 and phorbol esters, all of which translocate the transcription factor $NF{\kappa}B$ from cytoplasm to nucleus by releasing an inhibitory protein subunit, $I{\kappa}B$. Activation of $NF{\kappa}B$ is mimicked by exposure to mild oxidant stress, and inhibited by agents that remove oxygen radicals. It means the cytoplasmic form of the inducible tanscription factor $NF{\kappa}B$ might provide a physiologically important target for oxygen radicals. At the same time, it is well known that LPS induces the release of oxygen radicals in neutrophil with the activation of $NF{\kappa}B$. From above facts, we can assume the expression of IL-8 and IL-$1{\beta}$ gene by LPS stimulation may occur through the activation of $NF{\kappa}B$, which is mediated through the release of $I{\kappa}B$ by increasing amounts of oxygen radicals. But definitive evidence is lacking about the role of oxygen free radicals in the expression of IL-8 and IL-$1{\beta}$ gene in mononuclear phagocytic cells. We conducted a study to determine whether oxygen radicals act a role in the expression of IL-8 and IL-$1{\beta}$ gene in mononuclear phagocytic cells. Method: Human peripheral blood monocytes were isolated from healthy volunteers. Time and dose relationship of $H_2O_2$-induced IL-8 and IL-$1{\beta}$ mRNA expression was observed by Northern blot analysis. To evaluate the role of oxygen radicals in the expression of IL-8 and IL-$1{\beta}$ mRNA by LPS stimulation, pretreatment of various antioxiants including PDTC, TMTU, NAC, ME, Desferrioxamine were done and Northern blot analysis for IL-8 and IL-$1{\beta}$ mRNA was performed. Results: In PBMC, dose and time dependent expression of IL-8 and IL-$1{\beta}$ mRNA by exogenous $H_2O_2$ was not observed. But various antioxidants suppressed the expression of LPS-induced IL-8 and IL-$1{\beta}$ mRNA expression of PBMC and the suppressive activity was most prominant when the pretreatment was done with TMTU. Conclusion: Oxygen free radical may have some role in the expression of IL-8 and IL-$1{\beta}$ mRNA of PBMC but that radical might not be $H_2O_2$.

• The korean journal of orthodontics
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• v.27 no.3 s.62
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• pp.431-444
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• 1997

This research was carried out to compares the treatment effects of Horizontal and Vertical type activators in Angle's Class II div. 1 maloccusion patients with mandibular retrusion dand to find out whether different treatment effects or growth pattern were observed between sexes in each study groups. The results were as follows: 1. In Horizontal activator group, forward positioning of mandible and vertical increase in anteror face as examplified by increase of LAFH and AEM were observed when pre and post-treatment datas were evaluated. 2. Males samples in Horizontal activator group showed increase in mandiular length accmpanied by posterior positioning of maxilla, wheras female samples in Horizontal activator group showed increase in mandibular body length, labial inclination of mandibular incisors and increase in lower anterior facial height .3. In vertical activator group, increase in AFH, LAFH, PFH and LPFH were observed when pre and post treatment datas were evaluated. 4. Male samples in Vertical activator group showed increase in mandibular body length and anterior and posterior facial heights, whereas females samples of Vertical activator group showed mainly increase in anterior facial height. 5. When pre and post treatment datas of Horizontal and Vertical activator groups were compared, skeletal difference were mainly observed in pretreatment datas but dental difference were observed in post treatment datas ,indicating that two actiators differ only in their effects to dental variables. 6. Difference between sexes were noted after treatment although no difference were observed between sexs in each groups before treatmentt. This indicates that inherent growth effects in each sex exerts more influence 1km appliances used for treatment.

• The Korean Journal of Pharmacology
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• v.18 no.2
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• pp.103-117
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• 1982

In an effort to provide evidence as to the regulatory role of the central dopaminergic system on the renal function, the effects of centrally administered dopamine and its specific antagonist haloperidol were investigated. Haloperidol (HA) given intracerebroventricularly (i.c.v.) induced antidiuresis in doses of 15 and $50{\mu}g/kg$. With $15{\mu}g/kg$ sodium reabsorption in the tubules was increased, while with $50{\mu}g/kg$ free-water reabsorption was increased. However, a marked diuresis with increased sodium and potassium was observed with $150{\mu}g/kg$. Hemodynamic changes were not evident, indicating that the diuresis is of tubular origin. Dopamine (DA), on the other hand, produced antidiuresis when given i.c.v. in a dose-related fashion. With smaller doses of 5 and $15{\mu}g/kg$ the antidiuresis was related to increased reabsorption of sodium in the tubules, but higher doses of 50 and $150{\mu}g/kg$ the decreases in renal blood flow and glomerular filtration rate were evident in addition to the tubular action. After pretreatment with $150{\mu}g/kg$ HA, the effects of $15{\mu}g/kg$ DA was abolished, but the antidiuretic actions of 50 and $150{\mu}g/kg$ were not blocked, and the natriuretic diuretic action of HA was overcome and became inconspicuous. These observations indicate that the central dopaminergic system influences the renal function by producing antidiuresis, and HA elicits diuresis and natriuresis by competitively antagonizing DA specifically on the central dopaminegic receptors. The antidiuresis observed with smaller doses of HA can be best explained by the facts that there are more than two types of DA-receptors in the brain and that the presynaptic autoreceptors on the dopaminergic neurones which affect the dopamine release at the synapse are more sensitive than the postsynaptic receptors. Overall, these data provide an evidence indicating that the central dopaminergic system plays a role in the regulation of renal function in the rabbit.

• Toxicological Research
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• v.8 no.2
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• pp.343-357
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• 1992

Tumor necrosis factor-${\alpha}$(TNF), a polypeptide hormone secreted primarily by activated macrophages, was originally identified on the basis of its ability to cause hemorrhagic necrosis and tumor regression in vivo. Subsequently, TNF has been shown to be an important component of the host responses to infection and cancer and may mediate the wasting syndrome known as cachexia. These systemic actions of TNF are reflected in its diverse effects on target cells in vitro. TNF initiates its diverse cellular actions by binding to specific cell surface receptors. Although TNF receptors have been identified on most of animal cells, regulation of these receptors and the mechanisms which transduce TNF receptor binding into cellular responses are not well understood. Therefore, in the present study, the mechanisms how TNF receptors are being regulated and how TNF receptor binding is being transduced into cellular responses were investigated in rat liver plasma membranes (PM) and ME-180 human cervical carcinoma cell lines. $^{125}I$-TNF bound to high ($K_d=1.51{\pm}0.35nM$)affinity receptors in rat liver PM. Solubilization of PM with 1% Triton X-100 increased both high affinity (from $0.33{\pm}0.04\;to\;1.67{\pm}0.05$ pmoles/mg protein) and low affinity (from $1.92{\pm}0.16\;to\;7.57{\pm}0.50$ pmoles/mg protein) TNF binding without affecting the affinities for TNF, suggesting the presence of a large latent pool of TNF receptors. Affinity labeling of receptors whether from PM or solubilized PM resulted in cross-linking of $^{125}I$-TNF into $M_r$ 130 kDa, 90 kDa and 66kDa complexes. Thus, the properties of the latent TNF receptors were similar to those initially accessible to TNF. To determine if exposure of latent receptors is regulated by TNF, $^{125}I$-TNF binding to control and TNF-pretreated membranes were assayed. Specific binding was increased by pretreatment with TNF (P<0.05), demonstrating that hepatic PM contains latent TNF receptors whose exposure is promoted by TNF. Homologous up-regulation of TNF receptors may, in part, be responsible for sustained hepatic responsiveness during chronic exposure to TNF. As a next step, the post-receptor events induced by TNF were examined. Although the signal transduction pathways for TNF have not been delineated clearly, the actions of many other hormones are mediated by the reversible phosphorylation of specific enzymes or target proteins. The present study demonstrated that TNF induces phosphorylation of 28 kDa protein (p28). Two dimensional soidum dodecyl sulfate-polyacrylamide gel electrophoresis(SDS-PAGE) resolved the 28kDa phosphoprotein into two isoforms having pIs of 6.2 and 6.1. The pIs and relative molecular weight of p28 were consistent with those of a previously characterized mRNA cap binding protein. mRNA cap binding proteins are a class of translation initiation factors that recognize the 7-methylguanosine cap structure found on the 5' end of eukaryotic mRNAs. In vitro, these proteins are defined by their specific elution from affinity columns composed of 7-methylguanosine 5'-triphosphate($m^7$GTP)-Sepharose. Affinity purification of mRNA cap binding proteins from control and TNF treated ME-180 cells proved that TNF rapidly stimulates phosphorylation of an mRNA cap binding protein. Phosphorylation occurred in several cell types that are important in vitro models of TNF action. The mRNA cap binding protein phosphorylated in response to TNF treatment was purifice, sequenced, and identified as the proto-oncogene product eukaryotic initiation factor-4E(eIF-4E). These data show that phosphorylation of a key component of the cellular translational machinery is a common early event in the diverse cellular actions of TNF.

• Journal of Food Hygiene and Safety
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• v.35 no.4
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• pp.291-303
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• 2020

Marine organism-derived toxins have negative effects not only on human health but also in aquaculture, fisheries, and marine ecosystems. However, traditional analytical methods are insufficient in preventing this threat. In this paper, we reviewed new rapid methods of toxin detection, which have been improved by adopting diverse types of nanomaterials and technologies. Moreover, we herein describe the main strategies for toxin detection and their related sensing performance. Notably, to popularize and commercialize these newly developed technologies, simplifying the process of pre-treating real samples real samples is very important. As part of these efforts, numerous studies have reported pretreatment methods based on the antibody-immobilized magnetic nanoparticles, and some cases have applied nanoparticles to enhance the sensing performance by utilizing the intrinsic catalytic activity. Furthermore, some reports have introduced fluorescent nanoparticles, such as quantum dots, to represent the lower detection limits of conventional enzyme-based colorimetric methods and lateral flow assays. Some studies using electrochemical measurements based on aptamer-nanoparticle complexes have also been announced. In addition, as the response to new toxins generated by changes in the marine environment is still lacking, further research on diagnostic and detection is also greatly needed for these kinds of marine toxins and their derivatives.

• Applied Biological Chemistry
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• v.49 no.3
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• pp.186-191
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• 2006

In the present study, an attempt has been made to produce hybrid yeast strains of different useful and dominant characteristics. The hybrid yeast strains were produced by electrofusion and their genetic analysis were performed by RAPD-PCR (random amplified polymorphic DNA-polymerase chain reaction). The protoplast of Saccharomyces cerevisiae KCTC 7904 and Zygosaccharomyces rouxii KCTC 7966 were obtained above 92% when treated with lyticase at $30^{\circ}C$ for $60{\sim}90$ min after the pretreatment of $1{\sim}2%$ 2-mercaptoethanol at $30^{\circ}C$ for $15{\sim}20$ min. The fusant was produced from paired protoplast stage under the electric pulse at high frequency conditions (1.5 MHz/50 pV, 615 $V/256\;{\mu}sec$) within glass-platinum made electrofusion chamber. Changes in RAPD patterns in mother cells and hybrid cells proved that the fusant contains two types of yeast gene originated from its parent. Furthermore, fermentation characters exhibits by the fusant cell confirmed its genetic changes. These results suggest that genetically stable hybrid yeast strains of economic importance can be produced by electrofusion technique and these electrofused yeast cells have an enormous impact in biotechnology and biomedicine.

• Tuberculosis and Respiratory Diseases
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• v.58 no.1
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• pp.31-42
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• 2005

Background : Peroxiredoxins (Prxs) are a relatively newly recognized, novel family of peroxidases that reduce $H_2O_2$ and alkylhydroperoxide into water and alcohol, respectively. There are 6 known isoforms of Prxs present in human cells. Normally, Prxs exist in a head-to-tail homodimeric state in a reduced form. However, in the presence of excess $H_2O_2$, it can be oxidized on its catalytically active cysteine site into inactive oxidized forms. This study surveyed the types of the Prx isoforms present in the pulmonary epithelial, macrophage, endothelial, and other cell lines and observed their response to oxidative stress. Methods : This study examined the effect of exogenous, excess $H_2O_2$ on the Prxs of established cell lines originating from the pulmonary epithelium, macrophages, and other cell lines, which are known to be exposed to high oxygen partial pressures or are believed to be subject to frequent oxidative stress, using non-reducing SDS polyacrylamide electrophoresis (PAGE) and 2 dimensional electrophoresis. Result : The addition of excess $H_2O_2$ to the culture media of the various cell-lines caused the immediate inactivation of Prxs, as evidenced by their inability to form dimers by a disulfide cross linkage. This was detected as a subsequent shift to its monomeric forms on the non-reducing SDS PAGE. These findings were further confirmed by 2 dimensional electrophoresis and immunoblot analysis by a shift toward a more acidic isoelectric point (pI). However, the subsequent reappearance of the dimeric Prxs with a comparable, corresponding decrease in the monomeric bands was noted on the non-reducing SDS PAGE as early as 30 minutes after the $H_2O_2$ treatment suggesting regeneration after oxidation. The regenerated dimers can again be converted to the inactivated form by a repeated $H_2O_2$ treatment, indicating that the protein is still catalytically active. The recovery of Prxs to the original dimeric state was not inhibited by a pre-treatment with cycloheximide, nor by a pretreatment with inhibitors of protein synthesis, which suggests that the reappearance of dimers occurs via a regeneration process rather than via the de novo synthesis of the active protein. Conclusion : The cells, in general, appeared to be equipped with an established system for regenerating inactivated Prxs, and this system may function as a molecular "on-off switch" in various oxidative signal transduction processes. The same mechanisms might applicable other proteins associated with signal transduction where the active catalytic site cysteines exist.