• Fisheries and Aquatic Sciences
• /
• v.19 no.10
• /
• pp.42.1-42.10
• /
• 2016

The objectives of this study were to identify the histamine-forming bacteria and bacteriocin- producing lactic acid bacteria (LAB) isolated from Myeolchi-jeot according to sequence analysis of the 16S rRNA gene, to evaluate the inhibitory effects of the bacteriocin on the growth and histamine accumulation of histamine-forming bacteria, and to assess the physico-chemical properties of the bacteriocin. Based on 16S rRNA gene sequences, histamine-forming bacteria were identified as Bacillus licheniformis MCH01, Serratia marcescens MCH02, Staphylococcus xylosus MCH03, Aeromonas hydrophila MCH04, and Morganella morganii MCH05. The five LAB strains identified as Pediococcus acidilactici MCL11, Leuconostoc mesenteroides MCL12, Enterococcus faecium MCL13, Lactobacillus sakei MCL14, and Lactobacillus acidophilus MCL15 were found to produce an antibacterial compound with inhibitory activity against the tested histamine-producing bacteria. The inhibitory activity of these bacteriocins obtained from the five LAB remained stable after incubation at pH 4.0-8.0 and heating for 10 min at $80^{\circ}C$; however, the bacteriocin activity was destroyed after treatment with papain, pepsin, proteinase K, ${\alpha}$-chymotrypsin, or trypsin. Meanwhile, these bacteriocins produced by the tested LAB strains also exhibited histamine-degradation ability. Therefore, these antimicrobial substances may play a role in inhibiting histamine formation in the fermented fish products and preventing seafood-related food-borne disease caused by bacterially generated histamine.

• Proceedings of the Korean Society of Applied Pharmacology
• /
• 1993.04a
• /
• pp.87-87
• /
• 1993

항 Histamine쟤의 효과적인 응용과 그 개발율 위한 자료를 얻고자 이들 약물의 H$_1$-receptor와 muscarinic receptor에 대한 작용의 상대적 역가를 비교하였다. 본 실험에 이용된 기니픽 회장에는 [$^3$H]QHB어 대한 단일 muscarinic receptor가 존재하였으며 [$^3$H]QNB의 affinity와 결합부위농도는 각각 54 pM 및 156 fmol/mg이었다. 항 histamine제는 muscarinic receptor에 대한 [$^3$H]QNB결합을 억제하였으며 [$^3$H]QNB 결합억제로부터 추정된 항 histamine제의 Ki치가 0.008$\mu$M-1.6$\mu$M로서 항 histamine제의 종류에 따라 현저한 차이가 있었고, 이 결과는 carbachol 반응억제로부터 추정된 각 항 histamine제의 muscarinic receptor에 대한 affinity(K$_{M}$)와 유사하였다. 한편 histamine수축반응 억제로부터 추정된 항 histamine재의 H$_1$-receptor에 대한 affinity(K$_{H}$ ) 역시 0.15nM-56.5nM로서 약물에 따라 차이가 있었고 각 약물의 $K_{M}$ /K$_{H}$ 비가 3-2300으로 H$_1$-receptor에 대한 역가와 muscarinic receptor에 대한 역가 사이에는 상관성이 없었다. 즉 유사한 항 allergy 작용을 일으킬 수 있는 치료혈중농도에서도 muscarinic receptor 차단작용이 다르며 본 실험에 사용한 13종의 기존 항 histamine제중 triprolidine이 $K_{M}$ /K$_{H}$ 비가 가장 높았고 diphenidol이 가장 낮았다. 이상의 결과로 보아 항 histamine제의 muscarinic receptor 차단작용은 이들 약물의 항 alleragy 효과에 필요한 작용이 아니며 본 실험에서 추정된 항 histamine제의 H$_1$-receptor와 muscarinic receptor에 대한 상대적 역가는 이들 약물의 선택과 평가에 중요한 지표가 될수 있을 것으로 생각된다.

• Korean Journal of Clinical Laboratory Science
• /
• v.47 no.4
• /
• pp.306-312
• /
• 2015

The measurement of histamine is to determine the degree of allergy because the allergic reaction can lead to the release of histamine. In general, the antigen-antibody reaction was quantified by measuring absorbance using a microplate reader. In this study, we compare the method using a general antigen-antibody reaction and the method using a high performance liquid chromatography mass spectrometer (HPLC-MS) of chemical analysis in the measurement of histamine secretion. The cell line used was RBL-2H3, an allergic reaction was induced by stimulation with C48/80 (compound 48/80). Allergy-induced cells degranulation rate was confirmed by measurement of ${\beta}$-hexosaminidase and cytotoxicity was performed for the validity of the experiment. The quantitative determination of histamine showed a significant difference, since the quantitative limit of the measurement by the antigen-antibody reaction was 10.257 ppm while the quantitative limit of the measurement by HPLC-MS was 0.020 ppm. Measurement of histamine in allergic activity and anti-allergy tests showed that the HPLC-MS analysis rather than the analysis of the antigen-antibody reaction is a more precise and accurate test.

• KSBB Journal
• /
• v.5 no.2
• /
• pp.113-118
• /
• 1990

This experiment was carried out to investigate the immuno-regulatory effects of histamine on IL-1 synthesis and Ca2+ uptake in P388Dl macrophage-like cell line. The addition of histamine (10-8-10-3 M) increased IL-1 production in P388D1, cells, in a dose dependent manner, the treatment of EGTA (10-7-10-4M) and Co2+ ion (10-5-10-4M) decreased macrophage-derived IL-1 activity, and the pretreatment of histamine at the peak of 10-4M significantly enhanced Ca2+ uptake to P388Dl Cells. These results suggested that exogenous histamine was effective on IL-1 production from macrophage and the intracellular Ca2+ uptake play a important role in histamine-stimulated IL-1 synthesis.

• Journal of Pharmacopuncture
• /
• v.19 no.3
• /
• pp.239-245
• /
• 2016

Objectives: This study was conducted to clarify the effects of agarwood on histamine release from mast cells in rats and on the scratching behaviors in mice. Methods: Histamine release from rat mast cells induced by compound 48/80 or concanavalin A (Con A) and compound 48/80-induced scratching behavior in mice were examined to investigate the effects of agarwood. The hyaluronidase activity and the 3',5'-cyclic adenosine monophosphate (cAMP) levels in mast cells were examined to investigate the mechanisms for the inhibition of histamine release. The correlation between the inhibitory effects of agarwood on histamine release and the content of its typical ingredients, a 2-(2-phenylethyl)chromone derivatives, was analyzed using thin-layer chromatography. Results: Agarwood showed an inhibitory effect on mast-cell histamine release induced by compound 48/80 or Con A without any effect on hyaluronidase activity; this effect involves an increase in the cAMP levels in mast cells. Oral administration of agarwood showed an inhibitory effect on compound 48/80-induced scratching behavior in mice. The inhibitory effects of agarwood on histamine release were quite different, depending on the area where the agarwood was produced, its quality, and its market price. No correlation was found between the inhibitory effects of agarwood on histamine release and the typical ingredients of agarwood, which are 2-(2-phenylethyl)chromone derivatives. Conclusion: These results show that agarwood inhibits histamine release from mast cells partially through an increase in the cAMP levels in cells. We suggest that some active ingredients of agarwood must be effective on oral intake and that agarwood can be used to treat patients with a number of conditions, including urticaria, atopic dermatitis, and bronchial asthma, in which an increase in histamine release occurs. Differences in the pharmacological effects of this crude drug among markets may provide important information for the quality control of this herbal medicine.

• The Korean Journal of Pharmacology
• /
• v.29 no.1
• /
• pp.43-55
• /
• 1993

The present study was conducted to examine the characteristics of histamine on catecholamine secretion in the isolated perfused rat adrenal gland and to clarify the mechanism of its secretory action. Histamine (37.5 to 150 ug) injected into an adrenal vein evoked a dose-dependent significant secretory response of catecholamines (CA) from the rat adrenal gland. However, upon the repeated injection of histamine (150 ug) at 120 min intervals, CA secretion was rapidly decreased after third injection of histamine. Tachyphylaxis to releasing effects of CA evoked by histamine was observed by the repeated administration. The histamine-induced CA secretion was markedly inhibited by the pretreatment with chlorisondamine, diphenhydramine, ranitidine, $Ca^{++}-free$ Krebs solution, nicardipine and TMB-8 while was not affected by pirenzepine. Moreover, the CA secretion evoked by ACh was considerably reduced by the prior perfusion of histamine $(6.8{\times}10^{-5} M)$ for 30 min. These experimental data suggest that histamine causes secretion of CA in a calcium dependent manner from the perfused rat adrenal gland and that its secretory effect is mediated through activation of both $H_1-$ and $H_2-histaminergic$ receptors located in adrenal medulla, which may be associated with stimulation of cholinergic nicotinic receptors.

• The Korean Journal of Physiology
• /
• v.22 no.2
• /
• pp.259-272
• /
• 1988

Type I allergic reaction and it's related clinical manifestations are known to occur by the effects of various chemical mediators. These chemical mediators are released from circulating basophils and tissue mast cells, which become 'sensitized' through the binding of antigens and antibodies of the IgE type to their cell surface receptors. Efforts to elucidate the mechanism of the release of these mediators, especially that of histamine, have been persued for years. The mechanism is not yet clarified at the present time. Recent reports of hyaluronidase, an enzyme known to be involved in the tissue inflammatory process, as possible participant in type I allergic reaction, initiated this study. Relationships between the hyaluronidase activity and histamine release from the sensitized rat peritoneal mast cells were investigated. Also anti-allergic agents, tranilast and disodium cromoglycate, along with known histamine releasers, morphine and compound 48/80, were used to observe the inhibitory and stimulatory effects of these substances on the hyaluronidase activity as well as histamine release from the rat mast cells. The results obtained are summarized as follows: 1) Hyaluronidase activity and histamine release from sensitiaed rat peritoneal mast cells started to increase on the 4th day of postsensitization. Hyaluronidase activity reached it's peak value on the 7th day of postsensitization and that of histamine release on the 14th day of postsensitization. 2) Hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells, pre-treated with tranilast revealed significant decrease in comparison with those of non-treated cells. 3) Hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells, pre-treated with tranilast, followed by morphine injection, revealed significant increase in comparison with those of tranilast treated cells. 4) In vitro study of hyaluronidase activity and histamine release from un-sensitized rat peritoneal mast cells, using morphine and compound 48/80 as activators, revealed significant increase compared to those of non-activator used cells. 5) In vitro study of hyaluronidase activity and histamine release from un-sensitized rat peritoneal mast cells, pre-treated with tranilast and disodium cromoglycate, using confound 48/80 and morphine as activators revealed significant decrease in comparison with those of tranilast and disodium cromoglycate treated cells. From above results, participation of enzyme hyaluronidase in the process of histamine release from sensitized rat pertioneal mast cells, could be suggested. It was also quite evident that the clinically used anti-allergic agents, tranilast and disodium cromoglycate, have significant inhibitory function on the hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells, while morphine significantly increased the hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells.

• Journal of the East Asian Society of Dietary Life
• /
• v.22 no.1
• /
• pp.88-94
• /
• 2012

Histamine is a kind of primary biogenic amine arising from the decarboxylation of the amino acid L-histidine. The toxicology of histamine and its occurrence and formation in foods are especially emphasized in fermented foods. In this study, the biosensor for detection of histamine with functionalized multi-walled carbon nanotubes (MWCNT) was developed. We also searched for an appropriate insoluble substrate to immobilize the enzyme. The developed biosensor showed a detection limit of $0.1{\mu}M$ hydrogen peroxide. The enzyme reactor was prepared with diamine oxidase immobilized on insoluble carriers including CNBr-activated sepharose 4B, calcium alginate, and controlled pore size glass beads. The coupling efficiency of CNBr-activated sepharose 4B, calcium alginate, and controlled pore size glass beads were 48.5%, 40.3%, and 51.0%, respectively. In addition, the response currents on histamine with each immobilized enzyme reactor prepared with CNBr-activated sepharose 4B, calcium alginate, and controlled pore size glass beads were 120 nA, 110 nA, and 140 nA at $100{\mu}M$ of histamine concentration, respectively. Therefore, it is suggested that controlled pore size glass beads are the best carriers for immobilizing diamine oxidase to detect histamine in this biosensor.

• Korean Journal of Veterinary Research
• /
• v.29 no.2
• /
• pp.19-24
• /
• 1989

To elucidate the physiological characteristics of histamine receptor of the isolated renal artery in dog, effects of various receptor blockers and $Ca^{{+}{+}}$ channel blockers on the contractile responses of histamine were investigated in the isolated renal artery of dog. The results were summarized as follows: 1. Histamine caused the contraction in the isolated renal artery of dog, and the contractile responses increased between the concentration of $5{\times}10^{-6}M$ and $10^{-2}M$ in dose-dependent manner. 2. The contractile response induced by histamine ($10^{-3}M$) was not blocked by pretreatment with atropine ($10^{-6}M$), phentolamine ($10^{-6}M$), propranolol ($10^{-6}M$) or cimetidine ($10^{-6}M$), but was completely blocked by pretreatment with pyrilamine ($10^{-6}M$). 3. The contractility induced by histamine ($10^{-3}M$) was decreased in the $Ca^{{+}{+}}$ free medium. 4. The contractile response induced by histamine ($10^{-3}M$) was markedly inhibited by pretreatment with papaverine ($5{\times}10^{-5}M$) or verapamil ($5{\times}10^{-5}M$). 5. After the pre-contraction induced by norepinephrine ($10^{-7}M$) or prostaglandin $F2{\alpha}$ ($5{\times}10^{-6}M$), the contractile response induced by the additional treatment of histamine ($10^{-3}M$) was markedly increased compared with that of histamine ($10^{-3}M$) alone.

• Archives of Pharmacal Research
• /
• v.24 no.6
• /
• pp.552-556
• /
• 2001

Histamine and arachidonic acid (AA) release was measured using the P2-purinoceptor antaongists, phospholipase $A_2{\;}(PLA_2)$ and cyclooxygenase (COX)/lipoxygenase (LOX) inhibitors to determine whether or not ATP-induced histamine release is associated with arachidonic acid (AA) release in rat peritoneal mast cells. ATP increased histamine release in a dose dependent manner, whereas adenosine did not. PPADS (a selective P2X-purinoceptor antagonist) and suramin (a nonselective P2X,2Y-purinoceptor antagonist) inhibited ATP-induced histamine release in a dose dependent manner. However, RB-2 (a P2Y-purinoceptor antagonist) did not block ATP-induced histamine release. Manoalide and oleyloxyethyl phosphorylcholine (OPC), secretory PLA$_2$ inhibitors, also inhibited ATP-induced histamine release dose-dependently. Both COX inhibitors (ibuprofen and indomethacin) and LOX inhibitors (baicalein and caffeic acid) inhibited ATP-induced histamine in a dose dependent manner. ATP significantly increased [$^3H$]AA release by 54%. PPADS and suramin significantly inhibited ATP-induced [3H]Ph release by 81% and 39%, respectively. ATP-induced histamine release was significantly inhibited by a variety of protein kinase inhibitors, such as bisindolmaleimide, genistein, methyl 2,5-dihydroxycinnamate, W-7 and trifluoperazine. Overall, the results suggest that ATP-induced histamine release is in part related to the PLA2-mediated AA metabolism and P2X-purinoceptors.