• Journal of Food Hygiene and Safety
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• v.39 no.5
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• pp.444-451
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• 2024

The tissue distribution of tetrodotoxin (TTX) and its analogs in farmed Takifugu rubripes pufferfish sold in Korean markets was determined using ultra-high performance liquid chromatography coupled to triple quadrupole mass spectrometry in the multiple reaction monitoring mode. The method detection limit for TTX ranged from 0.019 to 0.022 mg/kg in high-fat and low-fat matrices. The intra-day (n = 5) and inter-day (3 d, n = 15) accuracy and precision results met the Codex guidelines. Tetrodotoxin was not detected in most of the analyzed tissue samples. In the farmed T. rubripes tissues, TTX levels reached a maximum of 0.07 mg/kg in the liver. Among the TTX analogs, dideoxyTTX, trideoxyTTX, and norTTX were detected in all samples. This study contributes to the database of marine toxicity information for farmed Takifugu species sold in Korean markets.

• Journal of Food Hygiene and Safety
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• v.39 no.5
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• pp.436-443
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• 2024

Tetrodotoxin (TTX) is a potent neurotoxin responsible for pufferfish poisoning. The tissue distribution of TTX and its analogs in Takifugu porphyreus pufferfish sold in the Korean market was determined using ultra-high-performance liquid chromatography coupled to triple quadrupole mass spectrometry in multiple reaction monitoring mode. The method detection limit for TTX was 0.006-0.009 mg/kg in high-fat and low-fat matrices. The intra-day (n = 5) and inter-day (3 days, n = 15) accuracy and precision results met the Codex guidelines. The ovaries of T. porphyreus pufferfish showed higher levels of TTX (up to 67.7 mg/kg) and its analogs compared to other tissues. Lower levels of TTX (non-detectable to 1.10 mg/kg) were found in the muscle and testis tissues, usually the edible parts of the pufferfish, than in other tissues. TrideoxyTTX was the major TTX analog across all tissues. This study contributes to the database of marine toxicity information on T. porphyreus species sold in Korea.

• Journal of Microbiology and Biotechnology
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• v.27 no.4
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• pp.725-730
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• 2017

A heteronemertean, Yininemertes pratensis, was collected in Han River Estuary, South Korea. This estuarine nemertean has been known by the local fishermen for harmful effects to the glass eels, juveniles of Japanese eel Anguilla japonica, migrating to fresh water. The present study confirmed the neurotoxic effects of this heteronemertean ribbon worm at the cellular level. Derivative types of neurotoxic tetrodotoxin (TTX), 5,11-dideoxy TTX (m/z 288) and 11-norTTX-6(S)-01 (m/z 305.97), were identified through HPLC and MALDI-TOF MS. However, significant neurotoxicity was confirmed in the fraction containing an undefined molecule corresponding to the 291.1 (m/z) peak, when tested in rat primary astrocytes and dorsal ganglion cells. This study is the first to report neurotoxins of the estuarine nemertean, fairly abundant in the Han River estuary, and suggests the long-term monitoring of population dynamics and surveillance of the toxicity in this river estuary.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.2
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• pp.389-396
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• 2002

In the present work, we examined the mechanism of vasorelaxant effect of scopoletin, an active constituent of Artemisia capillaris on rat thoracic descending aortic rings. Scopoletin induced a concentration-dependent relaxation in rat thoracic descending aortic rings pre-contracted with phenylephrine (EC/sub 50/ = 238.94±37.4 μM), while it was less effective in rat thoracic descending aortic rings precontracted with high potassium solution (KCI 30 mM). Vasorelaxation by scopoletin was significantly inhibited after endothelial removal, but recovered at high concentration. Pretreatment of rat thoracic descending aortic rings with N/sup G/-nitro-L-arginine (100 μM), a nitric oxide synthase inhibitor, and atropine (1 μM), a muscarinic receptor antagonist, significantly inhibited scopoletin-induced relaxation of rat thoracic descending aortic rings. Neither indomethacin (3 μM), an inhibitor of cydooxygenase, nor propranolol (1 μM), a β -adrenoceptor antagonist, modified the effect of scopoletin. The combination of N/sup G/ -nitro-L-arginine (100 μ M) and miconazole (10 μ M), an inhibitor of cytochrome P 450, did not modify the effect of scopoletin, when compared with pretreatment with N/sup G/-nitro-L-arginine(100 μM) alone. Vasorelaxant effect of scopoletin was inverted by pretreatment with diltiazem (10 μM), a Ca/sup 2+/-channel blocker, at low concentration, while restored at high concentration. Apamin (K/sub ca/-channel blocker, 1 μM), 4-aminopyridine (4-AP, K/sub v/-channel blocker, 1 mM), and tetrodotoxin (TTX, Na/sup +/-channel blocker 1 μM) potentiated the vasorelaxant effect of scopoledn, but glibendamide (K/sub ATP/-channel blocker, 10 μM), tetraetylammonium(TEA, non-selective K-channel blocker, 10 mM) did not affect the relaxation of scopoletin. Free radical scavengers (TEMPO, catalase, mannitol) did not modify vascular tone. These results suggest that nitric oxide, Ca/sup 2+/ -channels play a role in endothelium-dependent relaxations to scopoletin in rat aortas, that apamin, 4-AP, TTX but not glibenclamide, TEA potentiated relaxation to scopoletin mediated by these channels, and that free radicals do not concern to the vasorelaxant effect of scopoletin.

• The Korean Journal of Pharmacology
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• v.19 no.2
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• pp.25-34
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• 1983

In this isolated study, it was aimed to elucidate the pharmacological properties of non-cholinergic, non-adrenergic inhibitory responses in the longitudinal strips of rabbit portal vein. 1) The portal vein responded inhibitory to electrical field stimulation in a frequency - and calcium-dependent manner after pretreatment with atropine, guanethidine and ergotamine, simultaneously. 2) When exogenous ATP, ADP, adenosine and cyclic AMP were added, respectively, they only showed the relaxations in the higher concentration without mimicing or affecting the inhibitory response induced by the electrical stimulation. The antagonist of purine substances, neither quinine nor isobutyl-methyl xanthine did influence on the relaxation. 3) The inhibitory response was significantly increased in the presence of $1{\mu}g/ml 4-amino-pyrineine (4-AP) which is $K^+-conduction$ blockade, but higher concentration of 4-AP directly decreased the vascular tone. 4) Though repeated application of ATP revealed the inhibitory effect on the relaxation, however, that of adenosine resulted rather increase of the amplitude. 5) After pretreatment with $^3H-adenosine$, $^3H-efflux$ induced by ATP or adenosine was markedly enhanced, but the electrical stimulation caused less $^3H-efflux$. 6) ^3H-efflux by electrical stimulation was not affected by the administration 4-AP, tetrodotoxin and adenosine.

• The Korean Journal of Pharmacology
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• v.32 no.2
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• pp.127-138
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• 1996

The effects of adenosine analogues on the electrically-evoked acetylcholine(ACh) release and the influence of ischemia on the effects were studied in the rat hippocampus. Slices from the rat hippocampus were equilibrated with $0.1{\mu}M$ $[^3H]-choline$ and the release of the labelled product, $[^3H]-ACh$, was evoked by electrical stimulation(3 Hz, 2 ms, 5 $VCm^{-1}$ and rectangular pulses for 2 min), and the influence of various agents on the evoked tritiumoutflow was investigated. Ischemia(10 min with 95% $N_2$ + 5% $CO_2$) increased both the basal and evoked ACh release. These increases were abolished by glucose addition into the superfused medium, and they significantly inhibited either by 0.1 & $0.3{\mu}M$ TTX pretreatment or by removing $Ca^{++}$ in the medium. MK-801($1{\sim}10{\mu}M$), a specific NMDA receptor antagonist, and glibenclamide $(1{\mu}M)$, a $K^+-channel$ inhibitor, did not alter the evoked ACh release and nor did they affect the ischemia-induced increases In ACh release. However, polymyxin B(0.03 mg), a specific protein kinase C inhibitor, significantly inhibited the effects of ischemia on the evoked ACh release. Adenosine and $N^6-cyclopentyladenosine$ decreased the ACh release in a dose dependent manner in ischemic condition, though the magnitude of inhibition was far less than those in normal(normoxic) condition. However, the treatment with $5{\mu}M$ DPCPX, a potent $A_1-adenosine$ receptor antagonist, potentiated the ischemia-effect. These results indicate that the evoked-ACh release is potentiated by ischemia, and this process being most probably mediated by protein kinase C, and that the decreased effect of ACh release mediated by $A_1-adenosine$ receptor is significantly inhibited in ischemic state.