• Journal of Life Science
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• v.28 no.8
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• pp.885-891
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• 2018

Clostridium difficile (C. difficile) toxin A is known to cause acute gut inflammation in humans and animals by triggering cytoskeletal disorganization in gut epithelial cells. In human colonocytes, toxin A blocks microtubule assembly by directly increasing the enzymatic activity of histone deacetylase-6 (HDAC-6), a tubulin-specific deacetylase, thereby markedly decreasing tubulin acetylation, which is essential for microtubule assembly. Microtubule assembly dysfunction-associated alterations (i.e., toxin A-exposed gut epithelial cells) are believed to trigger barrier dysfunction and gut inflammation downstream. We recently showed that potassium acetate blocked toxin A-induced microtubule disassembly by inhibiting HDAC-6. Herein, we tested whether acetic acid (AA), another small acetyl residue-containing agent, could block toxin A-induced tubulin deacetylation and subsequent microtubule assembly. Our results revealed that AA treatment increased tubulin acetylation and enhanced microtubule assembly in an HT29 human colonocyte cell line. AA also clearly increased tubulin acetylation in murine colonic explants. Interestingly, the AA treatment also alleviated toxin A-induced tubulin deacetylation and microtubule disassembly, and MTT assays revealed that AA reduced toxin A-induced cell toxicity. Collectively, these results suggest that AA can block the ability of toxin A to cause microtubule disassembly-triggered cytoskeletal disorganization by blocking toxin A-mediated deacetylation of tubulin.

• Journal of Food Hygiene and Safety
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• v.15 no.4
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• pp.287-292
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• 2000

The toxicity and toxin composition between blue mussel, Mytilus edulis and oyster, Crassostrea gigas collected at Woepori in Ko je island in South Coast of Korea in 1996 and 1997 were compared. The highest toxicity score was about 10 times higher in blue mussel than oyster (blue mussel, 8,670 $\mu\textrm{g}$; oyster, 860$\mu\textrm{g}$ in 1996, blue mussel, 5,657 $\mu\textrm{g}$/100g in 1997). The blue mussel also retained its toxicity for slightly longer period than oyster. In the both shellfish, PSP was composed almost exclusively of C toxicity (Cl and C2, 20~65%) and gonyautoxins (GTXl, 2, 3, and 4, 38~78%). In the early period of toxin accumulation, the ratio of 11$\beta$-epimer toxins (C2, GTX4) whose amount was 25~56 mole% (5th March to 12th April in 1996) and 25~80 mole% (18th March to 7th April in 1997), were higher than that of 11-epimer toxins (Cl, GTX2) whose amount was 41~57 mol%(27th May to 3rd June in 1996) and 25~56 mole% (29th April to 12th May in 1997), became higher than that of 11-epimer toxins. The toxin compositions in the both samples changed on a daily basis, presumably owing to metabolism of the toxin in the bivalves.

• The Korean Journal of Zoology
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• v.29 no.3
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• pp.181-189
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• 1986

The present study was undertaken to investigate whether the known adenylate cyclase activators, forskolin and cholera toxin, would affect the germinal vesicle breakdown (GVBD) and the production of cAMP in mouse oocytes in vitro. To do this, in vitro oocyte culture method and adenylate cyclase assay were employed. In response to different concentrations of forskolin (20 to 80 $\\mu$g/ml) added to a culture medium, the percentage of GVBD significantly decreased (56 to 31%) in a dose-dependent manner as compared to that of control (63%). This inhibitory phenomenon by forskolin was reversible since the rate of GVBD was returned to the control level when the oocytes were transferred to a control medium following exposure to forskolin (80 $\\mu$g/ml). Treatment of cholera toxin (10 to 1, 000 ng/ml) was, however, ineffective in suppressing GVBD. When forskolin (10 to 80 $\\mu$g/ml) was added to the mouse oocyte extracts, cAMP production significantly increased by 5 to 18 fold, whereas cholera toxin (10 to 1, 000 ng/ml) was no longer effective. In addition, treatment of guanidyl-imidodiphosphate (GppNHp, 100 $\\mu$M), which is an activator of the regulatory unit of adenylate cycleas, with forskolin did not exhibit any changes in cAMP production as compared to that induced by forskolin alone. Neither cholera toxin nor cholera toxin plus GppNHp (100 $\\mu$M) exhibited any differences in mouse oocytes. From the above results, the suppression of GVBD by forskolin may be mediated by a high level of intracellular cAMP in mouse oocytes. It appears that the changes in intracellular cAMP level may an important role in the mouse oocyte maturation.

• Korean journal of applied entomology
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• v.26 no.3 s.72
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• pp.171-178
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• 1987

Pathogenic isolates of Alternaria mali produced host-specific toxin(AM-toxin) in liquid culture. The toxin was also released by germinating spores of the fungus. The physiological event of apple leaves induced by germinating spores was an increased loss of electrolytes from susceptible leaves. This reaction was evident soon after spore inoculation, indicating that the leakage was caused by AM-toxin from germinating spores. Typical symptoms were developed only in susceptible leaves of apple within 48hr after inoculation with pathogenic spores. Similar symptoms occurred on susceptible leaves when non-pathogenic isolates plus AM-toxin were used.

• Journal of Life Science
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• v.29 no.1
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• pp.97-104
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• 2019

Streptococcus iniae is a typical fish pathogen causing streptococcosis and it can also cause zoonotic infectious diseases. We studied S. iniae FP5228 isolated from infected olive flounder in Wando, Korea. In a study to find virulence factors in FP5228, we found that the number of live bacteria decreased dramatically in culture medium containing S. iniae FP5228 for more than 24 hr. This phenomenon was hypothesized to be related to Toxin ${\zeta}$ and Antitoxin ${\varepsilon}$ genes, components of the Toxin/ Antitoxin (TA) system on the 14 kb plasmid of FP5228. We used a protein overexpression system to identify it. The pBP1140 vector system was constructed to regulate the expression of Toxin ${\zeta}$ and Antitoxin ${\varepsilon}$ by IPTG and Arabinose. E. coli/pBP1140 strain grew slowly in early growth under toxin expression condition, and it was confirmed by microscopic observation that the strain became longer. S. iniae CK287, lacking a 14 kb plasmid of S. iniae FP5228 strain, was constructed. CK287 bacterial cells did not show rapid killing during culture, and the ability to produce biofilm was also decreased, and toxicity was weakened in cytotoxicity test and fish test. These results suggest that the TA system is involved in physiological regulation and expression of virulence factors in S. iniae FP5228.

• Proceedings of the Korean Aquaculture Society Conference
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• 2003.10a
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• pp.128-128
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• 2003

The annually outbreak of paralytic shellfish poisoning (PSP) were caused by toxic dinolagellate A. tamarense and A. catenella in Korea. The purpose of this study were to investigate the distribution of PSP-causative organisms, A. tamarense and A. catenella and their species classification. Sediment (Saemangeum, the south open sea) and water samples (southeastern coast) were sampled to establish clonal isolates in 2003. After isolation and purification, strains were cultured under $17^{\circ}C$, f/2 media, 14:10=L:D cycle. PST analysis and species identification were performed by HPLC-FD method and specific DNA probe, respectively. Thirty-ons strains were isolated from the Saemangeum reclamation, southeastern coast including Jinhae Bay and south open sea. PSTs were detected in all cultured strains. In eight strains from south offshore, major toxin components are GTX5, C1/2 and minors are GTX3/4, dcGTX3, neoSTX. Sixteen strains from south coastal area have GTX1/4, neoSTX, C1/2 as major toxin components and GTX2/3 as minors. Seven strains from the Saemangeum reclamation have GTX5, C1/2 as major toxin components and GTX1/2/3/4 as minors. Thus, among eight south offshore isolates, four A. tamarense have more toxic (38.31~l19.16 fmol.$cell^{-1}$) than A. catenella (3.78~13.13 fmol.$cell^{-1}$). With the previous results of different toxin composition, toxin components and toxin contents, .it is toxin profile that could used to diagnosis of regional toxic population and geographical distribution of both A. tamarense and A. catenella and their toxigenic strains.

• Archives of Craniofacial Surgery
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• v.10 no.2
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• pp.114-119
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• 2009

Purpose: Several therapeutic approaches have been introduced and tried to treat Frey syndrome following parotidectomy. However they were not proved as an effective treatment. A new therapeutic modality using botulinum toxin injections was presented previously by several study groups. But, the duration of the demonstrated positive effect was essentially unknown so far. The purpose of this clinical investigation is to demonstrate the effectiveness of Botulinum toxin type A(BTXA) in patients with Frey syndrome. Methods: For this study, 12 patients were treated, They were assessed with the Minor's iodine-starch test and interviewed before and after treatment. Botulinum toxin is injected with $1.0cm^2$ apart into the skin where symptoms of Frey's syndrome has manifestated. The patients were classified according to the concentration of botulinum toxin and dosage of botulinum toxin. Results: The outcome measures were the time of reappearance of gustatory sweating(subjective study), and the results of an Minor's iodine-starch test(objective study) of 3 weeks, 3 months, 6 months, 9 months, 12 months after treatment. This treatment was effective in all groups of patients. The concentrations and the amount of dosages did not affect the treatment. But high concentration produced faster effectiveness in subjective. Conclusion: Botulinum toxin type A(BTXA) for Frey syndrome is easy, convenient and effective withouts severe complication. And the patients has no difficulty and limitation in their life.

• Journal of Acupuncture Research
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• v.33 no.2
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• pp.1-9
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• 2016

Objectives : I investigated whether snake venom can synergistically strengthen the cytotoxic effects of NK-92 cells, and enhance the inhibition of the growth of lung cancer cells including NCI-H358 through the induction of death receptor dependent extrinsic apoptosis. Methods : Snake venom toxin inhibited cell growth of NCI-H358 Cells and exerted non influence on NK-92 cell viability. Moreover, when they were co-cultured with NK cells and concomitantly treated with $4{\mu}g/m{\ell}$ of snake venom toxin, more influence was exerted on the inhibition of growth of NCI-H358 cells than BV or NK cell co-culture alone. Results : The expression of Fas, TNFR2 and DR3 and in NCI-H358 lung cancer cells was significantly increased by co-culture of NK-92 cells and treatment of $4{\mu}g/m{\ell}$ of snake venom toxin, compared to co-culture of NK-92 cells alone. Coincidentally, Bax, caspase-3 and caspase-8 - expressions of pro-apoptotic proteins in the extrinsic apoptosis pathway, demonstrated significant increase. However, in anti-apoptotic NF-${\kappa}B$ activities, activity of the signal molecule was significantly decreased by co-culture of NK-92 cells and treatment of $4{\mu}g/m{\ell}$ of snake venom toxin, compared to co-culture of NK-92 cells or snake venom toxin treated by NCIH358 alone. Meanwhile, in terms of NO generation, there is a significant increase, in co-culture of NK-92 cells with NCI-H358 cells as well as the co-culture of NK-92 cells and concomitant treatment of $4{\mu}g/m{\ell}$ of snake venom toxin. However, no synergistic increase of NO generation was shown in co-culture of NK-92 cells and treatment of $4{\mu}g/m{\ell}$ of snake venom toxin, compared to co-culture of NK-92 cells with NCI-H358 cells. Conclusion : Consequently, this data provides that snake venom toxin could be useful candidate compounds to suppress lung cancer growth along with the cytotoxic effect of NK-92 cells through extrinsic apoptosis.

• Korean Journal of Agricultural Science
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• v.15 no.1
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• pp.1-7
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• 1988

Out of 24 isolates of Alternaria collected from pear leaves, only 7 isolates from cv. Nijiseiki leaves were specifically pathogenic to susceptible pear cultivar(Nijiseiki). Other isolates from cv. Chojuro, Oksankichi and Sinko did not show any pathogenicity to pear leaves. Pathogenic isolates of Alternaria kikuchiana produced host-specific toxin (AK-toxin) in liquid culture which caused veinal necrosis only on susceptible pear leaves, while nonpathogenic isolates did not produce this toxin. Varietal susceptibility among pear cultivars to the pathogen was investigated by evaluating HST (AK-toxin) sensitivity of pear leaves, as a substitute for spore inoculation. AK-toxin which the fungus produces was toxic to pear cultivars susceptible to the pathogen such as Isipsegi and Sinsu, but was harmless to resistant pear cultivars such as Chojuro, Oksankichi, Niitaka etc. Changes in disease susceptibility and toxin sensitivity of pear leaves with aging was investigated. Disease susceptibility and toxin sensitivity in cv. Sinsu leaves appeared to vary with leaf aging; the young leaves were visibly susceptible, but older leaves (more than 2 week old leaves) became resistant.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.23 no.2
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• pp.93-98
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• 2012

Botulinum toxins are the most potent toxins known to mankind. Botulinum toxin acts by blocking the cholinergic neuromuscular or the cholinergic autonomic innervation of exocrine glands and smooth muscles. Seven distinct antigenic botulinum toxins (A, B, C, D, E, F and G) produced by different strains of Clostridium botulinum have been described and only A and B type of botulinum toxins were clinically used. Toxins were consisted of a heavy chain with a molecular weight of 100 kD and a light chain with a molecular weight of 50 kD. Toxins are bound with an astounding selectivity to glycoprotein structures located on the cholinergic nerve terminal. Subsequently light chain of toxin is internalized and cleaves different proteins of the acetylcholine transport protein cascade transporting the acetylcholine vesicle from the intracellular space into the synaptic cleft. After a decade of therapeutic application of the toxin, no anaphylaxis or deaths have been reported and systemic adverse effects have not been reported so far. However the toxin's immunologic properties can lead to the stimulation of antibody production, potentially rendering further treatments ineffective. Botulinum toxin is a safe and effective treatment. Use of botulinum toxin in clinical medicine has grown exponentially in recent years, and many parts of the human body are now being targeted for therapeutic purposes.