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톨라신의 용혈활성에 대한 Ni<sup>2+</sup>의 저해효과
최태근,왕희성,김영기,Choi, Tae-Keun,Wang, Hee-Sung,Kim, Young-Kee 한국응용생명화학회 2009 Journal of Applied Biological Chemistry (J. Appl. Vol.52 No.1
세균독소인 톨라신은 재배버섯에서 버섯균사 및 자실체의 구조를 파괴하여 갈반병을 일으킨다. 톨라신의 세포독성은 톨라신이 적혈구의 세포막에 pore를 형성하여 세포구조를 파괴하기 때문에 용혈활성을 측정하여 평가한다. 저자들은 $Zn^{2+}$와 $Cd^{2+}$에 의한 톨라신의 용혈활성 저해효과를 측정하는 중에 $Ni^{2+}$이 또 다른 저해제로 톨라신의 독성을 억제하는 것을 발견하였다. $Ni^{2+}$에 의한 톨라신 용혈활성의 저해는 농도의존적이었으며, Ki 값은 대략 10mM이었고, 이것은 $Ni^{2+}$이 $Cd^{2+}$에 비하여 저해효과가 높음을 의미한다. 용혈활성은 50mM 이상의 $Ni^{2+}$농도에서 완전히 제거되었으며, $Ni^{2+}$의 효과는 EDTA 첨가에 의해 가역적임을 확인하였다. 톨라신에 의한 용혈활성이 20mM $Ni^{2+}$에 의해서 완전히 억제된 상태에서 EDTA를 가하면 즉각 용혈활성이 나타났다. $Ni^{2+}$에 의한 톨라신 독성의 저해기작은 알 수 없지만, $Ni^{2+}$은 톨라신의 독성과정인 막결합, 분자중합체 형성, pore 형성, pore를 통한 막대한 양의 이온이동 등에 작용할 수 있을 것이다. 된 연구의 결과는 $Ni^{2+}$이 독성과정의 마지막 단계인 pore를 통한 이온이동 과정을 저해함을 보여준다. The bacterial toxin, tolaasin, causes brown blotch disease on the cultivated mushrooms by collapsing fungal and fruiting body structure of mushroom. Cytotoxicity of tolaasin was evaluated by measuring hemolytic activity because tolaasins form membrane pores on the red blood cells and destroy cell structure. While we investigated the inhibitions of hemolytic activity of tolaasin by $Zn^{2+}$ and $Cd^{2+}$, we found that $Ni^{2+}$ is another antagonist to block the toxicity of tolaasin. $Ni^{2+}$ inhibited the tolaasin-induced hemolysis in a dose-dependent manner and its Ki value was $\sim10$ mM, implying that the inhibitory effect of $Ni^{2+}$ is stronger than that of $Cd^{2+}$. The hemolytic activity was completely inhibited by $Ni^{2+}$ at the concentration higher than 50 mM. The effect of $Ni^{2+}$ was reversible since it was removed by the addition of EDTA. When the tolaasin-induced hemolysis was suppressed by the addition of 20 mM $Ni^{2+}$, the subsequent addition of EDIA immediately initiated the hemolysis. Although the mechanism of $Ni^{2+}$ -induced inhibition on tolaasin toxicity is not known, $Ni^{2+}$ could inhibit any of fallowing processes of tolaasin action, membrane binding, molecular multimerization, pore formation, and massive ion transport through the membrane pore. Our results indicate that $Ni^{2+}$ inhibits the pore activity of tolaasin, the last step of the toxic process.
생태관광 개발과 환경복원 사업으로 지역의 지속가능한 발전 방안에 관한 연구 -시흥시 토취장을 중심으로-
최태근 ( Tae Keun Choi ) 관광경영학회 2013 관광경영연구 Vol.57 No.-
This study takes a look at how many citizens in South Korea have recently been having interest in various leisure themes depending on changes in the environment. In particular, the desire to want to enjoy a variety of eco-tourism is on the rise in order to improve the health and quality of life. Siheung`s borrow pit has been compromised by the development of neglect and environmental restoration projects in the region. If eco-tourism is to be developed, the satisfaction of local citizens and the creation of a regional eco-city brand are the cornerstones of a sustainable development plan. A separate survey targeting residents, government officials, and opinion leaders regarding a sustainable development plan is proposed. Looking at the analysis of empirical results, many residents hold a necessity in regards to the development of Siheung`s borrow pit. However, in order to propel the eco-tourism business, education for residents` understanding, participation, and knowledge will be carried out and specialists will be trained. It is deduced that the proceedings and direction of eco-tourism development must be presented in an integrated manner.
Zn<sup>2+</sup>와 Ni<sup>2+</sup>에 의한 톨라신 용혈활성 저해효과의 pH 의존성
윤영배 ( Yeong-bae Yun ),최태근 ( Tae-keun Choi ),김영기 ( Young-kee Kim ) 한국응용생명화학회 2018 Journal of Applied Biological Chemistry (J. Appl. Vol.61 No.3
Tolaasin secreted by Pseudomonas tolaasii is a peptide toxin and causes brown blotch disease on the cultivated mushrooms by collapsing cellular and fruiting body structure. Toxicity of tolaasin was evaluated by measuring hemolytic activity because tolaasin molecules form membrane pores on the red blood cells and destroy cell membrane structure. In the previous studies, we found that tolaasin cytotoxicity was suppressed by Zn<sup>2+</sup> and Ni<sup>2+</sup>. Ni<sup>2+</sup> inhibited the tolaasin-induced hemolysis in a dose-dependent manner and its Ki value was 1.8 mM. The hemolytic activity was completely inhibited at the concentration higher than 10 mM. The inhibitory effect of Zn<sup>2+</sup> on tolaasininduced hemolysis was increased in alkaline pH, while that of Ni2+was not much dependent on pH. When the pH of buffer solution was increased from pH 7 to pH 9, the time for 50% hemolysis (T50) was increased greatly by 100 μM Zn<sup>2+</sup>; however, it was slightly increased by 1 mM Ni<sup>2+</sup> at all pH values. When the synergistic effect of Zn<sup>2+</sup> and Ni<sup>2+</sup> on tolaasin-induced hemolysis was measured, it was not dependent on the pH of buffer solution. Molecular elucidation of the difference in pH-dependence of these two metal ions may contribute to understand the mechanism of tolaasin pore formation and cytotoxicity.