• Bulletin of the Korean Chemical Society
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• 제26권10호
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• pp.1582-1584
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• 2005

• The Korean Journal of Physiology and Pharmacology
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• 제13권3호
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• pp.195-200
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• 2009

Zinc released from excited glutamatergic neurons accelerates amyloid ${\beta}$ (A ${\beta}$) aggregation, underscoring the therapeutic potential of zinc chelation for the treatment of Alzheimer's disease (AD). Zinc can also alter A ${\beta}$ concentration by affecting its degradation. In order to elucidate the possible role of zinc influx in secretase-processed A ${\beta}$ production, SH-SY5Y cells stably expressing amyloid precursor protein (APP) were treated with pyrrolidine dithiocarbamate (PDTC), a zinc ionophore, and the resultant changes in APP processing were examined. PDTC decreased A ${\beta}$ 40 and A ${\beta}$ 42 concentrations in culture media bathing APP-expressing SH-SY5Y cells. Measuring the levels of a series of C-terminal APP fragments generated by enzymatic cutting at different APP-cleavage sites showed that both ${\beta}$-and ${\alpha}$-cleavage of APP were inhibited by zinc influx. PDTC also interfered with the maturation of APP. PDTC, however, paradoxically increased the intracellular levels of A ${\beta}$ 40. These results indicate that inhibition of secretase-mediated APP cleavage accounts -at least in part- for zinc inhibition of A ${\beta}$ secretion.

• 폴리머
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• 제37권3호
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• pp.269-275
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• 2013

화학적 구조가 다른 thiuram계 TMTD(tetramethyl thiuram disulfide), DPTT(dipenta-methylene thiuram tetrasulfide), thiazole계 MBT(2-mercapto benzothiazole), MBTS(2,2-dithiobis(benzo-thiazole)), sulfenamide계 CBS(n-cyclohexyl benzothiazyl-2-sulfenamide), NOBS(n-oxydiethylene benzo-thiazyl-2-sulfenamide), 아연이 포함된 thiuram계 ZDBC(zinc di-n-butyl-dithiocarbamate)를 사용하여 각각의 촉진제가 실리카와 카본블랙으로 충전된 천연 고무 복합소재의 가황 속도 및 가황 지수에 미치는 영향을 비교 평가하였다. 양 시스템에서 가황 속도는 thiuram계, thiazole계, sulfenamide계의 순서로 동일한 경향을 보였다. 각 촉진제에 대하여 실리카 컴파운드는 카본블랙 컴파운드에 비해 $t_{s2}$, $t_{10}$, $t_{90}$에 도달하는 시간이 느리게 나타났으며 느린 가황 지수(CRI)를 나타내었다.

• 대한화학회지
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• 제16권6호
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• pp.373-377
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• 1972

미량 구리의 sodium diethyl dithiocarbamate의 chelate를 ethyl acetate로 추출하고 이 추출액을 구리(원자번호 29번)의 이웃원소인 아연(원자번호 30번) 분말에 흡착시켰다. 추출액을 날려보낸 뒤에 $250kg/cm^2$ 으로 압축성형하여 구리의 $K_{\alpha}2(2{\theta}_{LiF} = 45.08^{\circ})$에서 형광 X-선을 측정한 결과 구리 $10{\mu}g$까지 측정할 수 있었으며 표준물질첨가법에 의하여 상대오차를 ${\pm}10$%이내로 낮출수가 있었다.

• 대한화학회지
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• 제38권12호
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• pp.898-907
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• 1994

킬레이트제로 zinc diethyldithiocabamate $[Zn(DDC)_2]$를 사용하여 해수중 흔적량 무기수은(Ⅱ)의 용매추출에 관하여 연구하였다. $Zn(DDC)_2$는 추출과정동안 산성 수용액에서 DDC-의 안정도를 유지하여 준다. 본 실험실에서 NaDDC와 $ZnSO_4$로부터 $Zn(DDC)_2$를 합성하였다. 흔적량 수은을 pH 3.0의 해수 100ml로부터 0.05 M $Zn(DDC)_2$의 클로포름 용액 10ml에 5분간 흔들어 추출하였다. 그리고 클로로포름 유기상으로부터 $Hg(DDC)_2$를 각 3% (v/v)인 질산과 염산의 1:1혼합산 용액 10ml에 25분간 흔들어 역추출하였다. 역추출된 수은을 냉증기 원자흡수 분광광도법으로 정량하였다. 본 추출과정을 해수중 수은의 정량에 응용하였고, 일정량의 수은을 첨가한 해수시료에서 90.0%와 93.3%의 회수율을 보여주었다.

• The Korean Journal of Physiology and Pharmacology
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• 제7권2호
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• pp.65-71
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• 2003

Increasing evidences suggest that ischemia-induced vascular damage is an integral step in the cascade of the cellular and molecular events initiated by cerebral ischemia. In the present study, employing a mouse brain endothelioma-derived cell line, bEnd.3, and oxygen-glucose deprivation (OGD) as an in vitro stroke model, the role of nuclear factor kappa B (NF-${\kappa}B$) activation during ischemic injury was investigated. OGD was found to activate NF-${\kappa}B$ and to induce bEnd.3 cell death in a time-dependent manner. OGD phosphorylated neither 32 Ser nor 42 Tyr of $I{\kappa}B{\alpha}$. OGD did not change the amount of $I{\kappa}B{\alpha}$. The extents of OGD-induced cell death after 8 h, 10 h, 12 h and 14 h of OGD were 10%, 35%, 60% and 85%, respectively. Reperfusion following OGD did not cause additional cell death, indicating no reperfusion injury after ischemic insult in cerebral endothelial cells. Three known as NF-${\kappa}B$ inhibitors, including pyrrolidine dithiocarbamate (PDTC) plus zinc, aspirin and caffeic acid phenethyl ester (CAPE), inhibited OGD-induced NF-${\kappa}B$ activation and increased OGD-induced bEnd.3 cell death in a dose dependent manner. There were no changes in the protein levels of bcl-2, bax and p53 which are modulated by NF-${\kappa}B$ activity. These results suggest that NF-${\kappa}B$ activation might be a protective mechanism for OGD-induced cell death in bEnd.3.