• Bulletin of the Korean Chemical Society
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• v.26 no.10
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• pp.1582-1584
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• 2005

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.3
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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.

• Polymer(Korea)
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• v.37 no.3
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• pp.269-275
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• 2013

Thiuram (DPTT, TMTD), thiazole (MBT, MBTS), sulfenamide (CBS, NOBS), and zinc containing thiuram (dithiocarbamate) (ZDBC) type accelerators were added into silica and carbon black filled natural rubber (NR) compounds. Their effects on vulcanization time and rate were compared. The vulcanization rate of thiuram type accelerator added compounds showed the fastest rate, followed by thiazole and sulfenamide types. Silica filled natural rubber (NR) compounds showed a slower vulcanization time ($t_{s2}$, $t_{10}$, $t_{90}$) and lower cure rate index (CRI) than carbon black filled ones upon each accelerator.

• Journal of the Korean Chemical Society
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• v.16 no.6
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• pp.373-377
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• 1972

The analytical conditions for the fluorescence X-ray determination of small amount of cupper in solution were established. Copper in solution was extracted by diethyldithiocarbamate ethyl acetate and adsorbed by zinc powder. After drying, it was pressed to tablet under the pressure of $250Kg/cm^2.$$K_{\alpha}2(2{\theta}_{LiF} = 45.08^{\circ})$. The limit of detection was estimated to be about $10{\mu}g$ by the method of standard addition with an error of 10 %.

• Journal of the Korean Chemical Society
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• v.38 no.12
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• pp.898-907
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• 1994

The solvent extraction of an inorganic trace mercury in sea water samples was studied using zinc diethyldithiocabamate $Zn(DDC)_2$ as chelating agent. The $Zn(DDC)_2$ which maintained the stability of DDC- in the acidic aqueous solution in the course of extraction was synthesized from NaDDC and $ZnSO_4$ in this laboratory. The trace of mercury(Ⅱ) was extracted at pH 3.0 from 100 ml of sea water into 10ml of chloroform containing 0.05 M $Zn(DDC)_2$ by shaking for 5 minutes. And from the organic phase, the $Hg(DDC)_2$ was back-extracted into 10ml of 1 to 1 mixed acid of each 3% (v/v) nitric acid and hydrochloric acid by shaking for 25 minutes. The mercury back-extracted was determined by a cold vapor atomic absorption spectrophotometry. The trace mercury(Ⅱ) was so successfully extracted that this procedure could be applied to its determination in the sea water. That is, the recoveries of mercury in two kinds of samples into which as given amount of Hg(Ⅱ) was spiked were 90.0% and 93.3%, respectively.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.2
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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.