• 분석과학
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• 제12권2호
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• pp.125-129
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• 1999

고농도의 과산화수소(10-75%)를 생산현장에서 손쉽게 측정할 수 있는 전극 센서 시스템을 연구하였다. Teflon 전극체는 휴대에 간편하도록 길이 10 cm, 지금 1.5 cm의 봉 형태로 제작하였고, 작업 극으로는 직경 3 mm의 glassy carbon을, 보조전극으로는 내경 5 mm, 외경 9 mm의 흑연을 전극물질로 사용하였다. 과산화수소 산화전위는 0.8 V의 전위를 걸어주었다. 공장에서 생산된 고농도의 과산화수소를 일정 이온강도의 전해질 용액으로 희석해 10% 이하의 농도가 되도록 하면 과산화수소에 첨가된 안정제의 방해작용과 과산화수소의 산화작용으로 인한 전극표면의 변성을 최소화할 수 있었고, 손쉽게 정량적인 측정을 할 수 있었다. 또한 과산화수소 투과막(teflon membrane${\leq}100{\mu}m$)을 입힌 전극을 이용하면 고농도의 과산화수소를 희석하지 않고 재현성 있게 정량할 수 있었다. 반면 투과막을 이용하는 방법을 내부전해질을 자주 교환해야 하는 단점이 있었다.

• 대한한의학회지
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• 제21권4호
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• pp.193-203
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• 2000

Objectives : Hindered barrier function of vascular endothelium has been implicated in the initiation and progression of degenerative vascular diseases such as atherosclerosis. In this study, the effect of Sunghyangchungisan(SHCS) as a protectant against oxidant-induced destruction of endothelial barrier function was assessed. Methods : Toward this end, endothelial cells derived from the human umbilical vein were cultured as monolayers on permeable membrane filters. Endothelial permeability was monitored by measuring transendothelial electrical resistance and movement of low density lipoprotein (LDL) across the endothelial monolayer. Results : Along with increased movement of LDL, $H_2O_2$-induced increase in endothelial permeability was paralleled by a decrease in transendotheliaI electrical resistance. The effect of $H_2O_2$ was mimicked by phorbol 12-myristate 13-acetate (PMA), a potent activator of proteinkinase C. Calphostin-C, a protein kinase C inhibitor, effectively blocked the increase in endothelial permeability induced by $H_2O_2$ or PMA, indicating that activation of protein kinase C is associated with the $H_2O_2-induced$ permeability change. SHCS effectively protected the endothelial monolayer against $H_2O_2-induced$ increase in permeability, whereas, it did not affect PMA-induced change. Forskolin, a potent activator of adenylyl cyclase, antagonized $H_2O_2$ to increase endothelial permeability. In addition, in ${H_2O_2}-treated$ cens, intracenular cAMP concentration was significantly decreased, indicating that impaired cAMP production as well as activation of proteinkinase C is a mechanism underlying ${H_2O_2}>-induced$$H_2O_2$ with regard to its effect on intracellular cAMP content. However, SHCS itself did not affect resting cAMP concentration in endothelial cells. Conclusions : These results suggest that SHCS might operate as an effective protectant against oxidant-induced destruction of endothelial barrier function. The mechanism does not appear to involve direct interaction with protein kinase C- or cAMP-associated signaling mechanism.