• Analytical Science and Technology
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• v.12 no.2
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• pp.125-129
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• 1999

Portable-type two electrode system for the determination of highly concentrated hydrogen peroxide (10-75%) has been studied. The electrode body was made with teflon rod (length=10 cm, diameter=1.5 cm) to withstand the highly corrosive power of hydrogen peroxide. Glass carbon rod (diameter=3 mm) was used as the working electrode and a carbon cylinder (i.d.=5 mm; o.d.=9 mm) was used as counter electrode. The applied voltage for the determination of $H_2O_2$ was 0.8 V. Diluting the highly concentrated samples taken from the industrial batch to 10% or less, it was possible to make quantitative determinations, while eliminating the interference from the stabilizer contained in the sample and preventing the surface of the electrode from oxidative corrosion. Employing hydrogen peroxide permeable membrane (teflon membrane${\leq}100{\mu}m$) for the electrode system, it was possible to measure the content of $H_2O_2$ in highly concentrated samples directly, quantitatively and reproducibly with no extra dilution step. However, it was necessary to change the internal electrolyte frequently to maintain the analytical performance of the electrode.

• The Journal of Korean Medicine
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• v.21 no.4
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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.