• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.288.3-289
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• 2002

Increasing evidence regarding free radical generating agents and inflammatory processes suggests that accumulation of reactive oxygen species can cause hepatotoxicity. A short-chain analog of lipid hydroperoxide, t-butyl hydroperoxide (t-BHP), can be metabolized to free radical intermediates by cytochrome P-450 in hepatocytes. which in turn can initiate lipid peroxidation, affect cell integrity and result in cell injury. (omitted)

• 공업화학
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• 제3권4호
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• pp.649-656
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• 1992

t-Butyl hydroperoxide(TBHP)에 의한 염화알릴의 에폭시화에 의해서 에피클로로히드린을 합성하는데 실리카에 담지된 몰리브데늄 촉매를 사용하였다. 속도론적 연구는 회분 반응기를 사용하여 $60-80^{\circ}C$, 10기압에서 TBHP/염화알릴의 농도비를 0.01-0.1의 범위내에서 수행하였다. t-butyl alcohol(TBA)에 의해서 염화알릴의 에폭시화 반응이 억제되었고, 반응속도는 Michaelis-Menten 형태의 속도식으로 표현할 수 있었다. 반응기구는 TBHP와 TBA의 가역흡착과 $Mo/SiO_2$에 흡착된 TBHP와 염화알릴의 표면반응으로 설명할 수 있었다.

• Natural Product Sciences
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• 제14권4호
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• pp.244-248
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• 2008

It is well known that excessive production of reactive oxygen species (ROS) leads to oxidative stress, loss of cell function, and ultimately apoptosis or necrosis. To search for natural antioxidants able to modulate cellular oxidative stress, we investigated the protective effect of ethanol extracts of 17 medicinal plants selected from the preliminary antioxidant screening on tert-butyl hydroperoxide (t-BuOOH)-induced oxidative stress in human keratinocytes. The result showed that extracts of the four plants, Distylium racemosum, Astilbe chinensis, Cercis chinensis and Sapium japonicum, exhibited significant cytoprotective activity (over 50% protection) against t-BuOOH-induced cellular injury.

• BMB Reports
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• 제42권10호
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• pp.648-654
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• 2009

Overexpression of phospholipid hydroperoxide glutathione peroxidase (PHGPx) genes has been reported to play an important role in protecting host cells from oxidative injury in several model systems. A radish phospholipid hydroperoxide glutathione peroxidase (RsPHGPx) known to have high catalytic activity was applied to mouse 3T3 fibroblasts to determine the protective effects of PHGPx against oxidative injury triggered by hydroperoxides such as hydrogen peroxide ($H_2O_2$), tert-butyl hydroperoxide (t-BHP) and phosphatidylcholine hydroperoxide (PCOOH). We observed that preincubation of cells with RsPHGPx significantly increased cell viability, reduced levels of malondialdehyde (MDA), inhibited generation of reactive oxygen species (ROS), and maintained natural cell shapes after treatment with $H_2O_2$, t-BHP or PCOOH, indicating that the exogenous RsPHGPx can act as an effective hydroperoxide-scavenger and may also protect target cells from oxidative damage. These results suggest the possibility for use of RsPHGPx as a therapeutic protectant.

• 대한한의학회지
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• 제20권3호
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• pp.77-86
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• 1999

This study was undertaken to evaluate the effect of Sunghyangchungi-san (SHCS) on the oxidant-induced contraction and lipid peroxidation in rabbit carotid artery. Vascular rings isolated from rabbit carotid artery were exposed to t-butyl hydroperoxide (t-BHP), an extrinsic oxidant, and the effect of SHCS on the changes of vascular tension and lipid peroxidation induced by t-BHP was determined. t- BHP induced a slowly developing and sustained contraction of the arterial rings. SHCS effectively relaxed the arterial rings that were pre-contracted by t-BHP. The responses to SHCS were partially dose-dependent at concentrations lower than 0.5 mg/ml. When SHCS was applied prior to the exposure to t-BHP, it inhibited the t-BHP-induced contraction as well. t- BHP increased lipid peroxidation in a dose-dependent manner. SHCS as well as well-known anti-oxidants GSH and DPPD reduced significantly lipid peroxidation induced by t-BHP. SHCS partially blocked the increase in $^{45}Ca$ uptake induced by t-BHP. In contrast to SHCS, anti-oxidants GSH and DPPD failed to inhibit significantly the t- BHP-induced contraction or $^{45}Ca$ uptake. From the above results, it is suggested that SHCS relaxed t-BHP-induced contraction of rabbit carotid artery independently of its anti-oxidant action, and inhibition of $Ca^{2+}$ influx may contribute to the underlying mechanism.

• Journal of Acupuncture Research
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• 제17권3호
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• pp.176-187
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• 2000

Objectives : This study was purposed to investigate the antioxidative effects of Paeoniae radix aqua-acupuncture solution(PR) on culture liver cell system, lipid peroxidation and antioxidative enzyme activities in tert-butyl hydroperoxide(t-BHP) treatmented conditions. Methods : Cultured normal rat liver cell(Ac2F) were prepared and incubated with or without PR(at 2% volume in culture medium). After 16~18hr, cells placed in DMEM medium without serum, and then incubated with 1mM t-BHP for 2hr. Viable cells were detected by MTT assay, and the levels of lipid peroxide(LPO) were measured by TBA method. And catalase activity was measured as the decrease in hydrogen peroxide absorbance at 240nm on spectrophotometer using 30mM hydrogen peroxide. Superoxide dismutase(SOD) were assayed by recording the inhibition of nitro blue tetrazolium reduction with xanthine and xanthine oxidase. Glutathione peroxidase(GPX) activity was determined by the modified coupled assay developed by Paglia and Lawrence. The reaction was started by addition of 2.2mM hydrogen peroxide as substrate. The change in absorbance at 340nm was measured for 1min on spectrophotometer. Glutathione-S-transferase(GST) activity was assayed with CDNB as substrate and enzyme activity of GST towards the glutathione conjugation of CDNB. Results : Cell killing was significantly enhanced by addition of t-BHP compared to those of untreated group. PR pretreated cell resisted the toxic effects of t-BHP. LPO levels of t-BHP treatment group were significantly higher than other groups. This increased level was significandy reduced by PR pretreatment. The t-BHP treatment resulted in a decrease of catalase, GPX and GST activities. By contrast, PR pretreatment markedly increased compare to those of untreated groups. Conclusions : T-BHP which can produce intracellular free radical was used for inducer of the peroxidation of cellular lipids. PR protected the cell death induced by t-BHP and significantly increased cell viabiliry in the normal rat liver cell, and showed effective inhibition of lipid peroxidation, and elevations of catalase, GPX and GST activities. These results suggested that PR might play a protective role in lipid peroxidation by free radicals.

• Bulletin of the Korean Chemical Society
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• 제17권2호
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• pp.116-117
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• 1996

• Bulletin of the Korean Chemical Society
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• 제19권3호
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• pp.319-323
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• 1998

The phodissociation dynamics of t-butyl hydroperoxide at 280-285 nm has been investigated by measuring laser induced fluorescence spectra of the fragment OH. Measured fractions of the available energy distributed among the fragments are ft=0.56, fr(OH)=0.044, fint(t-BuO)=0.40, and negligible populations of OH are found in vibrationally excited states. By analyzing the Doppler profiles of the spectra of OH, the positive ν-J vector correlation has been obtained. From the measured ν-J correlation and A" propensity in the two Λ-doublets of OH, it is concluded that the dissociation takes place directly from the repulsive surface induced by the σ* ← n transition with the fragment OH rotating in the plane perpendicular to the dissociating O-O bond axis.

• 대한한의학방제학회지
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• 제26권3호
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• pp.251-259
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• 2018

Objective : Kurarinone is one of the flavonoids isolated from Sophorae Radix with various biological activities including anti-microbial effect. In this study, we investigated the effects of Kurarinone on tert-butyl hydroperoxide (tBHP)-induced oxidative stress finally leading to apoptosis in human hepatoma cell line HepG2. Methods : To determine the effects on cell viability, the cells were exposed to tBHP ($100{\mu}mol/l$) after pretreatment with kurarinone (0.5 and $1{\mu}g/ml$). Cell viability was measured by MTT assay. To reveal the possible mechanism of cytoprotectivity of kurarinone, levels of reactive oxygen species, intracellular glutathione, mitochondrial membrane potential, and expression of caspase were examined. Results : tBHP-induced cell death was due to oxidative stress and the resulting apoptosis. Kurarinone dose-dependently protected cells from apoptosis when determined by MTT and TUNEL assay. Consistent with this observation, decreased expression of pro-caspase 3/9 protein by tBHP was restored by kurarinone. Kurarinone also showed anti-oxidative effects by inhibiting generation of ROS and depletion of GSH in tBHP-stimulated HepG2 cells. In addition, kurarinone significantly recovered disruption of mitochondrial membrane potential (MMP) as a start sign of hepatic apoptosis induced by oxidative stress. Conclusion : From these results, it was concluded that kurarinone protected tBHP-induced hepatotoxicity with anti-oxidative and anti-apoptotic activities. Our results suggest that kurarinone might be beneficial to hepatic disorders caused by oxidative stress.

• 대한한의학방제학회지
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• 제31권1호
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• pp.29-39
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• 2023

Objective : Gardeniae Fructus (GF) is the ripe fruit of Gardenia jasminoides Ellisa with a bitter taste and cold properties. Ingredient compounds including geniposide are known to have anti-inflammatory, antioxidant, and neuroprotective effects. The purpose of this study was to investigate the neuroprotective effect of GF on tBHP-induced PC12 cells. Methods : Cell viability was measured by the MTT assay, and apoptosis was determined by the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression level of each protein was monitored by Western blot analysis, and reactive oxygen species (ROS) were analyzed using DCFH-DA. Results : In PC12 cells, tBHP induced cell death through apoptosis with caspase activation and PARP inactivation. Cells treated with tBHP showed an increase in intracellular ROS and depletion of GSH. Pretreatment with GF prevented tBHP-induced apoptosis, reduced ROS, and increased GSH. GF also maintained increased Nrf2 expression in the presence of tBHP. Phosphorylation of JNK and p38 MAPK was increased by tBHP, whereas phosphorylation of ERK was decreased. GF restored changes in ERK and p38 phosphorylation, but not JNK phosphorylation. Conclusion : These results indicate that GF has neuroprotective effects through anti-apoptotic and antioxidant effects mediated by regulation of Nrf2 expression and phosphorylation of ERK and p38. It also demonstrates the potential use of GF as a source of antioxidant and neuroprotective substances.