• Asian Pacific Journal of Cancer Prevention
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• 제17권3호
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• pp.1325-1332
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• 2016

Radioprotective effects of ginger essential oil (GEO) on mortality, body weight alteration, hematological parameters, antioxidant status and chromosomal damage were studied in irradiated mice. Regression analysis of survival data in mice exposed to radiation yielded LD50/30 as 7.12 and 10.14 Gy for control (irradiation alone) and experimental (GEO-treated irradiated) mice, respectively, with a dose reduction factor (DRF) of 1.42. In mice exposed to whole-body gamma-irradiation (6 Gy), GEO pre-treatment at 100 and 500 mg/kg b.wt (orally) significantly ameliorated decreased hematological and immunological parameters. Radiation induced reduction in intestinal tissue antioxidant enzyme levels such as superoxide dismutase, catalase, glutathione peroxidase and glutathione was also reversed following administration of GEO. Tissue architecture of small intestine which was damaged following irradiation was improved upon administration of GEO. Anticlastogenic effects of GEO were studied by micronuclei assay, chromosomal aberration and alkaline gel electrophoresis assay. GEO significantly decreased the formation of micronuclei, increased the P/N ratio, inhibited the formation of chromosomal aberrations and protected agaisnt cellular DNA damage in bone marrow cells as revealed by comet assay. These results are supportive of use of GEO as a potential radioprotective compound.

• 한국환경성돌연변이발암원학회지
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• 제25권4호
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• pp.129-133
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• 2005

We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown seaweed), against oxidative stress induced cell damage in Chinese hamster lung fibroblast(V79-4) cells. Phloroglucinol was found to scavenge intracellular reactive oxygen species (ROS) generated by $\gamma-ray$ radiation. In addition, Phloroglucinol inhibited cell damage induced by radiation through scavenging ROS. Phloroglucinol increased the superoxide dismutase and glutathione peroxidase activity, Taken together, the results suggest that phloroglucinol protectes V79-4 cells against oxidative damage by enhancing the cellular antioxidant enzymes activity.

• 한국전자현미경학회:학술대회논문집
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• 한국현미경학회 2005년도 제36차 추계학술대회 및 제4회 HVEM 이용자 워크샵
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• pp.56-60
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• 2005

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2001년도 춘계학술발표회요약집
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• pp.399.2-399
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• 2001

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 1999년도 춘계학술발표회요약집
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• pp.388-388
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• 1999

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2005년도 춘계학술발표회
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• pp.998-999
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• 2005

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2005년도 추계학술발표회
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• pp.330-331
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• 2005

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 1999년도 춘계학술발표회요약집
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• pp.292-292
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• 1999

• Radiation Oncology Journal
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• 제31권2호
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• pp.57-65
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• 2013

Beta-lapachone (${\beta}$-Lap; 3,4-dihydro-2, 2-dimethyl-2H-naphthol[1, 2-b]pyran-5,6-dione) is a novel anti-cancer drug under phase I/II clinical trials. ${\beta}$-Lap has been demonstrated to cause apoptotic and necrotic death in a variety of human cancer cells in vitro and in vivo. The mechanisms underlying the ${\beta}$-Lap toxicity against cancer cells has been controversial. The most recent view is that ${\beta}$-Lap, which is a quinone compound, undergoes two-electron reduction to hydroquinone form utilizing NAD(P)H or NADH as electron source. This two-electron reduction of ${\beta}$-Lap is mediated by NAD(P)H:quinone oxidoreductase (NQO1), which is known to mediate the reduction of many quinone compounds. The hydroquinone forms of ${\beta}$-Lap then spontaneously oxidizes back to the original oxidized ${\beta}$-Lap, creating futile cycling between the oxidized and reduced forms of ${\beta}$-Lap. It is proposed that the futile recycling between oxidized and reduced forms of ${\beta}$-Lap leads to two distinct cell death pathways. First one is that the two-electron reduced ${\beta}$-Lap is converted first to one-electron reduced ${\beta}$-Lap, i.e., semiquinone ${\beta}$-Lap $(SQ)^{{\cdot}-}$ causing production of reactive oxygen species (ROS), which then causes apoptotic cell death. The second mechanism is that severe depletion of NAD(P)H and NADH as a result of futile cycling between the quinone and hydroquinone forms of ${\beta}$-Lap causes severe disturbance in cellular metabolism leading to apoptosis and necrosis. The relative importance of the aforementioned two mechanisms, i.e., generation of ROS or depletion of NAD(P)H/NADH, may vary depending on cell type and environment. Importantly, the NQO1 level in cancer cells has been found to be higher than that in normal cells indicating that ${\beta}$-Lap may be preferentially toxic to cancer cells relative to non-cancer cells. The cellular level of NQO1 has been found to be significantly increased by divergent physical and chemical stresses including ionizing radiation. Recent reports clearly demonstrated that ${\beta}$-Lap and ionizing radiation kill cancer cells in a synergistic manner. Indications are that irradiation of cancer cells causes long-lasting elevation of NQO1, thereby sensitizing the cells to ${\beta}$-Lap. In addition, ${\beta}$-Lap has been shown to inhibit the repair of sublethal radiation damage. Treating experimental tumors growing in the legs of mice with irradiation and intraperitoneal injection of ${\beta}$-Lap suppressed the growth of the tumors in a manner more than additive. Collectively, ${\beta}$-Lap is a potentially useful anti-cancer drug, particularly in combination with radiotherapy.

• Journal of Radiation Protection and Research
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• 제32권4호
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• pp.178-183
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• 2007

중성자선은 고 LET (linear energy transfer) 방사선으로 X선이나 감마선 등의 저 LET 방사선보다 세포에 더욱 큰 손상을 입힌다. 중성자에 의한 손상은 일반적으로 세포에 있어서 치명적이며, 중성자선은 X선이나 감마선에 비하여 직접작용을 통하여 세포사를 일으키는 경향이 있다. 본 연구에서는 고속중성자선의 성장지연비 및 산소증강비를 동물실험을 통하여 측정하고자 하였다. BALB-c 마우스의 우측 하지에 EMT-6 세포주를 이식한 후 종양의 평균용적이 $200-300mm^3$가 되었을 때 X선 및 고속중성자선을 조사하였다. 정상산소환경 및 저산소환경의 종양에 대하여 X선은 0, 11, 15.4 Gy를 조사하였고 고속중성자선은 0, 5, 7, Gy를 조사하였다. 방사선조사 후에는 종양의 용적을 주 3회 측정하였다. 정상산소환경 실험군의 경우 저산소환경 실험군에 비하여 X선 11 Gy를 조사하였을 때 성장지연비가 1.34였고, 15.4 Gy를 조사하였을 때 1.33였다. 고속중성자선을 조사한 경우정상산소환경 실험군이 저산소환경 실험군에 비하여 고속중성자선 5 Gy를 조사하였을 때 성장지연비는 0.94였고, 고속중성자선 7 Gy를 조사하였을 때 0.98였다. 고속중성자선의 산소증강비는 0.97이었다. 고속중성자선은 X선에 비하여 저산소환경에 있는 종양의 성장억제에 있어서 보다 효과적이었다.