• Environmental Analysis Health and Toxicology
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• 제19권3호
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• pp.251-259
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• 2004

Xenoestrogens are chemicals with diverse structure that mimic estrogen. Bisphenol A, a monomer of polycarbonate and epoxy resins, has been detected in canned food and human saliva. Bisphenol A stimulate cell proliferation and induce expression of estrogen -response genes in vitro. The purpose of the this study was to evaluate cell proliferation of bisphenol A in the presence of a rat liver 59 mix contaning cytochrome P450 enzymes and Cu (II). The fragmentation of intact DNA, a parameter of apoptotic cell death, was evaluated quantitatively by diphenylamine reaction method. Bisphenol A induced apoptotic cell death in a dose-dependent manner The effect of radical scavenger on the apoptotic cell death induced bisphenol A was investigated. The DNA fragmentation induced by bisphenol A was significantly inhibited by addition of radical scavenger to the culture medium. This indicated that elevated oxidative stress caused by imbalance between the production and removal of free radicals occurred in cells. Taken together, these results suggest that free radical reacts with Cu (II) leading oxidative stress.

• 동의생리병리학회지
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• 제18권1호
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• pp.236-242
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• 2004

Cerebral ischemia resulting from transient or permanent occlusion of cerebral arteries leads to neuronal cell death and eventually causes neurological impairments. Bee venom has been used for the treatment inflammatory disease. In the present study, the effects of bee venom on apoptosis and cell proliferation in the hippocampal dentate gyrus following transient global ischemia in gerbils were investigated using immunohistochemistry for cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), caspase-3, and 5-bromo-2'-deoxyuridine (BrdU). It was shown that apoptotic cell death and cell proliferation in the hippocampal dentate gyrus were significantly increased following transient global ischemia in gerbils and that treatment of bee venom suppressed the ischemia-induced increase in apoptosis and cell proliferation in the dentate gyrus. The present results also showed that 1 mg/kg bee-venom treatment suppressed the ischemia-induced increasing apoptosis, cell proliferation, and COX-2 expression in the dentate gyrus. It is possible that the suppression of cell proliferation is due to the reduction of apoptotic cell death by treatment of bee venom. In the present study, bee venom was shown to prosses anti-apoptotic effect in ischemic brain disease, and this protective effect of bee venom against ischemia-induced neuronal cell death is closely associated with suppression on caspase-3 expression.

• Radiation Oncology Journal
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• 제19권3호
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• pp.252-258
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• 2001

목적 : 사람의 두경부종양 세포주를 대상으로 방사선 조사 후에 일어나는 아포토시스를 측정하여 전체 세포사에서의 중요성 및 방사선감수성과의 관련성을 알아보고자 하였다. 대상 및 방법 : 방사선치료가 주 치료방법인 두경부종양 세포주(PCI-1, PCI-13, SNU-1066)와 정상세포 중 섬유모세포 세포주(LM217), 혈액종양 세포주 중 백혈병 세포주(CCRF-CEM)를 대상으로 하였다. 방사선 조사는 동물실험용 Cs-137 방사선조사기를 사용하였다. 전체 세포사는 집락형성능측정을 이용하였고, 아포토시스의 측정은 annexin-V와 propidium iodide를 이용하는 염색법을 사용하였다. 결과 : 2 Gy 방사선 조사 시의 생존분획인 $SF_2$는 PCI-1, PCI-13, SNU-1066, CCRF-CEM, LM217 세포주에서 각각 0.741, 0.544, 0.313, 0.302, 0.100으로, LM217 세포주가 방사선감수성이 가장 높았고 PCI-1 세포주의 방사선감수성이 가장 낮았다. 두경부암 세포주인 PCI-1, PCI-13, SNU-1066에서는 모두 72시간이 경과한 후 아포토시스지수가 최대치에 도달하였으며, LM217과 CCRF-CEM에서는 24시간 후에 최대치에 도달하였다. 방사선량의 증가에 따라서 전체세포사는 현저하게 증가하였으나 아포토시스지수의 변화는 매우 작았다. 전체 세포사에 대한 아포토시스의 분획(아포토시스분획)은 2 Gy 조사 시 PCI-1, PCI-13, SNU-1066, CCRF-CEM, LM217에서 각각 $46\%,\;48\%,\;46\%,\;24\%,\;19\%$이었고, 6 Gy 조사 시 각각 $20\%,\;33\%,\;35\%,\;17\%,\;20\%$이었다. 아포토시스의 정도와 6 Gy 조사 시의 방사선 감수성과는 일정한 관계를 보이지 않았으나, 2 Gy조사 시 방사선에 감수성이 비교적 높은 세포주가 아포토시스분획이 작았다. 결론 : 본 연구에서 사용한 두경부암세포주에서 방사선 조사 후 아포토시스가 관찰되었으며, 발생 양상이 시간적으로 정상 섬유모세포 및 백혈병세포주와 다른 것을 확인하였다. 또한 아포토시스보다는 다른 종류의 세포사인 증식사가 더 중요하게 작용하고 있음을 알 수 있었다. 아포토시스분획과 2 Gy 조사 시 방사선감수성 사이에 관련 가능성이 제시되었다.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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• pp.153-153
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• 2001

Capsaicin, a major pungent ingredient in red hot pepper, has long been used in food additives and drugs. We have previously reported that capsaicin induces apoptosis in Korean stomach cancer cell line, SNU-1. In the present study, the mechanism of capsaicin-induced apoptotic cell death was investigated in SNU-1. Treatment of capsaicin to SNU-1 produced dose-dependent increase of apoptotic cell death and ［Ca2＋］$_{i}$ concentrations.(omitted)d)

• 방사선산업학회지
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• 제4권1호
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• pp.91-94
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• 2010

A number of epidemiological studies as well as biological experiments, showed that genistein, one of the isoflavone, prevents prostate cancer occurrence. In this study, we showed that genistein inhibited the cell proliferation of human promyeoltic leukemia HL-60 cells and induced G2/M phase arrest. In addition, combination of genistein treatment and ${\gamma}$-irradiation displayed synergistic effect in apoptotic cell death of HL-60 cells. This means that the repair of genistein-induced DNA damage was hindered by ${\gamma}$-radiation and thus cell death was increased. In conclusion, genistein is one of the important chemicals that sensitize radiation-induced cell death.

• The Korean Journal of Physiology and Pharmacology
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• 제13권3호
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• pp.139-145
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• 2009

The purpose of this study was to evaluate the effects of the water extract of Samultang (SMT), a Chinese herb, on apoptotic cell death by $H_2O_2$-induced oxidative stress in SK-N-M C cells. A nuclear fragmentation was observed via fluorescence imaging 12 h after exposure to 30 ${\mu}M$ $H_2O_2$ and DNA laddering was detected via agarose electrophoresis gel. In addition, increases in sub-G1 phase and cleavage of the PARP protein were observed. However, treatment with SMT for 2 h prior to $H_2O_2$ exposure significantly reduced apoptotic cell death induced by incubation with 30 ${\mu}M$ $H_2O_2$ in SK-N-MC cells. Pre-incubation with water extract of SMT for 2 h prevented the $H_2O_2$-induced decrease in mitochondrial transmembrane potential. SMT also attenuated the increase in caspase-3 activity and the breakdown of PARP protein caused by $H_2O_2$-induced oxidative stress. These results suggest that the water extract of SMT provides inhibition of apoptotic cell death against oxidative injury in SK-N-MC cells.

• 대한화장품학회지
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• 제31권3호
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• pp.219-236
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• 2005

Glycolic acid 는 과일과 우유 사탕수수에서 비롯되는 알파-hydroxy 산의 일종의 화장품 성분으로 UV-irradiate된 피부에서는 광보호와 항 염증효과 및 산화 방지 효과가 있는 것으로 알려져 있다. 그러나 UV자극에 의한 피부세포증식에 관하여 glycolic acid의 기능은 거의 알려진바 없다. Glycolic acid는 UV에 의한 hairless mouse의 피부에서 종양 발전을 억제한다는 것을 본 연구자 등이 규명한바 있다. 따라서 이번 연구에서는 UV에 의한 피부의 종양발생억제 효과가 glycolic acid가 UV에 의한 피부의 세포성장을 억제하기 때문인지를 연구하였다 Glycolic acid 를 처치한 피부에서 UV에 의하여 유도된 세포증식과 apoptotic cell death을 감소시켰다. In vitro 연구에서도 glycolic acid 는 UVB 에 의하여 유도된 피부 유래세포인 keratinocyte의 세포성장억제와 apoptotic cell death 및 caspase-3 활동을 억제하였다. 이 결과들은 glycolic acid가 UV에 의하여 유도된 피부종양발생 억제가 UV에 의한 대한 피부세포성장과 apoptotic cell death를 억제하는 효과에 의한 것임을 시사한다.

• BMB Reports
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• 제35권1호
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• pp.28-40
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• 2002

Apoptosis is a mode of cell death that plays an important role in both pathological and physiological processes. Research during the last decade has delineated the entire machinery needed for cell death, and its constituents were found to pre-exist in cells. The apoptotic cascade is triggered when cells are exposed to an apoptotic stimulus. It has been known for several years that inhibitors of protein synthesis can potentiate apoptosis that is induced by cytokines and other inducers. Until 1996, it was not understood why protein synthesis inhibitors potentiate apoptosis. Then three reports appeared that suggested the role of the transcription factor NF-${\kappa}B$ activation in protecting the cells from TNF-induced apoptosis. Since then several proteins have been identified that are regulated by NF-${\kappa}B$ and are involved in cell survival, proliferation, and protection from apoptosis. It now seems that when a cell is attacked by an apoptotic stimulus, the cell responds first by activating anti-apoptotic mechanisms, which mayor may not be followed by apoptosis. Whether or not a cell undergoes proliferation, the survival, or apoptosis, appears to involve a balance between the two mechanisms. Inhibitors of protein synthesis seem to suppress the appearance of protein that are involved in anti-apoptosis. The present review discusses how NF-${\kappa}B$ controls apoptosis.

• 대한본초학회지
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• 제28권6호
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• pp.79-86
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• 2013

Objectives : The purpose of this study is to investigate neuroprotective effects and molecular mechanisms of luteolin against ${\beta}$-amyloid ($A{\beta}_{25-35}$)-induced oxidative cell death in BV-2 cells. Methods : The protective effects of luteolin against $A{\beta}_{25-35}$-induced cytotoxicity and apoptotic cell death were determined by MTT dye reduction assay and TUNEL staining, respectively. The apoptotic cell death was further analyzed by measuring mitochondrial transmembrane potential and expression of pro- and/or anti-apoptotic proteins. To elucidate the molecular mechanisms underlying the protective effects of luteolin, intracellular accumulation of reactive oxygen species, oxidative damages, and expression of antioxidant enzymes were examined. Results : Luteolin pretreatment effectively attenuated $A{\beta}_{25-35}$-induced apoptotic cell death indices such as DNA fragmentation, dissipation of mitochondrial transmembrane potential, increased Bax/Bcl-2 ratio, and activation of c-Jun N-terminal kinase and caspase-3 in BV-2 cells. Furthermore, $A{\beta}_{25-35}$-induced intracellular formation of reactive oxygen species and subsequent oxidative damages such as lipid peroxidation and depletion of endogenous antioxidant glutathione were suppressed by luteolin treatment. The neuroprotective effects of luteolin might be mediated by up-regulation of cellular antioxidant defense system via up-regulation of ${\gamma}$-glutamylcysteine ligase, a rate-limiting enzyme in the glutathione biosynthesis and superoxide dismutase, an enzyme involved in dismutation of superoxide anion into oxygen and hydrogen peroxide. Conclusions : These findings suggest that luteolin has a potential to protect against $A{\beta}_{25-35}$-induced neuronal cell death and damages thereby exhibiting therapeutic utilization for the prevention and/or treatment of Alzheimer's disease.

• 대한한방내과학회지
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• 제29권1호
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• pp.42-66
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• 2008

Aconiti Tuber is a traditional medicinal plant generally used in Oriental medicine therapy. In this study, we investigated the biochemical mechanisms of anti-proliferative effects by the methanol extract of Aconiti tuber (MEBJ) in Caki-1 human renal cell carcinoma cells. It was found that MEBJ could inhibit, in a dose-dependent manner, cell growth which was associated with apoptotic cell death such as formation of apoptotic bodies, DNA fragmentation and increased populations of apoptotic-sub G1 phase. Apoptosis of Caki-1 cells by MEBJ was associated with an up-regulation of pro-apoptotic Bax expression, and a down-regulation of anti-apoptotic Bcl-2 in a dose-dependent manner; however, the levels of IAP family were not affected. MEBJ treatment also induced the proteolytic activation of caspase-3 and -8, and a inhibition of poly(ADP-ribose) polymerase (PARP) and $PLC{\gamma}1$ protein. Furthermore, MEBJ treatment caused a dose-dependent inhibition of iNOS and cyclooxygenase-2 (Cox-2). Though further studies will be needed to identify the active compounds that confer the anti-cancer activity of MEBJ, the present findings provide important new insights into the possible molecular mechanisms of the apoptotic activity of MEBJ in cancer cells.