• 한국동물학회지
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• 제31권2호
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• pp.142-146
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• 1988

PAH화합물의 하나인 benzo(a)pyrene의 쥐 태반 microsomes에 의한 대사활성화를 조사하였다. B(a)P대사물은 C18- $\mu$ Bondapak칼럼을 사용하여 고압액체크로마토그래피로 분석하였다. 그 결과 B(a)P를 투여한 쥐의 태반 microsomes에 의한 주 대사산물은 발암성이 강한 7,8-diol B(a)P였으며, 또한 적은량의 4,5-diol B(a)P와 quinone류가 검출되었다. 3-methyl-cholanthrene을 투여한 경우 hydroxy B(a)P 와 quinone화합물이 주 대사산물이었으며 Phenobarbital을 전처리했을 경우 7,8-diol B(a)P이 주 대사산물인 것으로 나타났다.

• Nuclear Engineering and Technology
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• 제2권2호
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• pp.73-84
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• 1970

Solanum andigena의 괴경생성형상과 스테톨의 관계를 구명하기 위하여 방사성 매바론산을 이용하여 대사를 연구하였다. 괴경생성에 단일광조성수도를 요하는 단일식물과 괴경을 생성치 않는 장일식물을 접목 시켰을때 장일식물이 괴경생성 홀몬을 받아 괴경을 생성하는 현상을 스테로이드와 결부시켜 구명할려고한것이다. 이 연구에서 각종 방사성 스테톨이 특수장치한 까스 크로마토 그라피로서 분리 측정되었다. 여기서 분리된 각종 스테톨이 직정 괴경생성홀몬이라는 근거는 찾을 수 없으며, 이들이 괴경의 포대성장에 필요한 인자로서 관여하고 있는 것으로 논의되었다.

• Molecules and Cells
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• 제44권5호
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• pp.342-355
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• 2021

The microphthalmia-associated transcription factor family (MiT family) proteins are evolutionarily conserved transcription factors that perform many essential biological functions. In mammals, the MiT family consists of MITF (microphthalmia-associated transcription factor or melanocyte-inducing transcription factor), TFEB (transcription factor EB), TFE3 (transcription factor E3), and TFEC (transcription factor EC). These transcriptional factors belong to the basic helix-loop-helix-leucine zipper (bHLH-LZ) transcription factor family and bind the E-box DNA motifs in the promoter regions of target genes to enhance transcription. The best studied functions of MiT proteins include lysosome biogenesis and autophagy induction. In addition, they modulate cellular metabolism, mitochondria dynamics, and various stress responses. The control of nuclear localization via phosphorylation and dephosphorylation serves as the primary regulatory mechanism for MiT family proteins, and several kinases and phosphatases have been identified to directly determine the transcriptional activities of MiT proteins. In different immune cell types, each MiT family member is shown to play distinct or redundant roles and we expect that there is far more to learn about their functions and regulatory mechanisms in host defense and inflammatory responses.

• 동아시아식생활학회지
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• 제21권5호
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• pp.739-745
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• 2011

과실류는 대표적인 신선식품으로 식용되고 있으며, 소득의 증가에 따라 소비량이 크게 늘어나고 있다. 특히, 포도에 함유되어 있는 레스베라트롤과 같은 건강기능 성분의 효과가 과학적으로 밝혀지고 있어 포도는 단순한 영양 자원이나 기호 식품의 측면을 넘어서는 관심을 받고 있다. 이에 따라 본 연구에서는 포도의 대표적인 건강기능 성분인 레스베라트롤이 강화된 생식용 포도를 효과적으로 생산하는 방법을 찾고자 포도 수확 후 자외선을 처리하는 방법을 적용하였다. 본 연구를 통해 도출한 연구의 결론은 다음과 같다. 포도 세포에 외부에서 적당한 스트레스를 가할 경우, 레스베라트롤 생합성 유전자가 발현되어 레스베라트롤의 함량이 증가하는 현상을 확인하였다. 이 현상은 유전자 조작이 이루어지는 과정이 아니며, 단지 포도 세포의 대사를 조절하는 현상이므로 신선식품의 건강기능성분을 강화하는 효과적인 방법으로 사용될 수 있다. 특히, 자외선 조사는 간단한 장치와 단순한 처리로 가능한 방법이기 때문에 포도 산지에서 효과적으로 활용할 수 있는 방법으로 판단된다. 실제로, 수확이후 포도에 자외선을 조사하였을 때 품종에 무관하게 약 5배까지 레스베라트롤을 증폭할 수 있는 것으로 확인되었다. 본 연구에서 제시한 방법은 유전자 조작법이 아니라 세포대사조절에 의한 기법에 해당하므로 현장 활용이 크게 기대된다.

• Toxicological Research
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• 제6권1호
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• pp.51-59
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• 1990

Effects of altering hepatic mixed-function oxidase (MFO) enzyme activities on the metabolism and acute toxicity of parathio were investigated in adult female rats. In vitro hepatic metabolism of parathion to paraoxon was increased by phenobarbital pretreatment (50 mg/kg/day, ip, for 4 consecutive days) and SKF 525-A (50 mg/kg, ip, 1 hr prior to sacrifice) decreased paraoxon formation indicating that phenobarbital induces that form(s) of cytochrome P-450 catalyzing conversion of parathion to paraoxon. Degradation of paraoxon to p-nitrophenol was increased by phenobarbital pretreatment, but not affected by SKF 525-A suggesting that MFO activities play only a minor role in the detoxification of the active metabolite of this insecticide. The phenobarbital-induced increase in paraoxon formation was partially antagonized by SKF 525-A. Significant activity for both parathion activation and paraoxon degradation was also observed in the lung preparation, however, this extrahepatic parathion and paraoxon metabolizing activity was not induced by phenobarbital or inhibited by SKF 525-A pretreatment. Phenobarbital pretreatment increased paraoxon level in livers of rats when measured 3 hr following parathion injection (2 mg/kg, ip). SKF 525-A did not alter parathion or paraoxon levels in brain, blood and liver. Phenobarbital pretreatment decreased the toxicity of parathion (4mg/kg, ip) or paraoxon (1.5 mg/kg, ip) as determined by decreases in lethality and inhibition of brain and lung acetylcholinesterases. An additional SKF 525-A treatment failed to decrease the protective effects of phenobarbital against parathion or paraoxon toxicity. These results suggest that some unknown factors other than hepatic MFO induction are involved in the protective action of phenobarbital against parathion and paraoxon toxicity.

• Investigative Magnetic Resonance Imaging
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• 제20권1호
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• pp.53-60
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• 2016

Purpose: To develop a technique for quantifying the $^{13}C$-metabolites by performing frequency-selective hyperpolarized $^{13}C$ magnetic resonance spectroscopy (MRS) in vitro which combines simple spectrally-selective excitation with spectrally interleaved acquisition. Methods: Numerical simulations were performed with varying noise level and $K_p$ values to compare the quantification accuracies of the proposed and the conventional methods. For in vitro experiments, a spectrally-selective excitation scheme was enabled by narrow-band radiofrequency (RF) excitation pulse implemented into a free-induction decay chemical shift imaging (FIDCSI) sequence. Experiments with LDH / NADH enzyme mixture were performed to validate the effectiveness of the proposed acquisition method. Also, a modified two-site exchange model was formulated for metabolism kinetics quantification with the proposed method. Results: From the simulation results, significant increase of the lactate peak signal to noise ratio (PSNR) was observed. Also, the quantified $K_p$ value from the dynamic curves were more accurate in the case of the proposed acquisition method compared to the conventional non-selective excitation scheme. In vitro experiment results were in good agreement with the simulation results, also displaying increased PSNR for lactate. Fitting results using the modified two-site exchange model also showed expected results in agreement with the simulations. Conclusion: A method for accurate quantification of hyperpolarized pyruvate and the downstream product focused on in vitro experiment was described. By using a narrow-band RF excitation pulse with alternating acquisition, different resonances were selectively excited with a different flip angle for increased PSNR while the hyperpolarized magnetization of the substrate can be minimally perturbed with a low flip angle. Baseline signals from neighboring resonances can be effectively suppressed to accurately quantify the metabolism kinetics.

• Preventive Nutrition and Food Science
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• 제11권3호
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• pp.210-217
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• 2006

This study was performed to investigate effects of the experimental mixture containing soybean peptides, L-carnitine and Garcinia Cambogia extract on body weight and lipid metabolism in rats. Male Sprague-Dawley rats (n=40) of eight weeks old were raised for four weeks with high fat diet (40% fat as calorie) to induce obesity. After induction of obesity, rats were feed control (C) diet, containing either 0.16% (+1D), 1.6% (+10D), 8% (+50D) of experimental mixture for eight weeks. Plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity and total protein and albumin concentration were not different among groups. The Body weight gain was significantly lower in experimental mixture diet group compared to control group. Weights of perirenal fat pad and epididymal fat pad in the +50D group were significantly lower than those in the +1D and +10D groups. Plasma total lipid and liver total cholesterol levels in the experimental groups were significantly lower than those in the control group. Fecal total lipid and total cholesterol excretions were highest in +50D group. These results suggest that the experimental mixture containing peptides, L-carnitine and Garsinia Canbogia extract is effective for reducing the body weight and adipose tissue weight which may be due to the modulation of lipid metabolism and the increased fecal excretion of lipid.

• Environmental Analysis Health and Toxicology
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• 제24권3호
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• pp.213-218
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• 2009

1-bromopropane (1-BP) has been used in numerous purposes such as an intermediate in the synthesis of pharmaceuticals, a solvent for fats, waxes, or resins and a substitute for chlorofluorocarbons that destroy the ozone layer. However, the studies related to the modulation of activities of hepatic cytochrome P450s (CYPs) are not reported yet. This study was the first study to investigate the potential effect for the activities of hepatic CYPs by the treatment of 1-BP in vivo. When 1-BP was treated to male ICR mice by dose-dependently at the dose levels of 200, 500 and 1,000 mg/kg of body weight once, the activity of CYP2E1 was selectively increased for 24 h. The inductive potency for the activity of CYP2E1 by 1-BP was equal to induction by acetone a well-known selective CYP2E1 inducer. The present results indicated that 1-BP would affect the metabolism of 1-BP itself and/or other xenobiotics.

• Nutrition Research and Practice
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• 제3권3호
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• pp.192-199
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• 2009

Cadmium intoxication has been associated with the dysregulation of iron homeostasis. In the present study, we investigated the effect of cadmium on the expression of ferroportin 1 (FPN1), an important iron transporter protein that is involved in iron release from macrophages. When we incubated cadmium with J774 mouse macrophage cells, FPN1 mRNA levels were significantly increased in a dose- and time-dependent manner. Furthermore, the cadmium-induced FPN1 mRNA expression was associated with increased levels of FPN1 protein. On the other hand, cadmium-mediated FPN1 mRNA induction in J774 cells was completely blocked when cells were co-treated with a transcription inhibitor, acitomycin D. Also, cadmium directly stimulated the activity of the FPN1-promoter driven luciferase reporter, suggesting that the cadmium up-regulates FPN1 gene expression in a transcription-dependent manner. Finally, cadmium exposure to J774 macrophages increased intracellular reactive oxygen species (ROS) levels by ${\sim}2$-fold, compared to untreated controls. When J774 cells were co-treated with antioxidant N-acetylcystein, the cadmium-induced FPN1 mRNA induction was significantly attenuated. In summary, the results of this study clearly demonstrated that cadmium increased FPN1 expression in macrophages through a mechanism that involves ROS production, and suggests another important interaction between iron and cadmium metabolism.

• Biomolecules & Therapeutics
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• 제22권5호
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• pp.384-389
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• 2014

Adiponectin, an adipokine predominantly secreted from adipose tissue, exhibits diverse biological responses, including metabolism of glucose and lipid, and apoptosis in cancer cells. Recently, adiponectin has been shown to modulate autophagy as well. While emerging evidence has demonstrated that autophagy plays a role in the modulation of proliferation and apoptosis of cancer cells, the role of autophagy in apoptosis of cancer cell caused by adiponectin has not been explored. In the present study, we demonstrated that globular adiponectin (gAcrp) induces both apoptosis and autophagy in human hepatoma cell line (HepG2 cells) and breast cancer cells (MCF-7), as evidenced by increase in caspase-3 activity, Bax, microtubule-associated protein light chain 3-II (LC3 II) protein levels, and autophagosome formation. Interestingly, gene silencing of LC3B, an autophagy marker, significantly enhanced gAcrp-induced apoptosis in both HepG2 and MCF-7 cell lines, whereas induction of autophagy by rapamycin, an mTOR inhibitor, significantly prevented gAcrp-induced apoptosis in hepatoma cells HepG2. Furthermore, modulation of autophagy produced similar effects on gAcrp-induced Bax expression in HepG2 cells. These results implicate that induction of autophagy plays a regulatory role in adiponectin-induced apoptosis of cancer cells, and thus inhibition of autophagy would be a novel promising target to enhance the efficiency of cancer cell apoptosis by adiponectin.