• 한국식품영양과학회지
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• 제23권2호
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• pp.187-191
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• 1994

The present stduy was undertaken to investigate the possible effect of Puffer fish skin extract (Pf) on the heptic acetaldehyde metabolism . It was obsrved that PF markedly decreased the acetaldehyde levels in blood and liver. The activity of mitochondrial aldehyde dehydrogenase (Ald DH) increased by induction of acute intoxicatiion of alcohol (5 g/kg) was further increased through pretreatment with PF for 2 weeks. When PF was given to rat fed with 25% alcohol solution instead of water for 6 weeks. the activity of Ald DH in mitochondrial fraction decreased to about 28% compared with sucrose-treated group. But after pretreatemnt of PF, the activity was restored to the normal level. By the treatment with disulfiram (300 mg/kg, once a day for 3days) was restored to the control after the pretreatment with PF. And also mitochondrial Ald DH activity in vitro was not changed. All these observations suggest that reduction of acetaldehyde levels are partly due to increase activity of mitochondrial Ald DH. Therefore, the recovery from intoxication of acetaldehyde may be enhanced by treatment with PF.

• Journal of Applied Biological Chemistry
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• 제66권
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• pp.159-164
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• 2023

Ferroptosis is a type of regulated cell death recently discovered, characterized by the accumulation of iron-dependent lipid peroxides in the cell membrane, and it involves a complex network of signaling pathways, including iron metabolism, lipid peroxidation, and redox regulation. The dysregulation of these pathways can lead to the induction of ferroptosis and the development of liver diseases, such as alcoholic liver disease, non-alcoholic fatty liver disease, viral hepatitis, and liver cancer. Studies have demonstrated that targeting key molecules involved in iron metabolism, lipid peroxidation, and redox regulation can reduce liver injury and improve liver function in different liver diseases by inhibiting ferroptosis. Thus, modulation of ferroptosis presents a promising therapeutic target for treating liver diseases. However, further research is required to gain a more comprehensive understanding of the mechanisms underlying the role of ferroptosis in liver diseases and to develop more effective and targeted treatments.

• Toxicological Research
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• 제3권1호
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• pp.1-8
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• 1987

In vitro induction of cytochrome 450 associated monooxygenase activities by phenobarbital (PB) and 3-methylcholanthrene (MC) was investigated in primary cultures of adult rat hepatocytes. PB and MC were added to the culture 24 hr after the initial plating of hepatocytes. A signiftcant increase of the activities of 7-ethoxycoumarin 0-deethylase and aryl hydrocarbon hydroxylase were observed in MC and PB treated culture. MC caused about 500% induction of the initial oxidation rates of both enzymes in 48 hr. However the PB maintained both enzyme activities close to the level of freshly isolated hepatocytes. Biphenyl 4-hydroxylase and aminopyrine N-demethylase activities were also induced by MC and PB. But the level of induction was less than that occuring with 7-ethoxycoumarin 0-deethylase and aryl hydrocarbon hydroxylase. When aflatoxin $B_1$ was added to the hepatocyte cultures which have been treated with MC or PB, it caused a significant increase of the unscheduled DNA synthesis at higher dose of aflatoxin $B_1$ as compared to those of untreated control hepatocyte cultures. The results suggest that microsomal enzyme activities can be selectively controlled preferably in hepatocyte cultures by the in vitro induction method. This principle may be useful for studying the metabolism and other toxicological studies.

• Asian Pacific Journal of Cancer Prevention
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• 제15권1호
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• pp.495-499
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• 2014

Estrogens are considered the major breast cancer risk factor, and the carcinogenic potential of estrogens might be attributed to DNA modification caused by derivatives formed during metabolism. $17{\beta}$-estradiol ($E_2$), the main steroidal estrogen present in women, is metabolized via two major pathways: formation of 2-hydroxyestradiol (2-OH $E_2$) and 4-hydroxyestradiol ($4-OH\;E_2$) through the action of cytochrome P450 (CYP) 1A1 and 1B1, respectively. Previous reports suggested that $2-OH\;E_2$ has putative protective effects, while $4-OH\;E_2$ is genotoxic and has potent carcinogenic activity. Thus, the ratio of $2-OH\;E_2/4-OH\;E_2$ is a critical determinant of the toxicity of $E_2$ in mammary cells. In the present study, we investigated the effects of berberine on the expression profile of the estrogen metabolizing enzymes CYP1A1 and CYP1B1 in breast cancer MCF-7 cells. Berberine treatment produced significant induction of both forms at the level of mRNA expression, but with increased doses produced 16~ to 52~fold greater induction of CYP1A1 mRNA over CYP1B1 mRNA. Furthermore, berberine dramatically increased CYP1A1 protein levels but did not influence CYP1B1 protein levels in MCF-7 cells. In conclusion, we present the first report to show that berberine may provide protection against breast cancer by altering the ratio of CYP1A1/CYP1B1, could redirect $E_2$ metabolism in a more protective pathway in breast cancer MCF-7 cells.

• 대한본초학회지
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• 제21권1호
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• pp.63-69
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• 2006

Objectives : This study was designed to investigate the effects of Cervi Pantotrichum Cornu and Cervi Cornu on the growth of longitudinal bone in the adolescent male rats. Methods : Longitudinal bone growth was measured by fluorescence microscopy. To examine the effects on the growth plate metabolism, the heights of growth plate and the induction of local bone morphogenetic protein-2 were measured. Results : Treatment of Cervi Pantotrichum Cornu significantly enhanced longitudinal bone growth compared with control group. However, Cervi Cornu did not show the significant effects. Conclusion : Cervi Pantotrichum Cornu enhanced longitudinal bone growth and promoted the induction of local bone morphogenetic protein-2 of growth plate in adolescence male rats.

• 한국환경성돌연변이발암원학회지
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• 제24권3호
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• pp.143-150
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• 2004

In mammalian, cytochrome P4501A1 (CYP1A1) is very important for metabolism of xenobiotics such as PAHs(Polycyclic aromatic hydrocarbon) and heterocyclic amine, and it is induced by environmental contaminants such as PAHs, TCDD(2,3,7,8-tetrchlorodibenzo-p-dioxin) and 3-MC (3-methylcholanthrene). In fish, like mammalian, when it is exposed to environmental contaminants, they cause specific and sensitive induction of CYP1A. Therefore, induction of CYP1A in fish and mammalian is widely used as a biomarker for exposure of environmental contaminants. In this study, to compare the function of Cyp1a1 in fish with it in mammalian, we have used rainbow trout(Oncorhynchys mykiss) hepatoma cells (RTH-149) and mouse hepatocyte (Hepa-I). in order to examine induction of Cyp1a1 by TCDD, we have used the bioassay system. We examined effects of TCDD on the Cyp1a1-luciferase reporter gene activity, 7-ethoxyresorufin O-deethylase(EROD) activity and Cypa mRNA level.

• 고려인삼학회:학술대회논문집
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• 고려인삼학회 1998년도 Advances in Ginseng Research - Proceedings of the 7th International Symposium on Ginseng -
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• pp.63-70
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• 1998

Superoxide dismutase (SOD) and catalase constitute the first coordinated unit of defense against reactive oxygen species. Here, we examined the effect of ginseng saponins on the induction of SOD and catalase gene expression. To explore this possibility, the upstream regulatory promoter region of Cu/Zn superoxide dismutase (SODI) and catalase genes were linked to the chloramphenicol acetyl-transferase (CATI structural gene and introduced into human hepatoma HepG2 cells. Total saponin and panaxatriol did not activate the transcription of SODI and catalase genes but panaxadiol increased the transcription of these genes about 2-3 fold. Among the Panaxadiol ginsenosides, the Rb2 subtraction appeared to is a major induce of SODI and catalase genes. Using the deletion analyses and mobility shift assays, we showed that the 5051 gene was greatly activated by ginsenoside Rba through transcription factor AP2 binding sites and its induction. We also examined the effect of the content ratio of panaxadiol extracted from various compartment of ginseng on the transcription of 5031 gene. Saponin extract that contains 2.6-fold more PD than PT from the fine root Increased the SODI induction about 3-fold. These results suggest that the panaxadiol fraction and its ginsenosides could induce the antioxidant enzymes, which are important for maintaining cell viability by lowering level of oxygen radical generated from intracellular metabolism.

• 한국환경성돌연변이발암원학회지
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• 제24권4호
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• pp.155-162
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• 2004

In mammalian, cytochrome P4501A1 (CYP1A1) is very important for metabolism of xenobiotics such as PAHs(Polycyclic aromatic hydrocarbon) and heterocyclic amine, and it is induced by environmental contaminants such as PAHs, TCDD(2,3,7,8-tetrchlorodibenzo-p-dioxin) and 3-MC (3-methylcholanthrene). In fish, like mammalian, when it is exposed to environmental contaminants, they cause specific and sensitive induction of CYP1A. Therefore, induction of CYP1A in fish and mammalian is widely used as a biomarker for exposure of environmental contaminants. In this study, to compare the function of Cyp1a1 in fish with it in mammalian, we have used rainbow trout(Oncorhynchys mykiss) hepatoma cells (RTH-149) and mouse hepatocyte (Hepa-I). in order to examine induction of Cyp1a1 by TCDD, we have used the bioassay system. We examined effects of TCDD on the Cyp1a1-luciferase reporter gene activity, 7-ethoxyresorufin O-deethylase(EROD) activity and Cypa mRNA level.

• BMB Reports
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• 제56권12호
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• pp.651-656
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• 2023

Senescence, a cellular process through which damaged or dysfunctional cells suppress the cell cycle, contributes to aging or age-related functional decline. Cell metabolism has been closely correlated with aging processes, and it has been widely recognized that metabolic changes underlie the cellular alterations that occur with aging. Here, we report that fatty acid oxidation (FAO) serves as a critical regulator of cellular senescence and uncover the underlying mechanism by which FAO inhibition induces senescence. Pharmacological or genetic ablation of FAO results in a p53-dependent induction of cellular senescence in human fibroblasts, whereas enhancing FAO suppresses replicative senescence. We found that FAO inhibition promotes cellular senescence through acetyl-CoA, independent of energy depletion. Mechanistically, increased formation of autophagosomes following FAO inhibition leads to a reduction in SIRT1 protein levels, thereby contributing to senescence induction. Finally, we found that inhibition of autophagy or enforced expression of SIRT1 can rescue the induction of senescence as a result of FAO inhibition. Collectively, our study reveals a distinctive role for the FAO-autophagy-SIRT1 axis in the regulation of cellular senescence.

• 한국생명과학회:학술대회논문집
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• 한국생명과학회 2007년도 제48회 학술심포지움 및 추계국제학술대회
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• pp.90.2-90.2
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• 2007

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