• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.2
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• pp.175-180
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• 1993

The methanol extracts of perilla leaves reduced the mutagenicities mediated by of aflatoxin B$_1$(AFB$_1$), 3-amino-l-methyl-5H-pyrido (4,3-b) indole (Trp-P-2) and Benzo(a)pyrene (B(a)p) in Salmonella typhimurium TA98 and TA100. The methanol extracts were more fractionated, and the fractions of hexane and butanol revealed the antimutagenic activities against AFB$_1$ and B(a)p. The production of malondialdehyde (MDA) was decreased when the methanol extracts of perilla leaves were added to the system. The significantly higher antioxidative activity was observed in the butanol fraction. 2-Propyl furan, ethanedioic acid, dibutyl ester, benzaldehyde, 2-methyl-2-ethyl-3-hydroxy-propanoic acid and octahydro-3a-methyl-2H-inden-2-one were identified tentatively as major compounds from the butanol fraction.

• Development and Reproduction
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• v.16 no.4
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• pp.289-294
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• 2012

Gene expressions of cytochrome P4501A (CYP1A), aryl hydrocarbon receptor (AhR) and vitellogenin (Vg) by endocrine disruptors, benzo[${\alpha}$]pyrene (B[a]P) and tributyltin (TBT) were examined in cultured eel hepatocytes which were isolated from eels treated previously with B[a]P (10 mg/kg) or estradiol-$17{\beta}$ (20 mg/kg) in vivo, and the relationship between CYP1A, AhR and Vg genes were studied. When the cultured eel hepatocytes were treated with B[a]P ($10^{-6}-10^{-5}M$) the gene expressions of CYP1A and AhR were enhanced in a concentration-dependent manner. However, when treated with TBT ($10^{-9}-10^{-5}M$) the gene expressions of CYP1A and AhR were suppressed at high concentrations ($10^{-6}-10^{-5}M$), while having no effects at low concentrations ($10^{-9}-10^{-7}M$). Gene expression of Vg was also suppressed by TBT in a concentration-dependent manner in cultured eel hepatocytes which was previously treated in vivo with estradiol-$17{\beta}$.

• Journal of Ginseng Research
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• v.13 no.1
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• pp.42-48
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• 1989

The binding of bay region diol-epoxides of polycyclic aromatic hydrocarbons (PAHs) to target tissue DNA is thought to be essential for the initiation of cancer by these compounds. In this study we investigated the effect of polyacetylenes such as panaxynol and panaxydol on the formation of benzo(a)pyreno (BP)-metabolite-DNA adduct in the liver of ICR mice. Treatment of mice by i.p. administration of polyacetylenes produced a marked reduction in BP metabolite binding to DNA in vitro. Following i.v. administration of (3H)BP(300, ${\mu}$Ci/21 nmoles/0.1 nt DMSO) to mice, radioactivity was detected in the DNA of the liver in vivo. The result of tentative identification of the 4 peaks between the two standard markers for high pressure liquid chromatography showed that the peaks. I, II, III, and IV were BP-phenol oxide-DNA adduct (or BP-diol-epoxide-dCyt. adduct), (-) BP$.$diolepoxide I:dGuO adduct, (+) BP-diol-epoxide I: dGuo adduct, and BP-diol-epoxide II:dGuO adduct, respectively. The minor adduct, (-) BP-diol epoxide I: dGuo was reduced to 6971 of the amount of the control, while the major adduct, (+) BP-diolepoxide I: dGuO(peak II) which was produced from (-) BP-7, 8-diol was reduced to 78% of that of the control. The amount of the minor adduct, BP-diol-epoxide II:dGuo adduct(peak IV) which formed from (+) BP-7, 8-diol was 58% of the control. These results show that the panaxydol is more related to inhibition of the formation of the minor ad- ducts than of the major adducts, which were generally produced from ($\pm$) BP-7, 8-dihydro-dials.

• Environmental Mutagens and Carcinogens
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• v.19 no.2
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• pp.108-111
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• 1999

Correlation between the tumorigenic dose (TD) and the maximum tolerated dose (MTD) was examined to search for the most relevant TD values related to the MTD. Using benzo(a)pyrene (B(a)P) 2-yr bioassay data, correlation coefficients between values of $TD_{1-}$50/ and the MTD were estimated from linearized or non-linearlized dose-response curves. The highest correlation coefficients (0.9966-1.0000) were obtained from T $D_{1-}$10/ in linearized dose-response curves while the highest (0.9966-1.0000) were estimated from $TD _{5-}$10/ in non-linearized dose-response eurves. These data suggest that TDs-lo were more closely related to the MTD than the ,$TD_{5-}$10/ in B(a)P 2-yr bioassay and that in lieu of the $TD_{50}$ they could be efficiently applicable to risk assessment and management.ent.

• Preventive Nutrition and Food Science
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• v.2 no.2
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• pp.96-100
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• 1997

Carcinogenicity of di(2-ethylhexyl)phthalate(DEHP) to the mose forestomach and its inhibitor activity for the initiation of Benzo[a]pyrene(BP)-induced mouse forestomach neoplasia were studied on the mouse forestomach carcinogenesis regimen. One hundred female ICR mice(6~7 weeks of age) were hosed in a poly-carbonate cage (4 mice/cage) in a humidity- and temperature-controlled room subjected to a semipurified diet for a week. Mice were divided into 4 treatment groups (25 mice/treatment): Basal diet, DEHP, BP, and BP+DEHP. On Monday and wednesday, 0.1ML DEHP mixed with 0.1ml olive oil (for DEHP and DEHP+BP treatment groups) or 0.1ml saline+0.1ml olive oil (for basal diet group) was intubated, p.o., and on Friday, 2mg BP dissolved in 0.2ml olive oil (for BP and BP+DEHP treatment groups) was intubated, p.o. This cycle was repeated for 4 weeks. Beginning with the first intubation of BP an continuing thereafter, body weight and food intake were recorded once and twice weekly, respectively. All surviving mice were sacrificed 22 weeks after the first dose of BP intubation and countered forestomach tumor. No tumor was formed by DEHP treatment. 5.75 tumors per mouse was formed by BP treatment, whereas its number was reduced to 4.53 by BP+DEHP treatment. Similar results were seen in the tumor incidence. Body weight gain was not affected by DEHP treatment, when compared to that b basal diet treatment. The body weight was significantly reduced by BP treatment, but its reduction was recovered to the level of the basal diet group by BP+DEHP treatment. No significant difference was seen in food intake among all treatment groups. These results indicate that DEHP lacks carcinogenic activity to the mose forestomach and rather inhibits the initiation of BP-induced mose forestomach neoplasia.

• Korean Journal of Food Science and Technology
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• v.30 no.2
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• pp.439-445
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• 1998

The antimutagenic activity of the water extract of Rehmannia glutinosa Liboschitz (RG) on the mutagenicity induced by 4-nitroquinoline 1-oxide (4-NQO), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), mitomycin C (MMC), $aflatoxin\;B_1\;(AFB_1)$ and benzo(a)pyrene [B(a)P] were studied using the SOS Chromotest with Escherichia coli PQ37. The water extract of RG was separated into methanol soluble and methanol insoluble parts. The methanol soluble part exhibited higher inhibition effects than the methanol insoluble part against the mutagenic activities of five mutagens. Step-wise fractionation of methanol soluble part was done using methanol, ethyl acetate and water. Among these fractions, water fraction had the strongest inhibitory effects against the mutagenenicity of five model mutagens, showing $4.5{\sim}29.5%$ inhibition, but the $AFB_1$ mutagenic potency was increased slightly by ethyl acetate fraction. The water fraction was further partitioned by sephadex LH-20 column chromtography, and 9 subfractions were obtained. The fraction III showed the strongest inhibitory effects with dose response against the mutagenic activities induced by all the tested chemical mutagens. The inhibition rates of fraction III at concentration of $400\;{\mu}g/assay$ were 29%, 35%, 38%, 25% and 24% against 4-NQO, MNNG, MMC, AFBl and B(a)P, respectively. The fraction III also exhibited a strong bio-an-timutagenicity against 4-NQO and $AFB_1$ by showing more than 40% inhibition.

• Journal of the Korean Society of Food Science and Nutrition
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• v.29 no.2
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• pp.322-328
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• 2000

This study was performed to determine the antimutagenic and cytotoxic effect of the Phellinus linteus methanol extract on Salmonella typhimurium TA98, TA100 and human cancer cell lines. In the Ames test, methanol extract of P. linteus alone did not exhibit any mutagenicity but showed substantial inhibitory effects against mutation induced by N-methyl-N'-nitro-N-nitrosoguanidine(MNNG), 4-nitroquinoline-nitroquinoline-1-oxide(4NQO), 3-amino-1,4-dimethyl-5H-pyrdo[4,3-blindol(Trp-P-1) and benzo(α)pyrene(B(α)P). The methanol extracts of P. linteus(200㎍/plate) showed approximately 78.3%, 78.7% and 88.1% inhibitory effect on the mutagenesis induced by 4NQO, Trp-P-1 and B(α)P. The anticancer effects of P. linteus extract against human breast adenocarcinoma(MCF7), human lung carcinoma (A549), human fibrosarcoma (HT1080), human hepatocelular carcinoma (Hep3B) and human epitheloid carcinoma (HeLa) were investigated. The treatment of 1mg/mL P. linteus extracts had the highest cytotoxicity against MCF7 (92.0%), followed by Hep3B (84.9%), A549 (84.2%) and HT1080 (82.9%). In contrast 1mg/mL treatment of P. linteus extracts had only 10∼40% cytotoxicity on normal human liver cell (WRL68).

• Korean Journal of Acupuncture
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• v.18 no.1
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• pp.11-20
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• 2001

Cancer chemoprevention refer to the use of natural or synthetic substances to prevent the initiational and promtional events that occur during the process of carcinogenesis. The effect of Prunella Herba Vulgaris L. Aqua-acupuncture Solution (PVAS) and Prunella Herba Vulgaris L. Water-extracted Solution (PVWS) on the induction of phase II detoxification enzyme (quinone reductase, Glutathione S-transferase) and inhibition of phase I enzyme (cytochrome P4501A1) and benzo[a]pyrene-DNA adduct formation was examined. PVAS is potent inducers of quinone reductase activity. Glutathione levels were increased with PVAS, in cultured murine hepatoma Hepa1c1c7 cells. In addition glutathione S-transferase levels were increased with PVAS. However, there was 45.2% inhibition in the activity of cytochrome P4501A1 enzyme with the treatment of PVAS, $5{\times}$. At concentration of $1{\times}$ and $3{\times}$ of PVAS, the binding of $[^3H]B[a]P$ metabolites to DNA of NCTC-clone 1469 cell was inhibited by 25.3%, 45.0%, respectively. These results suggest that PVAS has chemopreventive potential by inducing quinone reductase and glutathione S-transferase activities, increasing GSH levels, inhibiting the activity of cytochrome P4501A1 and benzo[a]pyrene-DNA adduct formation.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.11
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• pp.1371-1376
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• 2007

The effect of Hovenia dulcis Thumb leaves on the mutagenicity in salmonella assay and inhibitory effects on the growth of cancer cells were studied. On antimutagenicity as evaluated by Ames test, the extract and fractions of Hovenia dulcis Thumb leaves had no effect on the mutagenicity by themselves. However, methanol extract and fractions from Hovenia dulcis Thumb showed strong inhibitory effect on the mutagenesis induced by N-methyl-N#-nitro-N-nitroso-guanidine (MNNG) and benzo(a)pyrene (B(a)P). Among the solvent fractions of methanol extract, the hexane, chloroform and butanol fraction exhibited stronger inhibitory activity against MNNG and B(a)P induced mutagenesis than water fraction. For anticancer effects, Hovenia dulcis Thumb loaves extract and fractions against cancer cell lines including HepG2 and HT29 were investigated. The methanol extract, the hexane fraction and the chloroform fraction of Hovenia dulcis Thumb leaves inhibited growth of cancer cells but they had no effect on the cytotoxicity of normal human liver cells under the same conditions.

• Toxicological Research
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• v.4 no.2
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• pp.131-142
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• 1988

The post-mitochondrial liver fractions (S-9) were prepared from rats and hamsters which have been treated with Aroclor 1254 (PCB) and the capacities of these S-9 fractions to generate mutagenic metabolites from several well known procarcinogens have been compared. Benzo(a)pyrene (B(a)P), 3-methylcholanthrene (3-MC), Aflatoxin B1(AFB1), 2-acetylamino-fluorene(AAF), and 2-aminofluorene (AF) were employed as promutagens in the Salmonella reverse mutation tests. Results showed that the rat and hamster S-9 fractions had differential abilities to produce mutagenic metabolites from a given promutagen.