• The Korean Journal of Zoology
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• v.26 no.4
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• pp.283-294
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• 1983

In order to study the change of protein synthesis in developing chick embryo under the influence of carcinogenic substances, we introduced a kind of potent carcinogen, 4-nitroquinoline-1-oxide (4 NQO) to the yolk sac of developing chick embryo. There are changes of synthetic pattern of protein abreast with proceeding of development is each tissue. Protein synthesis in samples which was treated with 4NQO was decreased as compared with untreated control samples. There are tissue specificity in 4NQO effect, showing the apparent decreasing at the 24 hr after drug treatment in the lung and gizzard muscle but not in heart muscle. The results in the present study suggested that 4NQO treated samples was decreased as compared with control samples. From the above data we could know that 4NQO also affected the synthesis of glycosaminoglycan.

• Journal of Food Hygiene and Safety
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• v.24 no.1
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• pp.46-49
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• 2009

The desmutagenic activity of the water extract of Cassia tara L on the mutagenicity induced by 4-nitroquinoline 1-oxide (4-NQO) and N-methyl-N-nitro-N'-nitrosoguani-dine (MNNG) was studied using the SOS Chromotest with Escherichia coli PQ37. The inhibition rates of water extract of Cassia tara L. at concentration of $100{\mu}g$/assay were 27.5% and 40% against 4-NQO and MNNG. The water extract of Cassia tara L. 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 4-NQO and MNNG. Step-wise fractionation of methanol soluble part was done to obtain methanol, ethyl acetate and water fractions. Among these fractions, water fraction had the strongest inhibitory effects of 23.0 and 19.0% against mutagenicities of MNNG and 4NQO, respectively. The results clearly indicated that the water fraction showed much stronger antimutagenicity against MNNG than 4NQO. The inhibition rates of aqueous fraction of methanol-soluble from water extracted Cassia tara L. at concentrations of 1.0, 10, 100 and $250{\mu}g$/assay were 8.0%, 12.0%, 25.5% and 43.0%, respectively. The water fraction showed the inhibitory effects with dose response against the mutagenic activities induced by MNNG.

• KSBB Journal
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• v.16 no.5
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• pp.486-492
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• 2001

The antimutagenic mechanism of the fraction III(RG III)separated from the water extract of Rehmannia glutionosa was investigated by Escherichia. coli GW and B/r strains. RG-III treatment did not affect the ${\beta}$-galactosidase activity E. coli GW-1060, 1106, 1107 and 1105. These results indicated that RG-III did not induce RecA protein amplification and did not also prevent the proteolytic cleavage of LexA. The bio-antimutagenicity and survival effect of RG-III on 4-nitroquinoline 1-oxide(4NQO), N-methyl-N-nitor-N\`-nitrosoguanidine(MNING) were investigate by E. coli B/r strains with have different pathway of DNA repai. RG-III slightly increased the survival of 4NQO-treated WP2, WP2s, WP67, CM561, CM611 cells, but the reactivation of survival cannot ve explained by the repair mode. RG-III caused the decrease of mutagenicity and lethality treated with MNNG in ZA159 despite of the increase in WP2, WP2s, WP67, CW561, CM611. Compared with bio-antimutagenic effects of RG-III on 4NQO, greatly increased antimutagenic effects of RG-III were observed with all the E. coli B/r strains tested, but less active in ZA159. These results suggest that RG-III was identified as a blocking agent for preventing the 4NQO induced mutagenesis, and may act as chl-products.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.4107-4112
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• 2012

4-Nitroquinoline 1-oxide (4-NQO) a potent oral carcinogen, widely used for induction of oral carcinogenesis, has been found to induce lipid peroxidation in vivo and in vitro. Green tea contains a high content of polyphenols, which are potent antioxidants. Thus green tea polyphenols (GTP) might be expected play a protective role against 4-NQO induced lipid peroxidation and bone marrow toxicity. In the present study, a dose of 200 mg of GTP/kg b.wt/day was given orally for a week, simultaneously animals received 0.2 ml of 0.5% 4-NQO in propylene glycol (5 mg/ml) injected intramuscularly for three times/week. Oxidants and antioxidants such as malendialdehyde (MDA) and thiols, glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT) were significantly decreased in 4-NQO induced animals except MDA, and these parameters were brought back to near normalcy on treatment with GTP. The results suggest that GTP treatment offers significant protection against 4-NQO induced lipid peroxidation and bone marrow toxicity and might be a promising potential candidate for prevention of mutations leading to cancer.

• Korean journal of food and cookery science
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• v.16 no.5
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• pp.390-393
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• 2000

Desmutagenic effects of water-soluble and ethanol-soluble extracts of dried green tea toward the mutagenicity of 4-nitroquinoline-N-oxide(4-NQO) and 3-Amino-1,4-dimethyl-5H-pyrido［4,3-b］indole(Trp-P-1) in streptomycin-dependent SD510 strains of Salmonella typhimurium TA98 were investigated. Inhibition effects toward the mutagenicity of 4-NQO and Trp-P-1 of water-soluble and ethanol-soluble extracts from green tea were high as increase of concentration of extracts. Desmutagenic effects toward 4-NQO of water-soluble and ethanol-soluble extracts from green tea harvested in May and August were up to 93% in 1,000 $\mu\textrm{g}$ of extract/plate. Desmutagenic effects toward Trp-P-1 of ethanol-soluble extracts from green tea were 53.3∼92.1%, but the effects of water-soluble extracts decreased as increase of concentration of extracts.

• Korean Journal of Food Science and Technology
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• v.28 no.4
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• pp.796-799
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• 1996

The antimutagenic properties of twenty-one strains of Bifidobacterium were examined using Salmonella typhimurium TA98 in an in vitro assay system. The mutagens utilized for testing included Trp-P-1 (3-amino-1, 4-dimethyl-$^{5}H-pyrido$ (4, 3-b) indole), benzopyrene, IQ (2-amino -3-methylimidazo [4,5-f] quinoline), and NQO. The lyophilized cells of strain showed inhibitory effect of 64, 38, 29 and 20% in average against Trp-P-1, benzopyrene, NQO and IQ, respectively. There was no marked variation between each strain or growth stage in the degree of antimutagenicity against Trp-P-1, benzopyrene and IQ. Twelve hour grown cells showed higher antimutagenicity against NQO than 5-day grown cells. The results indicate that Bifidobacterium cells had a antimutagenic effect against several well-known mutagens to some degree.

• Journal of Microbiology and Biotechnology
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• v.31 no.6
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• pp.794-802
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• 2021

In this study we investigated the role and mechanism of cardamonin on IL-1β induced injury in OA. CHON-001 cells were treated with cardamonin and IL-1β and transfected with silencing nuclear factor erythroid 2-related factor 2 (siNrf2). Cell viability was detected by Cell Counting Kit-8 assay and flow cytometer assay was utilized for cell apoptosis assessment. IL-6, IL-8, TNF-α and Nrf2 mRNA expression was tested by qRT-PCR. Western blot was employed to evaluate MMP-3, MMP-13, Collagen II, Nrf2, NQO-1, NLRP3, Caspase 1 and apoptosis-associated speck-like protein containing a caspase-1 recruitment domain (ASC) protein levels. In CHON-001 cells, IL-1β suppressed cell viability and Collagen II level while promoting cell apoptosis and expression of pro-inflammatory cytokines (IL-6, IL-8, TNF-α), MMPs (MMP-3, MMP-13), NQO-1, and NLRP3 inflammasome (NLRP3, Caspase 1 and ASC), with no significant influence on Nrf2. Cardamonin reversed the effect of IL-1β on cell viability, cell apoptosis, pro-inflammatory cytokines, MMPs, Collagen II, and NLRP3 inflammasome levels. In addition, cardamonin advanced Nrf2 and NQO-1 expression of CHON-001 cells. SiNrf2 reversed the function of cardamonin on IL-1β-induced cell apoptosis and expression of pro-inflammatory cytokines, Nrf2, NQO-1, and NLRP3 inflammasome in chondrocytes. Taken together Cardamonin inhibited IL-1β induced injury by inhibition of NLRP3 inflammasome via activating Nrf2/NQO1 signaling pathway in chondrocyte.

• Oncology Letters
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• v.42 no.4
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• pp.1621-1630
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• 2019

One million females are diagnosed worldwide every year with breast cancer, and the mortality rate of these patients remains high. Several treatments, including surgery, are available for breast cancer. β-Lapachone (β-Lap), a natural quinone compound, has been developed for cancer treatment due to its strong cytotoxic effect through its action on NAD(P)H:quinone oxidoreductase 1 (NQO1)-dependent activity. However, the mechanism in regards to how β-Lap induces cytotoxicity in breast cancer cells is still elusive. In the present study, we showed that β-Lap induced apoptotic cell death via activation of protein kinase A (PKA) in NQO1-overexpressing MDA-MB-231 human breast cancer cells. This PKA-dependent cell death was observed solely in NQO1-overexpressing 231 cells via the high production of reactive oxygen species (ROS). Cell survival of antioxidant [N-acetylcysteine (NAC)]-treated NQO1-overexpressing 231 cells was significantly recovered, and NQO1-negative 231 cells did not respond to β-Lap. Antiapoptotic proteins such as Bcl2 and Bcl-xL were decreased, while proapoptotic proteins, including cytochrome c, activation of caspase-3, and cleavage of PARP were increased after β-Lap treatment of NQO1-overexpressing 231 cells. Furthermore, PKA activators, forskolin or dibutyryl-cAMP, an analog of cAMP, aggravated the β-Lap-induced apoptotic cell death by decreasing antiapoptotic proteins and further activating proapoptotic proteins in NQO1-positive 231 cells. Treatment with a PKA inhibiter, H89, significantly increased cell viability even in NQO1-overexpressing cells treated with β-Lap. These data showed that β-Lap activated PKA via ROS accumulation, subsequently leading to apoptotic cell death in NQO1-positive breast cancer cells.

• Environmental Mutagens and Carcinogens
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• v.19 no.2
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• pp.112-115
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• 1999

The action mechanism of the inhibitory effect of some natural products on the DNA strand break and DNA damage was investigated in vitro and in vivo. In the E. coli chromosomal DNA strand break experiment in vitro, three mushroom water extracts were effective on the DNA strand breaking by daunorubicin. Phellinus linteus water extract inactivated daunorubicin, a DNA strand breaking agent, but did not protect DNA from daunorubicin-induced DNA strand breaking. Agaricus blazei water extract inhibited DNA strand breaking action of daunorubicin not only by daunorubicin inactivation, but also by DNA protection from daunorubicin. An inhibitory effect of Ganoderma lucidum water extract on the DNA strand break was based on the DNA protection rather than daunorubicin inactivation. In vivo mutagen assay system (SOS-chromotest), among three mushroom water extracts Phellinus linteus water extract was the most effective one on the inhibition of DNA damage by 4-NQO. The results suggest that all three mushroom water extracts inhibit daunorubicin-induced DNA damage and in vivo DNA damaging action of 4-NQO by the reaction of mutagen inactivation or DNA protection from the mutagen.

• Archives of Pharmacal Research
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• v.24 no.5
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• pp.390-396
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• 2001

Synthesized 6-arylamino-5,8-quinolinediones 4a-4j and 6-chloro-7-arylamino-5,8-isoquinolinediones 5a-5g were evaluated for effects on NAD(P)H quinone oxidoreductase (NQOl ) activity with the cytosolic fractions derived from cultured human lung cancer cells and their cytotoxicity in cultured several human solid cancer cell lines. The 5,8-quinolinediones 4 and 5,8-isoquinolinediones 5 affected the reduction potential by NQO1 activity and showed a potent cytotoxic activity against human cancer cell lines. The tested compounds 4a, 5c, 5f, and 5g were considered as more potent cytotoxic agents. The compounds 4d, 5b, 5c, 5e and 5g were comparable modulators of NQO1 activity.