• Title/Summary/Keyword: Genotoxic

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Mutation Spectrum of 1, 2-Dibromo-3-chloropropane, an Endocrine Disruptor, in the lacI Transgenic Big $\textrm{Blue}^{(R)}$ Rat2 Fibroblast Cell Line.

  • Kim, Youn-Jung;Chai, Young-Gyu;Lee, Kilchul;Kyounghee Oh;Ryu, Jae-Chun
    • Proceedings of the Korea Society of Environmental Toocicology Conference
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    • 2001.05a
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    • pp.129-129
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    • 2001
  • 1,2-Dibromo-3-chloropropane (DBCP), a soil fumigant against nematodes, is a genotoxic carcinogen and also is classified by World Wildlife Fund as endocrine disruptors. DBCP has been extensively studied on genotoxicity, carcinogenicity, and damage in male reproductive-related organs. However, information on precise mechanism of mutagenesis and carcinogenesis of DBCP is yet unknown. (omitted)

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Evaluation of Genotoxicity on Plant-Derived Dietary Sulfur

  • Lee Yoon-Ik;Lee Young-Seok;Park Jong-Cheol;Lee Kwan-Bok;You Kwan-Hee
    • Journal of Microbiology and Biotechnology
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    • v.16 no.5
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    • pp.817-820
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    • 2006
  • The potential genotoxicity of methylsulfonylmethane, a crystalline organic sulfur, derived from chemically modified lignin from plants was evaluated using in vitro and in vivo assays. In the bacterial reverse mutation test using Salmonella typhimurium TA98, TA100, TA1535, and TA1538, methylsulfonylmethane did not induce any significant increase of His' revertants. In the in vitro chromosome aberration test using Chinese Hamster Lung (CHL) cells, no aberration effects were seen. In the in vivo evaluation using a micronucleus test, negative results were obtained. Accordingly, the results indicated that methylsulfonylmethane is not genotoxic and its use is unlikely to present a potential hazard.

Nickel Toxicity and Carcinogenicity (니켈의 독성과 발암성)

  • Park Hyoung-Sook;Park Kwangsik
    • Environmental Analysis Health and Toxicology
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    • v.19 no.2
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    • pp.119-134
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    • 2004
  • Human exposure to highly nickel-polluted environments, such as those associated with nickel refining, electroplating, and welding, has the potential to produce a variety of pathologic effects. Among them are skin allergies, lung fibrosis, and cancer of the respiratory tract. The exact mechanisms of nickel-induced carcinogenesis are not known and have been the subject of numerous epidemiologic and experimental investigations. This review provides the evidence of the current state for the genotoxic and mutagenic activity of Ni (II) particularly at high doses. Such doses are best delivered into the cells by phagocytosis of sparingly soluble nickel-containing dust particles. Ni (II) genotoxicity may be aggravated through the generation of DNA-damaging reactive oxygen species (ROS) and the inhibition of DNA repair by this metal. The epigenetic effects of nickel includes alteration in gene expression resulting from DNA hypermethylation and histone hypoacetylation, as well as activation some signaling pathways and subsequent transcrziption factors.

Hygienic Quality and Genotoxicological Safety of Gamma Irradiated Pork (감마선조사에 의한 돈육의 위생화 및 유전독성학적 안전성 평가)

  • 강일준;윤정한;강영희;이효구;변명우
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.28 no.5
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    • pp.1092-1098
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    • 1999
  • Gamma irradiation was applied to pork for improving its hygienic quality and evaluating its possible genotoxicity. The effective dose of irradiation was 3 kGy in pork for the sterilization of all contaminated microorganisms tested. After 8 weeks of storage at 5oC, no growth of microorganisms except for psychrophile and total aerobic bacteria was observed in the more than 3 kGy irradiated pork. The genotoxicity of high dose irradiated pork(30 kGy) was evaluated by Salmonella typhimurium reversion assay, chromosomal aberration test and in vivo micronucleus assay. The results were negative in the bacterial reversion assay with S. typhimurium TA98, TA100, TA1535, TA1537. In chromosomal aberration tests with CHL cells and in vivo mouse micronucleus assay, no significant difference in the incidences of chromosomal aberration and micronuclei was seen between nonirradiated and 30 kGy irradiated porks. These results indicate that 30 kGy irradiated pork did not show any genotoxic effects under these experimental conditions.

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Genotoxicity of Capsaicin in Cultured Human Lymphocytes

  • Lee, Sang-Sup;Park, Young-Ho;Sohn, Yeowon;Ryu, Soo-Jung;Surh, Young-Joon
    • Environmental Mutagens and Carcinogens
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    • v.15 no.2
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    • pp.81-87
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    • 1995
  • The clastogenic activity of capsaicin, a major pungent and irritating constituent of hot chili pepper, was evaluated in cultured human lymphocytes. Capsaicin (125, 250, and 500 $\mu$M) caused cytogenetic damage as determined by increased frequency of chromosome/chromatid aberrations compared to the solvent control. The mitotic indices were also decreased in a concentration-related manner in capsaicin-treated cells. Moreover, capsaicin suppressed [$^3$]thymidine incorporation into lymphocytes. The clastogenicity and cytotoxicity of capsaicin towards human lymphocytes were evident without an external metabolic activation system. Taken together, these findings suggest that capsaicin is a genotoxic agent and may thus represent a potential health hazard in humans.

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Photocleavage of DNA by 4′-Bromoacetophenone- Pyrrole Carboxamides

  • Jeon, Raok
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2001.11a
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    • pp.79-79
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    • 2001
  • Genotoxic chemotherapeutics are irreversible DNA targeting agents, which can act as anticancer and antiviral drugs. Natural antibacterial and anticancer enediynes function through the formation of free radicals formed by Bergman-type cycloaromatization and being capable of cleavage of DNA strand. They have been focused primarily on the design and syntheses of simple enediyne structures, which can be mimic their mechanistic feature. Recently. I have been reported the possible application of 4'-bromoacetophenone as a simple photoactivatable DNA cleaving agent, which could be readily prepared and exhibit potent and selective DNA cleaving activity. Herein, we further investigated the activity of 4'-bromoacetophenone-pyrrolecarboxamides, which consist of both DNA cleaving element and recognition unit under various conditions in order to get more understanding of the mechanism of the action and find a broad spectrum of application.

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Nuclear DNA Damage and Repair in Normal Ovarian Cells Caused by Epothilone B

  • Rogalska, Aneta;Marczak, Agnieszka
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.15
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    • pp.6535-6539
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    • 2015
  • This study was designed to assess, whether a new chemotherapeutic microtubule inhibitor, Epothilone B (EpoB, Patupilone), can induce DNA damage in normal ovarian cells (MM14.Ov), and to evaluate if such damage could be repaired. The changes were compared with the effect of paclitaxel (PTX) commonly employed in the clinic. The alkaline comet assay technique and TUNEL assay were used. The kinetics of DNA damage formation and the level of apoptotic cells were determined after treatment with IC50 concentrations of EpoB and PTX. It was observed that PTX generated significantly higher apoptotic and genotoxic changes than EpoB. The peak was observed after 48 h of treatment when the DNA damage had a maximal level. The DNA damage induced by both tested drugs was almost completely repaired. As EpoB in normal cells causes less damage to DNA it might be a promising anticancer drug with potential for the treatment of ovarian tumors.

Evaluation of the Genetic Toxicity of Synthetic Chemical (XVIII)-in vitro Mouse Lymphoma Assay and in vivo Supravital Micronucleus Assay with Butylated Hydroxytoluene (BHT)

  • Kim, Youn-Jung;Ryu, Jae-Chun
    • Molecular & Cellular Toxicology
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    • v.3 no.3
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    • pp.172-176
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    • 2007
  • Butylated hydroxytoluene (BHT) is widely used antioxidant food additives. It has been extensively studied for potential toxicities. BHT appears adverse effects in liver and thyroid. In this study, we evaluated the genetic toxicity of BHT with more advanced methods, in vitro mouse lymphoma assay $tk^{+/-}$ gene assay (MLA) and in vivo mouse supravital micronucleus (MN) assay. BHT did not appear the significantly results in the absence and presence of metabolic activation system with MLA. Also, in vivo testing of BHT yielded negative results with supravital MN assay. These results suggest that BHT itself was not generally considered genotoxic.

Jab1 has negative effects on p53-mediated genotoxic stresses

  • Lee, Eun-Woo;Lee, Sang-Sik;Song, Jae-Whan
    • BMB Reports
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    • v.42 no.5
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    • pp.299-303
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    • 2009
  • In this study, we use promoter analysis to show that interaction between Jab1 and p53 induces suppression of p53 activation in U2OS and H1299 cells. Interaction between p53 and Jab1 was further confirmed by immunoprecipitation and immunofluorescent analyses. In particular, Jab1 was able to induce nuclear export of p53 as previously reported. When Jab1 was overexpressed in U2OS cells followed by etoposide or hydrogen peroxide ($H_2O_2$), cell death induced by such stresses was protected against. On the contrary, when the level of Jab1 was suppressed in U2OS cells, cytotoxicity imposed by etoposide and $H_2O_2$ was dramatically increased, suggesting a cell protective role for Jab1. These results indicate that Jab1 is a negative regulator of p53 and a plausible oncogene.

The Evaluation of Genotoxicities of Antifungal 6-[(N-Halophenyl)amino]-7- Chlore-5,8-Quinolinediones (항진균성 6-[(N-Halophenyl)amino]-7-Chloro-5, 8-Quinolinedione의 유전독성 평가)

  • 유충규;허문영;박윤미;윤여표
    • Biomolecules & Therapeutics
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    • v.3 no.3
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    • pp.182-187
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    • 1995
  • The clastogenecity and mutagenicity of antifungal 6-[(N-halophenyl)amino]-7-chloro-5, 8-quinolinedione (RCK 3, 7, 13, 14, and 15) had been evaluated. Salmonella typhimurium reversion assay (Ames test) was used to test the mutagenicity of RCKs. RCK14 was mutagenic in S. typhimurium(TA98 and TA100) with and without rat liver microsomal activation. Whereas RCK3, 7, 13 and 15 were negative in Ames test with Salmonella typhimurium(TA98 and TA100), The clastogenecity was tested on the RCKs with in vivo mouse micronucleus assay. All of RCKs tested did not show any clastogenic effect in mouse peripheral blood. Thus RCKs were not supposed to cause any chromosomal damage termed micronuclei. These results indicate that RCK 3, 7, 13 and 15 have no genotoxic potential under these experimental condition.

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