Antimutagen

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 1518 Experts worldwide ranked by ideXlab platform

John B Bremner - One of the best experts on this subject based on the ideXlab platform.

  • structure of an Antimutagen from carmona retusa leaves
    Carcinogenesis, 1993
    Co-Authors: Irene M Villaseñor, Deborah A Edu, John B Bremner
    Abstract:

    An Antimutagenic compound was isolated from the leaves of Carmona retusa (Vahl) Masam. Its structure has been elucidated by spectral analysis to be 4-hydroxy-7,8,11,12,15,7',8',11',12',15'-decahydro-beta, psi-carotene. The results of the Micronucleus Test, an in vivo method, showed that the isolated Antimutagenic compound reduced by approximately 68.4% the number of micronucleated polychromatic erythrocytes induced by tetracycline, a known mutagen.

Irene M Villaseñor - One of the best experts on this subject based on the ideXlab platform.

  • A new Antimutagen from Mentha cordifolia Opiz.
    Mutation research, 2002
    Co-Authors: Irene M Villaseñor, Deborah E Echegoyen, Jennifer S Angelada
    Abstract:

    The CHCl(3) extract of Mentha cordifolia Opiz. showed Antimutagenicity against tetracycline. An Antimutagen was purified by solvent partitioning and repeated normal phase-vacuum liquid chromatography (NP-VLC) using a micronucleus test-guided isolation and purification. Spectral analyses showed that the isolated Antimutagen is possibly 6,7-bis-(2,2-dimethoxyethene)-2,11-dimethoxy-2Z,4E,8E,10Z-dodecatetraendioic acid. It inhibited the mutagenicity of tetracycline by 68.7% at a dosage of 0.01 mg per 20 g mouse. Statistical analysis using Kruskal-Wallis one-way analysis of variance (ANOVA) by ranks showed that its variance differs from that of the solvent control group (tetracycline+dimethylsulfoxide (DMSO)) at alpha=0.001. Moreover, the isolated Antimutagen did not exhibit mutagenic activity at the same dosage. Statistical analysis showed that it is not mutagenic at 0.001 level of significance because its variance differs from that of tetracycline.

  • structure of an Antimutagen from carmona retusa leaves
    Carcinogenesis, 1993
    Co-Authors: Irene M Villaseñor, Deborah A Edu, John B Bremner
    Abstract:

    An Antimutagenic compound was isolated from the leaves of Carmona retusa (Vahl) Masam. Its structure has been elucidated by spectral analysis to be 4-hydroxy-7,8,11,12,15,7',8',11',12',15'-decahydro-beta, psi-carotene. The results of the Micronucleus Test, an in vivo method, showed that the isolated Antimutagenic compound reduced by approximately 68.4% the number of micronucleated polychromatic erythrocytes induced by tetracycline, a known mutagen.

  • Antimutagen from leaves of carmona retusa vahl masam
    Mutation Research\ genetic Toxicology, 1993
    Co-Authors: Irene M Villaseñor, Deborah A Edu
    Abstract:

    An Antimutagenic principle was extracted from the leaves of Carmona retusa with ethyl alcohol. This was then purified by solvent partition and liquid chromatography. The micronucleus test, an in vivo method, using albino mice as the test system was used for monitoring the Antimutagenic activity. At a dosage of 23.4 mg/kg body weight, the pure isolate reduced by 68.4% the number of micronucleated polychromatic erythrocytes induced by the mutagen tetracycline. Statistical analysis (one-way ANOVA) shows that the variance of the pure isolate differs significantly from that of tetracycline, a known mutagen.

G D Zasukhina - One of the best experts on this subject based on the ideXlab platform.

  • Cells of patients with Down syndrome—a model to study mechanisms of oncogenesis and hypersensitivity to genotoxicants and Antimutagenesis
    Biology Bulletin Reviews, 2016
    Co-Authors: G D Zasukhina, V F Mikhailov, I M Vasilyeva, L V Shulenina
    Abstract:

    Several molecular and genetic features of cells from Down syndrome patients are considered in comparison to those of healthy donors, as is the possibility of using these cells to study mechanisms of the transformation of normal cells to malignant ones, based on the study of the expression of the genes controlling these processes. The role of microRNAs in the regulation of gene activity is estimated. These investigations make it possible to detect the genes for a hereditary predisposition to oncogenesis. The application of Antimutagens-anticancerogens provides a new approach to the prophylaxis of this and other human pathologies. In addition, the data on the hypersensitivity of Down syndrome cells to genotoxicants (radiation and others) and the possibility of correcting these disturbances with Antimutagens are presented. A special section is devoted to specific changes in cells typical for Down syndrome and Alzheimer disease; the commonality of several elements of the pathogenesis of these diseases is emphasized. The research on Down syndrome cells in terms of an imbalance in the entire genome under this pathology opens new means for the prophylaxis and treatment of several human pathologies.

  • Comparative analysis of natural and synthetic Antimutagens as regulators of gene expression in human cells under exposure to ionizing radiation
    Russian Journal of Genetics, 2015
    Co-Authors: V F Mikhailov, A A Shishkina, I M Vasilyeva, L V Shulenina, N F Raeva, E A Rogozhin, M I Startsev, G D Zasukhina, S P Gromov, M V Alfimov
    Abstract:

    This paper studies the effect of plant peptides of thionine Ns-W2 extracted from seeds of fennel flower ( Nigella sativa ) and β-purothionine from wheat germs ( Triticum kiharae ), as well as a synthetic Antimutagen (crown-compound), on the expression of several genes involved in the control of cellular homeostasis, processes of carcinogenesis, and radiation response in human rhabdomyosarcoma cells (RD cells), T-lymphoblastoid cell line Jurkat, and blood cells. All of these agents acted as Antimutagens-anticarcinogens, reducing the expression of genes involved in carcinogenesis (genes of families MMP, TIMP, and IAP and G-protein genes) in a tumor cell. A pronounced reduction in the mRNA level of these genes was caused by thionine Ns-W2, and the least effect was demonstrated by β-purothionine. Antimutagens had very little effect on the mRNA levels of the several studied genes in normal blood cells. Thionine Ns-W2 in tumor cells resulted in a reduction of the content of oncogenic mature miR-21 but did not affect the mRNA level of gene p53 and mature miR-34, which was regulated by the activity of tumor suppressor p53 . It was established that thionine Ns-W2 has a cytotoxic effect by inducing the death of RD cells and lymphoma. The exposure of these cells to ionizing radiation enhanced the inhibitory effect of thionine on expression of the genes involved in oncogenesis. These data indicate that thionine can be regarded as a promising anticarcinogen.

  • Comparative analysis of natural and synthetic Antimutagens as regulators of gene expression in human cells under exposure to ionizing radiation
    Genetika, 2015
    Co-Authors: V F Mikhailov, A A Shishkina, I M Vasilyeva, L V Shulenina, N F Raeva, E A Rogozhin, M I Startsev, G D Zasukhina, S P Gromov, M V Alfimov
    Abstract:

    This paper studies the effect of plant peptides of thionine Ns-W2 extracted from seeds of fennel flower (Nigella sativa) and β-purothionine from wheat germs (Triticum kiharae), as well as a synthetic Antimutagen (crown-compound), on the expression of several genes involved in the.control of cellular homeostasis, processes of carcinogenesis, and radiation response in human rhabdomyosarcoma cells (RD cells), T-lymphoblastoid cell line Jurkat, and blood cells. All of these agents acted as Antimutagens-anticarcinogens, reducing the expression of genes involved in carcinogenesis (genes of families MMP, TIMP, and IAP and G-protein genes) in a tumor cell. A pronounced reduction in the mRNA level of these genes was caused by thionine Ns-W2, and the least effect was demonstrated by β-purothionine. Antimutagens had very little effect on the mRNA levels of the several studied genes in normal blood cells.

  • Mechanisms of human cell protection associated with genetic polymorphism
    Russian Journal of Genetics, 2005
    Co-Authors: G D Zasukhina
    Abstract:

    Systems ensuring protection of human cells against endogenous and exogenous mutagenic factors are considered in terms of genetic polymorphism. Some protection mechanisms are described, including those connected with capturing free radicals, biotransformation of xenobiotics, excision repair of DNA damage (excision of nitrous bases, nucleotides, mismatch repair). A special section is devoted to some issues of using Antimutagens in context of genetic polymorphism. The problem of adaptive response is discussed, providing evidence for independence (in some cases) of DNA repair systems and the formation of adaptive response. Some results of the author obtained many years ago but still relevant are presented.

  • Modification of Repair DNA Synthesis in Mutagen-Treated Human Fibroblasts during Adaptive Response and the Antimutagenic Effect of Garlic Extract
    Russian Journal of Genetics, 2002
    Co-Authors: G. N. Lvova, G D Zasukhina
    Abstract:

    Repair DNA synthesis (RDS) in human fibroblasts during the adaptive responses (ARs) induced by cadmium chloride (CdCl_2), γ-radiation, and 4-nitroquinoline-1-oxide (4NQO) was compared in cells pretreated and not pretreated with garlic extract. The RDS was increased during the ARs induced CdCl_2 and γ-irradiation. Garlic extract stimulated RDS in cells treated by the same mutagens. 3-Aminobenzamide (3AB), an inhibitor of poly(ADP-ribose) polymerase, decreased the RDS rate in cells treated with CdCl_2 and γ-irradiation but had no significant effect on cells treated with 4NQO. It was demonstrated that DNA repair was involved into cell protection in different ways in the cases of Antimutagen treatment and AR.

Deborah A Edu - One of the best experts on this subject based on the ideXlab platform.

  • structure of an Antimutagen from carmona retusa leaves
    Carcinogenesis, 1993
    Co-Authors: Irene M Villaseñor, Deborah A Edu, John B Bremner
    Abstract:

    An Antimutagenic compound was isolated from the leaves of Carmona retusa (Vahl) Masam. Its structure has been elucidated by spectral analysis to be 4-hydroxy-7,8,11,12,15,7',8',11',12',15'-decahydro-beta, psi-carotene. The results of the Micronucleus Test, an in vivo method, showed that the isolated Antimutagenic compound reduced by approximately 68.4% the number of micronucleated polychromatic erythrocytes induced by tetracycline, a known mutagen.

  • Antimutagen from leaves of carmona retusa vahl masam
    Mutation Research\ genetic Toxicology, 1993
    Co-Authors: Irene M Villaseñor, Deborah A Edu
    Abstract:

    An Antimutagenic principle was extracted from the leaves of Carmona retusa with ethyl alcohol. This was then purified by solvent partition and liquid chromatography. The micronucleus test, an in vivo method, using albino mice as the test system was used for monitoring the Antimutagenic activity. At a dosage of 23.4 mg/kg body weight, the pure isolate reduced by 68.4% the number of micronucleated polychromatic erythrocytes induced by the mutagen tetracycline. Statistical analysis (one-way ANOVA) shows that the variance of the pure isolate differs significantly from that of tetracycline, a known mutagen.

Michael D. Waters - One of the best experts on this subject based on the ideXlab platform.

  • Activity profiles of Antimutagens: in vitro and in vivo data.
    Mutation Research, 1996
    Co-Authors: Michael D. Waters, H. Frank Stack, Marcus A. Jackson, Herman E. Brockman, Silvio De Flora
    Abstract:

    Abstract In this review, retinol, chlorophyllin, and N -acetylcysteine are examined and compared with regard to their Antimutagenic activity against some promutagens and a group of direct-acting alkylating agents. The promutagens included aflatoxin B 1 , certain polycyclic aromatic hydrocarbons (e.g., benzo[ a ]pyrene), and certain heterocyclic amines (e.g., food pyrolysates). Results of Antimutagenicity testing selected from data surveyed in the published literature are displayed graphically as activity profiles of Antimutagens showing both the doses tested and the extent of inhibition or enhancement of mutagenic activity. All three Antimutagens are discussed in terms of their putative mechanisms of action in vitro and in vivo with emphasis on the xenobiotic metabolizing enzyme systems.

  • Antimutagenicity profiles of some natural substances.
    Mutation Research Fundamental and Molecular Mechanisms of Mutagenesis, 1992
    Co-Authors: Herman E. Brockman, H.f. Stack, Michael D. Waters
    Abstract:

    Abstract Selected Antimutagenicity listings and profiles have been prepared from the literature on the Antimutagenicity of retinoids and the carotenoid β-carotene. The Antimutagenicity profiles show: (1) a single Antimutagen (e.g., retinol) tested in combination with various mutagens or (2) Antimutagens tested against a single mutagen (e.g., aflatoxin B1). Data are presented in the profiles showing a dose range for a given Antimutagen and a single dose for the corresponding mutagen; inhibition as well as enhancement of mutagenic activity is indicated. Information was found in the literature on the testing of selected combinations of 16 retinoids and carotenoids vs. 33 mutagens. Of 528 possible Antimutagen-mutagen combinations, only 82 (16%) have been evaluated. The most completely evaluated retinoids are retinol (28 mutagens), retinoic acid and retinol acetate (7 mutagens each), and retinal and retinol palmitate (6 mutagens each). β-Carotene is the most frequently tested carotenoid (15 mutagens). Of the remaining retinoids and carotenoids, 8 were evaluated in combination with a single mutagen and the other 2 were tested against only 2 or 3 mutagens. Most of the data on Antimutagenicity in vitro are available for S. typhimurium strains TA98 and TA100. Substantial data also are available for sister-chromatid exchanges in vitro and chromosome aberrations in vitro and in vivo. This report emphasizes the metabolic as well as the Antimutagenic effects of retinoids in vitro and in vivo.

  • Antimutagenicity profiles for some model compounds
    Mutation Research Reviews in Genetic Toxicology, 1990
    Co-Authors: Michael D. Waters, H. Frank Stack, Ann L. Brady, Herman E. Brockman
    Abstract:

    Abstract The concept of activity profile listings and plots, already applied successfully to the display of mutagenicity data, has been modified for application to Antimutagenicity data. The activity profiles are bar graphs that have been organized in two general ways: for Antimutagens that have been tested in combination with a given mutagen and for mutagens that have been tested in combination with a given Antimutagen. Doses from both the mutagen and the Antimutagen are displayed and plotted together with results on enhancement or inhibition of mutagenic activity. The short-term tests that have been used extensively to identify mutagens and potential carcinogens are increasingly being used to identify Antimutagens and potential anticarcinogens. Three model mutagens, N -methyl- N ′-nitro- N -nitrosoguanidine, aflatoxin B 1 and benzo[ a ]pyrene, and 4 model Antimutagens, butylated hydroxyanisole, butylated hydroxytoluene, glutathione and disulfiram, were selected from the data surveyed in the published literature. It is not clear at the present time whether the inhibition of carcinogen-induced mutation is a good indicator of anticarcinogenic properties, and further research is needed. Nevertheless, the activity profiles are useful for the assessment of the available Antimutagenesis data by providing rapid visualization of considerable dose information and experimental results.

  • The concept of activity profiles of Antimutagens.
    Antimutagenesis and Anticarcinogenesis Mechanisms II, 1990
    Co-Authors: Michael D. Waters, H. Frank Stack, Ann L. Brady, Herman E. Brockman
    Abstract:

    There is considerable evidence that gene and chromosomal mutations are important factors in carcinogenesis (1,45). It follows, therefore, that the incidence of cancer can be reduced by decreasing the rate of mutation. The most obvious way to decrease the rate of mutation is to determine which environmental agents are mutagenic and then to reduce or prevent human exposure (1). Short-term genetic tests have been, and continue to be, useful in the detection of environmental mutagens and potential carcinogens (9).