Modifying role of Phyllanthus emblica and ascorbic acid against nickel clastogenicity in mice.
TL;DR: Aqueous extract of edible dried fruits of Phyllanthus emblica was fed to Mus musculus for seven consecutive days prior to treatment with different doses of nickel chloride, finding the greater efficacy of the fruit extract could be due to the interaction of its various natural components rather than to any single constituent.
About: This article is published in Cancer Letters.The article was published on 1991-07-26. It has received 59 citations till now. The article focuses on the topics: Dried fruit & Ascorbic acid.
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TL;DR: Seven plants contain antioxidant principles, that can explain and justify their use in traditional medicine in the past as well as the present, and are viewed for their historical, etymological, morphological, phytochemical and pharmacological aspects.
801 citations
01 Aug 2005
363 citations
Cites background from "Modifying role of Phyllanthus embli..."
...The nickel-induced DNA damage has resulted in the formation of chromosomal aberrations (Conway and Costa 1989; Dhir et al. 1991; Larramendy et al. 1981; Lechner et al. 1984; Sen and Costa 1986b; Sen et al. 1987; Waksvcik and Boysen 1982) that could result in deletion of senescence or tumor suppressor genes....
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...Chromosome gaps or chromosome aberrations have been reported in lymphocytes from nickel refinery workers (Waksvik and Boysen 1982), mouse bone marrow cells following intraperitoneal injection (Dhir et al. 1991), and in in vitro assays using hamster cells (Conway and Costa 1989; Larramendy et al....
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Journal Article•
TL;DR: Structural-activity relationship analysis suggested that the micronucleus assay is more sensitive to the genetic toxicity of some classes of chemicals than to those carcinogens with stronger evidence human carcinogenicity.
268 citations
TL;DR: In the 6th MMS/CSGMT collaborative study as mentioned in this paper, IARC groups 1 (human carcinogen), 2A (probable human carcinogen) and 2B (possible human carcinogens) were selected from 100 commercially available chemicals and chemical groups on which there was little or no micronucleus assay data.
Abstract: To assess the correlation between micronucleus induction and human carcinogenicity, the rodent micronucleus assay was performed on known and potential human carcinogens in the 6th MMS/CSGMT collaborative study Approximately 100 commercially available chemicals and chemical groups on which there was little or no micronucleus assay data were selected from IARC (International Agency for Research on Cancer) Groups 1 (human carcinogen), 2A (probable human carcinogen) and 2B (possible human carcinogen) As minimum requirements for the collaborative study, 5 male mice were treated by intraperitoneal injection or oral gavage once or twice with each chemical at three dose levels, and bone marrow and/or peripheral blood was analyzed Five positives and 2 inconclusives out of 13 Group 1 chemicals, 7 positives and 5 inconclusives of 23 Group 2A chemicals, and 26 positives and 6 inconclusives of 67 Group 2B chemicals were found Such low positive rates were not surprising because of a test chemical selection bias, and we excluded well-known micronucleus inducers The overall evaluation of the rodent micronucleus assay was based on the present data combined with published data on the IARC carcinogens After merging, the positive rates for Groups 1, 2A and 2B were 686, 545 and 456%, respectively Structure-activity relationship analysis suggested that the micronucleus assay is more sensitive to the genetic toxicity of some classes of chemicals Those to which it is sensitive consist of (1) aziridines and bis(2-chloroethyl) compounds; (2) alkyl sulfonate and sulfates; (3) acyl-type N-nitroso compounds; (4) hydrazines; (5) aminobiphenyl and benzidine derivatives; and (6) azo compounds Those to which it is less sensitive consist of (1) dialkyl type N-nitroso compounds; (2) silica and metals and their compounds; (3) aromatic amines without other functional groups; (4) halogenated compounds; and (5) steroids and other hormones After incorporation of structure-activity relationship information, the positive rates of the rodent micronucleus assay became 905, 652 and 600% for IARC Groups 1, 2A and 2B, respectively Noteworthy was the tendency of the test to be more sensitive to those carcinogens with stronger evidence human carcinogenicity
251 citations
TL;DR: There is no convincing evidence that any genotoxic rodent carcinogens or in vivo genotoxins would remain undetected in an in vitro test battery consisting of Ames+MNvit.
Abstract: In vitro genotoxicity testing needs to include tests in both bacterial and mammalian cells, and be able to detect gene mutations, chromosomal damage and aneuploidy. This may be achieved by a combination of the Ames test (detects gene mutations) and the in vitro micronucleus test (MNvit), since the latter detects both chromosomal aberrations and aneuploidy. In this paper we therefore present an analysis of an existing database of rodent carcinogens and a new database of in vivo genotoxins in terms of the in vitro genotoxicity tests needed to detect their in vivo activity. Published in vitro data from at least one test system (most were from the Ames test) were available for 557 carcinogens and 405 in vivo genotoxins. Because there are fewer publications on the MNvit than for other mammalian cell tests, and because the concordance between the MNvit and the in vitro chromosomal aberration (CAvit) test is so high for clastogenic activity, positive results in the CAvit test were taken as indicative of a positive result in the MNvit where there were no, or only inadequate data for the latter. Also, because Hprt and Tk loci both detect gene-mutation activity, a positive Hprt test was taken as indicative of a mouse-lymphoma Tk assay (MLA)-positive, where there were no data for the latter. Almost all of the 962 rodent carcinogens and in vivo genotoxins were detected by an in vitro battery comprising Ames+MNvit. An additional 11 carcinogens and six in vivo genotoxins would apparently be detected by the MLA, but many of these had not been tested in the MNvit or CAvit tests. Only four chemicals emerge as potentially being more readily detected in MLA than in Ames+MNvit--benzyl acetate, toluene, morphine and thiabendazole--and none of these are convincing cases to argue for the inclusion of the MLA in addition to Ames+MNvit. Thus, there is no convincing evidence that any genotoxic rodent carcinogens or in vivo genotoxins would remain undetected in an in vitro test battery consisting of Ames+MNvit.
203 citations
Additional excerpts
...Nickel chloride Nickel chloride hexhydrate 7718-54-9 7791-20-0 E + [985]; − TC [370,474,986, 987]; I [988]; − [989] + [990, 991]; gpt [992]; HPRT [388,993] + [392,785] + + [994–999]; Weak + [1000] E + [1001,1002]; − [120,1003] + [1002] + [1004,1005]...
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...[1002] H....
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References
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TL;DR: Cinnamomi cortex, Rhei rhizoma, Scutellariae radix and Rehmanniae radix were found to decrease the mutagenic activity of benzo[a]pyrene, and Aurantii nobilis pericarpium had an enhancing effect, but then neither of these extracts is itself Mutagenic.
Abstract: The effects of medicinal plants on the mutagenicity of benzo[a]pyrene were studied with Salmonella typhimurium tester strains. The chosen medicinal plants are very frequently used as Chinese herbal medicines. Each medicinal plant was extracted with hot water, which is similar to the method used in Chinese medicinal treatment. Cinnamomi cortex, Rhei rhizoma, Scutellariae radix and Rehmanniae radix were found to decrease the mutagenic activity of benzo[a]pyrene. Atractylodis rhizoma also reduced the mutagenicity of benzo[a]pyrene, but this was not certain, because it showed a killing effect on the cell survival test. Bupleuri radix and Aurantii nobilis pericarpium had an enhancing effect, but then neither of these extracts is itself mutagenic. Each medicinal plant extract showed a different effect on the mutagenicity of benzo[a]pyrene. These effects were classified into 5 types: (I) decreasing effect, (II) killing effect, (III) enhancing effect, (IV) enhancing and decreasing effect and (V) inactive.
20 citations
TL;DR: Findings show that AA prophylaxis alone cannot substantially reduce the hazards associated with exposure to anti-cancer drugs.
19 citations
Abstract: Chromosomal aberration and sister-chromatid exchange (SCE) base-line frequencies and SCE frequencies induced by 10 ng/ml mitomycin C (MMC) were analysed in cultured peripheral lymphocytes of 65 workers occupationally exposed to nickel carbonyl Ni(CO) 4 . The subjects were divided into 4 groups: (1) control; (2) exposed to nickel carbonyl ( = exposed); (3) cigarette smokers; (4) smoking-exposed. The results show that there are no significant differences in chromosomal aberration frequencies, breaks or gaps, between the various groups. However, the SCE base-line frequency of the smoking-exposed group, with an average of 7.7/cell, was significantly higher than that of the control group, with an average of 6.5/cell ( P P P P
17 citations
TL;DR: The inhibition by vitamins C and E of the formation of carcinogenic nitrosamines and nitrosamides (N-nitroso compounds), as well as effects of these vitamins on carcinogenesis and human cancer are reviewed.
Abstract: To introduce this subject, I will briefly review the inhibition by vitamins C and E of the formation of carcinogenic nitrosamines and nitrosamides (N-nitroso compounds), as well as effects of these vitamins on carcinogenesis and human cancer. I have previously reviewed the inhibition by vitamins C and E of N-nitroso compound formation (4, 5) and hope shortly to publish a more complete review on the subject (7).
11 citations
Journal Article•
TL;DR: In this paper, the authors studied the earliest changes and their sequence in the development of malignant tumors following implantation of 10 mg of nickel subsulfide (Ni3S2) into the right quadriceps muscle of seven male Fischer rats.
Abstract: Experiments were performed to study the earliest changes and their sequence in the development of malignant tumors following implantation of 10 mg of nickel subsulfide (Ni3S2) into the right quadriceps muscle of seven male Fischer rats. Biopsies were performed when nodules reached one to three mm, and, later, when they were five to seven mm, and, finally, at sacrifice, to confirm the fully developed tumor pattern. Light microscopy of the earliest samples showed groups of cells clumped and scattered among degenerating muscle fibers. Mitoses were seen and inflammatory cells were not a feature. Electron microscopy showed individual degenerating muscle fibers, but also cells with characteristic features of myofibroblasts. In many cells osmium, dense fragments suggestive of crystalline material, were seen in the cytoplasm and nuclei. In the second set of biopsy material, myofibroblasts with well defined and dilated rough endoplasmic reticulum, intracellular membrane-bound collagen, and microfilaments with focal "dense bodies" were numerous. Mitoses were frequent. Immunohistochemistry showed strongly positive reaction to Vimentin and muscle-specific Actin in the tumor cells. In the fully developed tumors, the previously described typical storiform cell pattern with spindle and spheroidal cells with frequent mitoses was seen. Vimentin and muscle-specific Actin stains were strongly positive. The long latent period, the evidence of cell degeneration, necrosis, foreign material (probably of nickel composition), cell invasion, and subsequent rapid myofibroblast-type cell development, proliferating to malignant tumors highly suggestive of malignant fibrous histiocytoma, seem to suggest an epigenetic form of carcinogenicity of cytotoxic variety. Whether the tumor cells derive from transformed myofibrils or from activated pluripotential mesenchymal cells, or from both, remains in doubt.
10 citations