Anticlastogenicity of two derivatives of 1,4-dihydroisonicotinic acid in mouse micronucleus test

Гончарова, Р. И.; Zabrejko, S.; Dalivelya, Olga; Kuzhir, Tatyana D.

doi:10.1016/s1383-5718(01)00223-6

Cited by 20 publications

(12 citation statements)

References 14 publications

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“…The mice were administered 60 mg/kg per day EMS in dimethyl sulfoxide, intraperitoneally (ip). The dose of EMS was determined following previous literature studies, in order to elicit mild response (Kondo and Ozawa, 1992;Goncharova et al, 2001).…”

Section: Methodsmentioning

confidence: 99%

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Randomly amplified polymorphic DNA as a tool for genotoxicity: an assessment

Noel

Rath

2006

Toxicol Ind Health

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Novel short-term assays are required to substantiate the battery of assessment methods for evaluating the genotoxicity of candidate drugs. In this study, an attempt has been made to evaluate randomly amplified polymorphic DNA (RAPD) analysis for its potential to establish genotoxic effect of a known genotoxicant, ie, ethyl methanesulfonate (EMS) in Swiss mice (Mus musculus). Based on the RAPD profiles, genetic damages were detected in EMS-exposed animals, suggesting its usefulness in scanning whole genome for assessing the genotoxic effects of candidate drugs. The profiles were generated using genomic DNA, isolated from liver prior to treatment and from liver, bone marrow and blood after treatment of the genotoxicant. Measurable differences indicative of genetic damages were observed when the pre- and post-treatment profiles were compared. This suggests that RAPD analysis may be useful for assessing the pre-clinical genotoxic effects of candidate drugs.

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Section: Methodsmentioning

confidence: 99%

“…EMS was used because it is an established genotoxicant, capable of inducing mutations in the genome (Goncharova et al, 2001;Guha and Khuda-Bukhsh, 2002;Wagner et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Randomly amplified polymorphic DNA as a tool for genotoxicity: an assessment

Noel

Rath

2006

Toxicol Ind Health

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“…Chemical isolation of the active compound is increasingly the method of choice. For example, 4-(methylthio)-3-butenyl isothiocyanate has been found to be the primary anti-mutagen in daikon (Raphanus sativus; Japanese white radish) (38), curcumin and its natural analogues (39-41), vanillins (25), 1,4-dihydroisonicotinic acid (42) or paraaminobenzoic acid (23). While many of these have been extracted from natural sources, chemical synthesis of anti-mutagens is also a common practice, especially as a potential means of producing chemopreventive agents (40,(43)(44)(45).…”

Section: Examples Of Anti-mutagens and Their Sourcesmentioning

confidence: 99%

Antimutagenesis Studies: Where Have They Been and Where Are They Heading?

Ferguson

2011

Genes and Environment

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An anti-mutagen is any substance that reduces the rate of spontaneous mutations or counteracts or reverses the action of a mutagen, or any technique that protects cells against the eŠects of mutagens. Studies as early as the 1940s reported on substances that delayed detection of radiation-induced mutations, or reduced the appearance of mutations induced by chemicals such as acridine orange. However, a far more sophisticated range of anti-mutagens is now being identiˆed. Mutagen scavengers act through absorption onto a larger molecule that is readily excreted. Good examples are provided by dietaryˆbre sources, such as wheat bran, or the planar molecule, chlorophyll and its stabilised derivative, chlorophyllin. Mutagens may be actively extruded from human cells through the action of one or more of a series of ATP-binding cassette (ABC) drug transporter proteins, including the multidrug resistance proteins (P-glycoproteins), multidrug resistance-associated proteins (MRP1-7) and the breast cancer resistance protein (BCRP). These proteins can aŠect the absorption, distribution and excretion of mutagens and carcinogens, as well as of their metabolites and conjugates. Even if the undesirable compound enters the cells, there are several mechanisms by which it may be prevented from interaction with DNA. Detoxiˆcation mechanisms are of increasing interest, especially those where transcription is regulated through the antioxidant response element (ARE), whose own transcription factor, Nrf2, is repressed under basal conditions. While much of the early literature on mutagenesis and carcinogenesis implicated exogenous chemicals, it is increasingly realised that unrepaired oxidative DNA lesions are important mutational precursors, and anti-oxidants represent an important class of anti-mutagens. It is also recognised that deˆciency of certain micronutrients may lead to cell mutation, and that restoring nutrient balance is an important mechanism of antimutagenesis. An increasing number of studies focus on DNA repair and stress responses as novel mechanisms of anti-mutagenesis.

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“…Эффективность антиму тагенного действия изученных соединений определя лась их антиоксидантной и электронодонорной актив ностью, что объясняло эффекты соединений против спонтанных мутаций и предполагало их защитное дей ствие против ионизирующей радиации, так как и в том, и другом случае велик вклад реактивных радикалов кис лорода. Однако дальнейшие исследования в различных тест системах, включая млекопитающих, показали, что антимутагены этой группы, в частности, натрий 3,5 бис этоксикарбонил 2,6 диметил 1,4 дигидропири дин 4 карбоксилат (ДГП), дилудин (Д) и глутапирон (ГП), существенно снижают уровень химического му тагенеза, индуцированного алкилирующим агентом этилметансульфонатом (ЭМС) [9,11,60,62].…”

Section: некоторые особенности и механизмы действия антимутагенов -прunclassified

Molecular basis of applying antimutagens as anticarcinogens

Гончарова

Иосифовна²,

Kuzhir

et al. 2005

Ecological genetics

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The paper presents a review of current data on mechanisms of natural and synthetic antimutagen action underlying the expediency and availability of their application as anticarcinogens. Previously, some molecular processes involved in carcinogenesis as well as some therapeutic targets are considered. The effects of antimutagens on those or other molecular targets have been summarized in table. Along with the literature data on plant antimutagens, some experimental results and supposed mechanisms of the 1,4-dihydropyridine derivatives have been analyzed.

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Anticlastogenicity of two derivatives of 1,4-dihydroisonicotinic acid in mouse micronucleus test

Cited by 20 publications

References 14 publications

Randomly amplified polymorphic DNA as a tool for genotoxicity: an assessment

Randomly amplified polymorphic DNA as a tool for genotoxicity: an assessment

Antimutagenesis Studies: Where Have They Been and Where Are They Heading?

Molecular basis of applying antimutagens as anticarcinogens

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