ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
环境与分子突变
ISSN: 0893-6692
自引率: 5.9%
发文量: 65
被引量: 3500
影响因子: 3.575
通过率: 暂无数据
出版周期: 月刊
审稿周期: 2
审稿费用: 0
版面费用: 暂无数据
年文章数: 65
国人发稿量: 18

投稿须知/期刊简介:

Environmental and Molecular Mutagenesis publishes original research articles on environmental mutagenesis. It will publish manuscripts in the six general areas of mechanisms of mutagenesis; genomics; DNA damage; replication recombination and repair; public health; and DNA technology. Subsumed under these six general areas are subject matters that are appropriate for inclusion in EMM. Mechanisms of Mutagenesis spontaneous and induced mutation in indigenous and transgene systems genomic instability mutation rates the consequence of mutation on fitness and evolution of organisms Genomics molecular epidemiology genetic susceptibility gene expression biomarkers small genomes and comparative genomics DNA Damage Indentification detection characterization and quantification of DNA damage metabolism of chemicals into DNA-damaging agents Replication Recombination and Repair genetic and biochemical mechanisms genetic and infectious disease insertions deletions rearrangements aneuploidy Public Health Issues impacting basic human health such as cancer genetic disease aging or acute and chronic disease methodologies that will lead to better methods to determine risk and help to define regulatory policy DNA Technology DNA microarrays differential dispaly and mutation detection analysis novel sequencing strategies bioimaging techniques bioinformatics and functional genomics The study of environmental mutagenesis is a multidisciplinary activity. The journal is intended for investigators in such fields as genetics microbiology biochemistry basic cancer research radiation biology and toxicology. It should as well be of interest to a wide audience of scientists in other areas of biology chemistry and medicine that are engaged in public health research or in formulating public health policy.

期刊描述简介:

Environmental and Molecular Mutagenesis publishes original research articles on environmental mutagenesis. It will publish manuscripts in the six general areas of mechanisms of mutagenesis; genomics; DNA damage; replication recombination and repair; public health; and DNA technology. Subsumed under these six general areas are subject matters that are appropriate for inclusion in EMM. Mechanisms of Mutagenesis spontaneous and induced mutation in indigenous and transgene systems genomic instability mutation rates the consequence of mutation on fitness and evolution of organisms Genomics molecular epidemiology genetic susceptibility gene expression biomarkers small genomes and comparative genomics DNA Damage Indentification detection characterization and quantification of DNA damage metabolism of chemicals into DNA-damaging agents Replication Recombination and Repair genetic and biochemical mechanisms genetic and infectious disease insertions deletions rearrangements aneuploidy Public Health Issues impacting basic human health such as cancer genetic disease aging or acute and chronic disease methodologies that will lead to better methods to determine risk and help to define regulatory policy DNA Technology DNA microarrays differential dispaly and mutation detection analysis novel sequencing strategies bioimaging techniques bioinformatics and functional genomics The study of environmental mutagenesis is a multidisciplinary activity. The journal is intended for investigators in such fields as genetics microbiology biochemistry basic cancer research radiation biology and toxicology. It should as well be of interest to a wide audience of scientists in other areas of biology chemistry and medicine that are engaged in public health research or in formulating public health policy.

最新论文
  • Genotoxicity evaluation of gene therapies: A report from the International Workshop on Genotoxicity Testing (IWGT) 2022.

    被引量:- 发表:1970

  • AOP report: Development of an adverse outcome pathway for deposition of energy leading to learning and memory impairment.

    Understanding radiation-induced non-cancer effects on the central nervous system (CNS) is essential for the risk assessment of medical (e.g., radiotherapy) and occupational (e.g., nuclear workers and astronauts) exposures. Herein, the adverse outcome pathway (AOP) approach was used to consolidate relevant studies in the area of cognitive decline for identification of research gaps, countermeasure development, and for eventual use in risk assessments. AOPs are an analytical construct describing critical events to an adverse outcome (AO) in a simplified form beginning with a molecular initiating event (MIE). An AOP was constructed utilizing mechanistic information to build empirical support for the key event relationships (KERs) between the MIE of deposition of energy to the AO of learning and memory impairment through multiple key events (KEs). The evidence for the AOP was acquired through a documented scoping review of the literature. In this AOP, the MIE is connected to the AO via six KEs: increased oxidative stress, increased deoxyribonucleic acid (DNA) strand breaks, altered stress response signaling, tissue resident cell activation, increased pro-inflammatory mediators, and abnormal neural remodeling that encompasses atypical structural and functional alterations of neural cells and surrounding environment. Deposition of energy directly leads to oxidative stress, increased DNA strand breaks, an increase of pro-inflammatory mediators and tissue resident cell activation. These KEs, which are themselves interconnected, can lead to abnormal neural remodeling impacting learning and memory processes. Identified knowledge gaps include improving quantitative understanding of the AOP across several KERs and additional testing of proposed modulating factors through experimental work. Broadly, it is envisioned that the outcome of these efforts could be extended to other cognitive disorders and complement ongoing work by international radiation governing bodies in their review of the system of radiological protection.

    被引量:- 发表:1970

  • Mutagenicity evaluation of methyl tertiary- butyl ether in multiple tissues of transgenic rats following whole body inhalation exposure.

    Methyl tertiary-butyl ether (MTBE) is used as a component of motor vehicle fuel to enhance combustion efficiency and to reduce emissions of carbon monoxide and nitrogen oxides. Although MTBE was largely negative in the in vitro and in vivo genotoxicity studies, isolated reports of positive findings along with the observation of tumors in the rat cancer bioassays raised concern for its in vivo mutagenic potential. To investigate this, transgenic male Big Blue Fischer 344 rats were exposed to 0 (negative control), 400, 1000, and 3000 ppm MTBE via whole body inhalation for 28 consecutive days, 6 h/day. Mutant frequencies (MF) at the cII locus of the transgene in the nasal epithelium (portal of entry tissue), liver (site of primary metabolism), bone marrow (rapidly proliferating tissue), and kidney (tumor target) were analyzed (5 rats/exposure group) following a 3-day post-exposure manifestation period. MTBE did not induce a mutagenic response in any of the tissues investigated. The adequacy of the experimental conditions to detect induced mutations was confirmed by utilizing tissue samples from animals treated with the known mutagen ethyl nitrosourea. These data provide support to the conclusion that MTBE is not an in vivo mutagen and male rat kidney tumors are not likely the result of a mutagenic mode of action.

    被引量:- 发表:1970

  • Establishment of a nonradioactive DNA ligation assay and its applications in murine tissues.

    被引量:- 发表:1970

  • Visualization strategies to aid interpretation of high-dimensional genotoxicity data.

    被引量:- 发表:1970

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