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Genes and Genomics
Published in Firdos Alam Khan, Biotechnology Fundamentals, 2020
It all started during the mid-twentieth century with scientists Conrad H. Waddington and Ernst Hadorn, who did extensive research focused on merging genetics and developmental biology, and has evolved into a new field, which we currently call epigenetics. The word epigenetics was coined by Waddington in 1942 and originally described the influence of genetic processes on development. During the 1990s, there was a renewed interest in genetic assimilation that led to the elucidation of the molecular basis of Waddington’s observations in which environmental stress caused genetic assimilation in fruit flies. Subsequently, research efforts focused on unraveling the epigenetic mechanisms related to these types of changes. Presently, DNA methylation is one of the most largely studied epigenetic modifications. The renewed interest in epigenetics has led to new findings about the relationship between epigenetic variations and many diseases such as cancers, immune disorders, mental retardation-associated disorders, and pediatric and psychiatric disorders.
Emerging Risks and Final Thoughts
Published in Ted W. Simon, Environmental Risk Assessment, 2019
The complexity of epigenetic regulation and the challenge of integrating epigenetics into risk assessment is just beginning to be appreciated. The regulation of gene expression by DNA methylation appears context-dependent.21 Histone proteins that surround DNA on the chromosomes carry many covalent modifications, and over 100 unique modifications have been identified.22,23 These patterns form a code or “alphabet” to facilitate an open structure of the chromosome for access to genomic DNA by transcription factors and movement into the transcription factory. Some epigenetic modifications may be repressive and would tend to prevent transcription. The overall pattern of gene expression is responsive to both new stimuli and exposures, but also conditioned by persistent epigenetic modifications that are both inherited and acquired.24
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
On the other hand, growing progress has been made in the recognition of epigenetic modifications in human chronic diseases, particularly cancer. Cancer is now considered as an epigenetic disease, the same as a genetic disease. There is tremendous evidence on the contribution of epigenetic events in the initiation, promotion, and progression of different types of cancers, mainly through silencing of tumor suppressor genes and/or activation of proto-oncogenes. These modifications have allocated such a fundamental role in cancer development that epigenetic therapy of cancer is rapidly growing in medical sciences.1124 In addition, epigenetic changes currently have been a powerful tool for studying the carcinogenesis mechanisms of occupational and environmental exposures.1125 The first note on pesticide-induced carcinogenesis through epigenetic mechanisms was from a study carried out by Maslansky and colleagues in 1981. They reported hepatocarcinogenesis of organochlorine pesticides with no genotoxic effects in hepatocytes and suspected to epigenetic modifications disrupting intracellular communications.1126 Later, reports presented about epigenetic actions of vinclozolin, a fungicide known to be an environmental endocrine disruptor, in association with adult-onset diseases, particularly tumor development.1127 Pesticides were introduced as carcinogens acting through epigenetic or nongenotoxic mechanisms.752
Epigenotoxicity: a danger to the future life
Published in Journal of Environmental Science and Health, Part A, 2023
Farzaneh Kefayati, Atoosa Karimi Babaahmadi, Taraneh Mousavi, Mahshid Hodjat, Mohammad Abdollahi
Recent attention has been chiefly turned to epigenetic toxicity due to four main reasons. First, early life environmental exposures lead to diseases in the late-life of a person, and the etiology of these disorders can be described via epigenetic mechanisms, but the diagnosis by physicians is not that easy. Second, when a genetic mutation occurs, epigenetic patterns and related enzymes can manage the accessibility of DNA; thus, epigenetic modifiers can control diseases’ severity. Third, some epigenetic modifications are not directly responsible for the etiology of diseases but can be promising biomarkers for diagnosing or treating conditions.[4] Last, depending on the type and extent of these changes, gene expression can be irreversibly altered in both fetuses and adults and can sometimes be transmitted to the next generation in humans despite the continuation of multiple cycles of cell proliferation.[1] Through various cellular and molecular mechanisms, environmental toxins can damage the function of stem cells and lead to changes in stem cell differentiation and the fate of cell transformation. Epigenetic intergenerational changes are among the most acute effects of various toxins on embryos and stem cells that can adversely affect the health of future generations.[5]
Pre-pubertal exposure to ibuprofen impairs sperm parameters in male adult rats and compromises the next generation
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Mariana Gazoli Barbosa, Bárbara Campos Jorge, Julia Stein, Dayana Agnes Santos Ferreira, Ana Carolina da Silva Barreto, Ana Carolina Casali Reis, Suyane Da Silva Moreira, Leonardo Cesar De Lima Inocencio, Luis Fernando Benitez Macorini, Arielle Cristina Arena
Even though changes in the sperm count were observed in F0, this was not observed in F1. On the other hand, the male descendants presented the same alterations in Leydig cell nuclei exhibited by treated progenitors. However, alterations in the testosterone or LH levels were not observed in these males. One possible explanation for maintaining testosterone levels could be a compensatory mechanism through an increased cellular activity in the Leydig cell (Agee, Parsa, and Huntrakoon 1988). The differences in the phenotypic characteristic observed between generations can be explained based on the possible scenarios for epigenetic mechanisms control genes and influence the occurrence of alterations. Thus, epigenetic modifications can be changed by environmental factors, lost during gametogenesis or affected by gene-environmental interactions (Briffa, Wlodek, and Moritz 2018). Consequently, some epigenetic changes can be lost whereas others can be passed on to the next generation.
DNA methylation modifications induced by hexavalent chromium
Published in Journal of Environmental Science and Health, Part C, 2019
Xinnian Guo, Lingfang Feng, Bernardo Lemos, Jianlin Lou
However, the exact mechanisms underlying the carcinogenesis of Cr (VI) are not well elucidated. Previous studies have investigated the pathogenesis of cancers induced by Cr (VI) from different perspectives, among which the hottest one is epigenetic modifications.14 Epigenetic modifications including chemical modifications to DNA or histone are heritable changes that alters the structure of chromatin without changing DNA nucleotide sequence.15 Among the various kinds of epigenetic modifications, DNA methylation is one of the most intensely studied in the context of Cr (VI) exposure. Many studies have investigated the features of DNA methylation induced by chromium (Table 1). In addition, previous studies showed, for instance, that changes in DNA methylation were related to the progress of tumor in lung cancer patients with chromate exposure.16–20