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Genes and Genomics
Published in Firdos Alam Khan, Biotechnology Fundamentals, 2020
Epigenetics changes may be reflected at various stages throughout a person’s life; for example, several studies have provided evidence that prenatal and early postnatal environmental factors influence human embryos and may cause the development of various chronic diseases and behavioral disorders in adulthood. For example, studies have shown that children born during the period of the famine from 1944 to 1945 in Holland have shown increased rates of coronary heart disease and obesity after maternal exposure to famine during pregnancy. Similarly, adults that were prenatally exposed to famine conditions have also been reported to have a higher frequency of schizophrenia. Cancer was the first human disease to be linked to epigenetics, for example, research performed by Feinberg and Vogelstein in 1983, found that genes of colorectal cancer cells were significantly hypo-methylated compared with normal tissues. It has been reported that DNA hypo-methylation can activate oncogenes and initiate chromosome instability; however, DNA hyper-methylation initiates silencing of tumor suppressor genes. The buildup of genetic and epigenetic faults can convert a normal cell into a metastatic tumor cell. Furthermore, DNA methylation patterns may cause abnormal expression of cancer-associated genes. The modification of global histone patterns is linked with prostate, breast, and pancreatic cancers. Therefore, epigenetic changes or modifications can be used as biomarkers for the diagnosis of early cancer.
Epigenomic alterations in the individuals exposed to arsenic through drinking water in West Bengal, India
Published in Yong-Guan Zhu, Huaming Guo, Prosun Bhattacharya, Jochen Bundschuh, Arslan Ahmad, Ravi Naidu, Environmental Arsenic in a Changing World, 2019
A.K. Giri, D. Chatterjee, N. Banerjee
Arsenic is not mutagenic but carcinogenic and human. There is a strong believe that arsenic follows the epigenetic pathways to induce cancer in humans. DNA methylation is an epigenetic modification of DNA that is tightly regulated in mammalian development and is responsible for maintaining the normal functioning of the adult organism (Schaefer et al., 2007). Micro RNAs(miRNA) are small 19–25 nucleotides long non-coding RNA molecules that functions in controlling gene expression post-transcriptionally by destabilizing the transcribed mRNA or translational repression (Filipowicz et al., 2008). Evidence showed that epigenetic modifications including DNA methylation and altered micro RNA expression patterns contribute to carcinogenesis (Watanabe et al., 2008). So here we have investigated the epigenetic alterations in arsenic exposed population in West Bengal, India.
Insights from ‘Omics on the Exposure and Effects of Engineered Nanomaterials on Aquatic Organisms
Published in Julián Blasco, Ilaria Corsi, Ecotoxicology of Nanoparticles in Aquatic Systems, 2019
Epigenetic responses to chemicals is arguably an understudied area of research, despite compelling examples of transgenerational effects being mediated by changes in the epigenome. Epigenetics refers to heritable phenotypic changes that occur independent of alterations to the genetic code through the processes of DNA methylation, histone tail modifications or small non-coding RNAs (ncRNAs) including microRNAs (miRNAs) (Vandegehuchte and Janssen 2011). Through these mechanisms, epigenetics induces long-term changes to gene transcription and protein translation, which can be passed down to daughter cells and in some cases, offspring (Vandegehuchte and Janssen 2011). For example, nutritional status and exposure to endocrine disrupting chemicals can induce transgenerational effects, which are mediated through inheritance of DNA methylation patterns (Vandegehuchte and Janssen 2011). For ENMs, there is preliminary evidence that they can cause transgenerational effects. Carbon-based ENMs and Au NPs have been shown to impact reproduction in subsequent generations in D. magna (Arndt et al. 2014) and C. elegans (Kim et al. 2013, Moon et al. 2017); although not yet investigated, it seems likely that epigenetic mechanisms are involved.
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A. Zeki, Christopher M. Royer, Urmila P. Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E. Pinkerton
In addition to RNA interference, other epigenetic modifications might be mediated by different mechanisms, including DNA methylation and histone modification, which might also play essential roles in COPD development. DNA methylation is a chemical modification that involves addition of a methyl group to cytosine residues in CpG dinucleotides, resulting in formation of 5-methylcytosine. DNA methylation might occur in promoter regions of genes, leading to gene silencing or reduced gene expression. In COPD, alterations in DNA methylation patterns were noted in genes involved in inflammation, oxidative stress, and tissue remodeling, which are critical processes in COPD pathogenesis (Alfahad et al. 2021). Previously Zeng et al. (2020) suggested that cigarette-induced oxidative stress plays a role in mediating pulmonary apoptosis and hypermethylation of the B-cell lymphoma/leukemia-2 (Bcl-2) promoter, an apoptosis regulator, in COPD through DNA methyltransferase enzyme 1 (DNMT1), a key DNA methyltransferase enzyme. Similarly, aberrant DNA methylation was reported to be a widespread occurrence in small airways of COPD patients and was associated with altered expression of genes and pathways related to COPD, such as NF-E2-related factor 2 oxidative response pathway (Vucic et al. 2014).
Role of DNA methylation regulation of miR-130b expression in human lung cancer using bioinformatics analysis
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Jin Wang, Xiao-Fan Yu, Nan OUYang, Qiulin Luo, Jian Tong, Tao Chen, Jianxiang Li
The interaction of DNA with smoking constituents is postulated to play an important role in the observed lung carcinoma in animals and humans. Numerous investigators reported that aberrant DNA methylation contributed to the initiation and subsequent development of many types of cancers (Brock et al. 2008; Chen et al. 2012; Hoque 2009). It is noteworthy that DNA methylation regulates gene expression (Gyorffy et al. 2016). In addition, regulation of gene expression also occurs due stimulation of a special class of small, 19–22 nucleotides long, non-coding RNA, called microRNA (miRNAs) (Ha and Kim 2014).
Global DNA methylation (LINE-1) associated with exposure to arsenic-contaminated environment and with type of arsenical skin lesions in Thailand
Published in Human and Ecological Risk Assessment: An International Journal, 2019
Witchaya Phetliap, Alan Geater, Laura S. Rozek, Shoko Oshikawa, Katherine Helmick, Katie Rentschler, Yasuko Kojo, Siriluck Thaicharoen
Epigenetic mechanisms are known to involve DNA methylation, histone modifications, and/or miRNA. DNA methylation is one of several epigenetic mechanisms that cells use to control gene expression. DNA methylation occurs when a methyl group is covalently attached to a cytosine at the 5’ position of a CpG dinucleotide (Relton and Davey 2010). Arsenic exposure has also been shown to cause change in global DNA methylation and loci-specific changes in DNA methylation.