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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
Abnormal and excessive blood pressure in the pulmonary artery causes PHD, eventually leading to right ventricular dysfunction. In recent decades, the importance of epigenetic therapy mediated by DNA methylation alterations and histone modifications has been highlighted in treating lung disease. Using di-methyltransferase SUV4-20H1, knockout mouse caused a PHD phenotype that further confirm the role of histone methyltransferase in the etiology of this disease. The methyl-CpG-binding domain protein family, is a regulatory factor in DNA methylation that was shown to increase in expression in PHD patients’ pulmonary arteries, cigarette smoke (CS)-exposed rat models’ pulmonary arteries, and human pulmonary artery cells exposed to CS, indicating the role of epigenetic modulator in CS-induced PHD. Indeed, epigenetic factors play an essential role in the elevation of blood pressure in the pulmonary arteries (Table 2).[11] According to the previous research, there is a substantial decrease in histone modification of H4K20me2/3 in human patients with COPD, unlike patients with PHD that makes them responsive to epigenetic drug effect.[171] The methylation of H4K20me2/3 was attributed to the activity of the H4K20 di-methyltransferase SUV4-20H1. Smoking or exposure to environmental CS significantly alters gene methylation in COPD-related diseases, especially PHD. One of the regulatory factors of DNA methylation is the methyl-CpG-binding domain protein family (MBD). The MBD2 protein is a factor of the MBD protein family, which acts as a reader in DNA methylation. MBD2 can intervene in transcriptional repression or activation by merging methylated DNA or collecting proteins to form a suppressive combination.[172]