Epigenotoxicology is an emerging field of study that investigates the non-genotoxic epigenetic effects of environmental toxicants resulting in alteration of normal gene expression and disruption of cell function. Recent findings on the role of toxicant-induced epigenetic modifications in the development of degenerative diseases have opened up a promising research direction to explore epigenetic therapy approaches and related prognostic biomarkers. In this review, we presented comprehensive data on epigenetic alterations identified in various diseases, including cancer, autoimmune disorders, pulmonary conditions as well as cardiovascular, gastrointestinal and bone disease. Although data on abnormalities of DNA methylation and their role in the development of diseases are abundant, less is known about the impact of histone modifications and microRNA expressions. Further, we discussed the effects of selected common environmental toxicants on epigenetic modifications and their association with particular abnormalities. A number of different environmental toxicants have been identified for their role in aberrant DNA methylation, histone modifications, and microRNA expression. Such epigenetic effects were shown to be tissue-type specific and highly associated with the level and duration of exposure. Finally, we described present and future therapeutic strategies, including medicines and dietary compounds for combating the toxicant-induced epigenetic alterations. There are currently seven histone deacetylase inhibitors and two DNA methyltransferase inhibitors approved for clinical use and many other promising candidates are in preclinical and clinical testing. Dietary compounds are thought to be the effective and safe strategies for treating and prevention of epigenetic pathophysiological conditions. Still more concentrated epigenetic researches are required for evaluation of chemical toxicity and identifying the causal association between key epigenetic alteration and disease.
Purpose: The current project aimed to design a simple, highly sensitive, and economical label-free electrochemical aptasensor for determination of prostate-specific antigen (PSA), as the gold standard biomarker for prostate cancer diagnosis. The aptasensor was set up using a screen-printed carbon electrode (SPCE) modified by gold nanoparticles (Au NPs) conjugated to thiolated aptamers. Methods: Cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS) were implemented for electrochemical (EC) characterization of the aptasensor. The determination of PSA was also performed through differential pulse voltammetry (DPV) in [Fe (CN) 6]3-/4- electrolyte solution. Results: The present aptasensor was shown an outstanding linear response in the concentration range of 1 pg/mL - 200 ng/mL with a remarkably lower limit of detection of 0.077 pg/mL. The optimum concentration for PSA separation and the optimum incubation time for antigen-aptamer binding were determined by observing and electing the highest electrochemical responses in a specified time or concentration. Conclusion: According to the results of the specificity tests, the designed aptasensor did not show any significant interactions with other analytes in real samples. Clinical functionality of the aptasensor was appraised in serum samples of healthy individuals and patients examining the PSA level through the fabricated aptasensor and the reference methods. Both methods are comparable in sensitivity. The present fabricated PSA aptasensor with substantial characteristics of ultra-sensitivity and cost-effectiveness can be conventionally built and used for the routine check-up of the men for prostate problems.
Sulfur mustard (SM), also known as mustard gas, is a chemical weapon which by now has been used in many wars. The most concerning SM toxic effect is probable carcinogenicity. In this study, the genetic and epigenetic mechanisms of SM carcinogenicity, by focusing on treatment of SM-associated malignancies, particularly gene therapeutics, cancer vaccines, and epigenetic medications, have been criticized. The required data were collected through an organized search on valid scientific databases. For SM carcinogenicity due to acute or chronic exposure, the entire original and review articles were evaluated. In addition, studies on the therapeutic effects of available genetic and epigenetic medications were included. Currently, four gene therapeutics, two cancer vaccines with genetic bases, and seven epigenetic medications are available for cancer treatment. Genetic and epigenetic cancer treatments including Gendicine, Imlygic, Provenge, Cimavax-EGF, Azacitidine, Vorinostat, Romidepsin, and Belinostat will yield outstanding benefits for SM-exposed patients who suffer from cancer.
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