Epigenetic Variation in Terms of the Extent of Methylation of the AhRR Gene as a Result of Smoking Behaviour

Abstract

A large volume of data accumulated and numerous studies published substantiate the strong association of smoking behaviour with a variety of adverse health effects in humans. It is well established that smoking exposure increases the risk of respiratory diseases, cardiovascular diseases, and different forms of cancer, including lung, liver, and colon. A wide variety of these exposures result in epigenetic modifications of the monocytes (cells most sensitive to these exposures). DNA methylation and histone modification are crucial epigenetic modifications of the genome that are involved in regulating many cellular processes and gene activity by alteration of DNA accessibility and chromatin structure. We now recognize that genetic variation is not the only source of phenotypic variation that may be passed down through generations, since genetic variance can only account for a small portion of the diversity in complex traits. Thus, epigenetics comes into play. The pathogenesis involves the release of pro-inflammatory cytokines as a result of activation of enzymes that regulate these epigenetic modifications when exposed to cigarette smoke. Any aberration in the DNA methylation is indicative of conditions far from normal and need for immediate attention. Hypomethylation of the aryl hydrocarbon Receptor Repressor (AhRR) gene indicates long-term smoking exposure and might therefore be a monitor for smoking-induced disease risk. Here, we reviewed the concepts of epigenesis and the identification of epigenetic markers for the study of smoking behaviour and its applicability in the recognition of various risks pertaining to health of an individual. Furthermore, we also discussed about their probable translation to clinical practice and therapeutics in order to enhance risk predictions of smoking related diseases.