Abstract
Polycyclic aromatic hydrocarbons (PAHs) are among the most prevalent environmental pollutants and result from the incomplete combustion of hydrocarbons (coal and gasoline, fossil fuel combustion, byproducts of industrial processing, natural emission, cigarette smoking, etc.). The first phase of xenobiotic biotransformation in the PAH metabolism includes activities of cytochrome P450 from the CYP1 family and microsomal epoxide hydrolase. The products of this biotransformation are reactive oxygen species that are transformed in the second phase through the formation of conjugates with glutathione, glucuronate or sulphates. PAH exposure may lead to PAH-DNA adduct formation or induce an inflammatory atherosclerotic plaque phenotype. Several genetic polymorphisms of genes encoded for enzymes involved in PAH biotransformation have been proven to lead to the development of diseases. Enzyme CYP P450 1A1, which is encoded by the CYP1A1 gene, is vital in the monooxygenation of lipofilic substrates, while GSTM1 and GSTT1 are the most abundant isophorms that conjugate and neutralize oxygen products. Some single nucleotide polymorphisms of the CYP1A1 gene as well as the deletion polymorphisms of GSTT1 and GSTM1 may alter the final specific cellular inflammatory respond. Occupational exposure or conditions from the living environment can contribute to the production of PAH metabolites with adverse effects on human health. The aim of this study was to obtain data on biotransformation and atherosclerosis, as well as data on the gene polymorphisms involved in biotransformation, in order to better study gene expression and further elucidate the interaction between genes and the environment.
Highlights
Polycyclic aromatic hydrocarbons (PAHs) are among the most prevalent environmental pollutants known to be involved in carcinogenesis [1]
The general aim of this review is to present the substantial data on PAH exposure as a factor in the development of atherosclerosis
The focus points of this paper include: 1) activation of PAH biotransformation, biotransformation mechanisms, production of specific metabolites that may increase the risk of atherosclerosis; 2) the most frequent genetic polymorphisms of genes involved in PAH biotransformations and atherosclerosis presented in biomedical literature; 3) the influence of certain common genetic variants of genes involved in xenobiotic biotransformations on the development of coronary artery disease (CAD); 4) an overview of different population studies related to the association of common genetic polymorphisms and atherosclerosis; and 5) gene–environment mechanisms involved in the process of atherosclerosis development
Summary
Polycyclic aromatic hydrocarbons (PAHs) are among the most prevalent environmental pollutants known to be involved in carcinogenesis [1]. These are aromatic hydrocarbons with 3 and more aromatic rings. The best known PAHs are naphthalene, benz(a)pyrene (b[A]P), phenantrene, and anthracite. PAHs mainly result from fossil fuel combustion, as byproducts of industrial processing, human activity, industrial emission, and natural emission [2,3]. The main channels through which PAHs enter the environment are coal production and processing, crude oils, natural gases, production of heavy and light metals, and waste incineration. There are over a hundred of various PAHs, but in practice, only six to sixteen are interesting for analyses and monitoring [4]
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