Abstract
Dibenzo[a,l]pyrene (DBP), an environmental pollutant, undergoes a series of enzymatic reactions yielding electrophilic diastereomeric diol-epoxides (DEs) that subsequently bind to DNA covalently and hampers the healing mechanism of cascaded biological pathways resulting in onset of different diseases. In the proposed work, we meticulously investigated and elucidated the mechanistic details of DNA adduct formation and nucleotide excision repair (NER) pathway proteins interaction with all possible diastereomers of dibenzo[a,l]pyrene-diol-epoxides (DBPDEs) namely- (±)-anti-, (±)-syn-, trans- and cis- forms of (-)-anti- and (+)-syn- DBPDEs through a computational simulation study. Our findings revealed that (±)-anti- and (-)-syn-DBPDEs interact more strongly with dT20 while (+)-syn-DBPDE exhibits strong interaction with dG6. Moreover, cis- and trans-conformations of (-)-anti- and (+)-syn-DBPDEs depicted strong binding towards N6-dA. Furthermore, aforesaid metabolic intermediates exhibited weak interactions with NER proteins. This imbalance of interaction tendencies relatively favors the DNA-adduct formation than the NER pathway. Based on our computational data, a robust understanding of the underlying molecular mechanism(s) of DBP-DNA interactions may subsequently lead to the design of novel potential compounds to exert inhibition and block its DNA binding ability and eventually facilitate cancer prevention.
Publisher
AMG Transcend Association
Subject
Molecular Biology,Molecular Medicine,Biochemistry,Biotechnology
Cited by
11 articles.
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