Chemical mutagens are electrophilic reagents or their metabolic precursors that covalently modify DNA bases or become incorporated into the DNA double helix, thereby generating lesions that alter base-pairing specificity, block replication, or distort the helical structure. A defining characteristic of chemical mutagens is their dependence on the chemical reactivity of the nucleophilic sites within DNA bases; alkylating agents transfer methyl or ethyl carbonium ions to atoms such as the O⁶ and N⁷ positions of guanine, producing modified nucleotides with altered pairing properties or forming interstrand cross-links that arrest replication ^[1]. Base analogs constitute a separate class of chemical mutagens whose structural similarity to canonical bases permits their incorporation during DNA replication, after which their distinct hydrogen-bonding or tautomeric properties direct the insertion of incorrect partner bases in subsequent rounds of synthesis ^[2]. Intercalating agents, by contrast, are planar aromatic molecules that insert between adjacent base pairs without covalent attachment, unwinding the helix and increasing the distance between bases, an event that promotes frameshift mutations through slippage during replication ^[3]. Promutagens, a further category, are chemically inert compounds that acquire mutagenic activity only after enzymatic transformation, typically by cytochrome P450-mediated oxidation, into reactive electrophilic species ^[4]. Within the DNA repair mechanisms framework, the biological significance of chemical mutagens resides in the specific lesion types they produce and in the repair pathways—such as direct reversal by alkyltransferases, base excision repair, and nucleotide excision repair—that are mobilized to remove the resulting damage and restore template integrity ^[5].