Molecular mechanisms of drug-induced mutagenesis: a narrative review

The act of changing an organism’s genetic material to produce mutations, heritable alterations in the nucleotide sequence of DNA or RNA, is known as mutagenesis. Although evolution and natural selection are thought to be primarily driven by mutations, a number of exogenous stimuli, especially some medications, can dramatically speed up the pace of mutation. Because it contributes to the development of resistance to medicinal medicines, the onset and progression of cancer, and congenital defects (teratogenesis), this drug-induced mutagenesis has significant effects on human health. The purpose of this work is to present a thorough analysis of modern drugs that are known to cause mutagenesis. Based on their main side effects, it classifies these medications as teratogenic, carcinogenic, or directly mutagenic. In order to represent the current state of knowledge in this crucial field of study, the review places special emphasis on discoveries that have been published since 2019. Recent data calls into question the widely held notion that mutations happen unintentionally and gradually. Rather, it implies that stress reactions brought on by medication exposure frequently initiate mutagenesis processes, which are present in all biological systems. This suggests that rather than directly interacting with genetic material, the carcinogenic effects of some medications may occur indirectly as a result of cellular stress. Furthermore, comprehending the intricacies of drug-induced mutagenesis requires an understanding of the interactions among cellular stress, drug exposure, and mutagenic mechanisms. The study highlights the need for ongoing research on the mutagenic effects of both new and existing medications. By focusing on studies primarily published since 2019, it aims to provide relevant insights into medication safety protocols and therapeutic approaches to decrease potential patient damage, particularly with relation to teratogenic issues during pregnancy.