The Process and Metabolism of Chemical Carcinogenesis

Abstract

The potential for DNA damage and the activation of specific oncogenic pathways that cause inflammation are present in a wide range of physical, chemical, and biological variables that are constantly present in human beings. According to certain theories, chemical carcinogens are the primary etiological factor in cancer. These substances interact either or non-covalently with the DNA, RNA, and proteins in human tissue, which helps to initiate carcinogenesis, a process in which genetic mutation and changes to the transcription of the genome take precedence. These carcinogens act as cancer cell growth initiators or promoters. When DNA, RNA, or proteins are alkylated, covalent connections are first formed with them and then the promoting action occurs. The process involves numerous molecular and cellular changes that turn normal cells into plastic cells. Although it is hypothesized that these endogenous chemical processes could cause DNA damage by inducing gene changes with the aid of reactive oxygen species. This review's focus is on the basic mechanism and metabolism of chemical carcinogenesis. Chemical carcinogens are supposedly considered to be the key etiological factor of malignancy. The covalent or non-covalent bonds between these chemical and the DNA, RNA, and proteins of human tissue help in the initiation of carcinogenesis wherein, genetic mutation and alteration in the genome transcription supervenes. These carcinogens behave as initiators or promoters of cancer cell growth. Alkylation of DNA, RNA, or proteins and the formation of covalent bonds with them begin initially followed by the promoting effect. Numerous molecular and cellular events causing the transformation of normal cells into neoplastic cells occur in the process. It is assumed though those endogenous molecular pathways could instigate mutations in respective genes with the support of reactive oxygen species, thus leading to DNA damage. Thus, this review deals with the basic mechanism and metabolism of chemical carcinogenesis.