Carcinogen refers to an agent which causes autonomous and new tissue growth in a multicellular organism. Carcinogens can be solid materials, chemicals, ionizing radiation, viruses or hormones. All these agents create cancer by altering the cell genomic DNA and then causing these altered cells to flourish instead of going through differentiation into ordinary operational cells. Carcinogens might be DNA reactive that is categorized as chemicals which relate with genomic DNA, yielding to damage or change of its structure, causing mutation. Other forms of carcinogens might alter how DNA articulates its information without direct structure modification, or might alter the environment in a tissue or cell, yielding to increased vulnerability to DNA destruction from other sources (Klaunig et al., 2014).
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Carcinogenic agents can be grouped into classes which include non-mutagenic and mutagenic, based on whether they damage the DNA or not. A mutagenic carcinogen refers to cancer agents which influence DNA change. These carcinogens increase the risk of acquiring cancer by altering its DNA or by causing mutation. Non-mutagenic refers to cancer agents which do not show any evidence activities of altering the DNA of the cell and hence no evidence on mutagenesis activity (Raymond, 2014).
Mutagens refer to chemical compounds or some kinds of X-rays or ultraviolent (UV) light which cause heritable and irreversible changes in the DNA genetic cellular material. Mutagenic adduct persist when they miss detection by repair mechanism of protective cellular DNA, when repair mechanisms are overpowered by extensive damage or when there is a mistake in the repair process (Klaunig et al., 2014). The following cellular replication causes the mutation to be fixed in the genome and they are passed on to all daughters cells. This makes mutagenesis a cumulative process, extending over the organism lifetime. Mutagens are the main causes of cancer by destruction of the DNA causing mutation. The carcinogenic mutagens include viruses, chemical carcinogens and different kinds of radiation which include ionized radiation that include alpha particles originating from radioactive decay, and gamma rays as well as UV light. The main characteristics of all carcinogenic mutagen is that they all cause cancer by causing DNA mutation despite their structural diversity (Basu, 2018).
According to Basu (2018), mutagens and carcinogens normally create multiple DNA adducts, with some adducts. When DNA replication takes place, the DNA adducts magnify the rate of error-prone duplications, with each DNA adduct containing a distinctive mutational signature that is directly associated to the DNA polymerase identity which bypass it and the nucleotide extension and insertion. Normally, a human cell has about 17 varying polymerases from seven families which include RT, A, B, C, D, X and Y. This implies that the kind of tumor developed will depend on the affected cell (Basu, 2018). The main cancers caused by mutagenic carcinogens include skin cancer where mutation is initiated by radiation, lung cancer where mutation is initiated by toxin chemicals in Tobacco, and cervical cancer where mutation is initiated by the presence of Human papillomaviruses (HPV) in the body. Mutagenic agents are said to be the main causes of cancer today. However, they are not the only main causes of cancer. Cancer can also be caused by a group of carcinogenic agents without damaging the cell DNA. Non-mutagenic carcinogens are said to create tumors through disruption of cellular structure and by altering the cell proliferation rate or the rate of process which augment the genetic error rate (Lee et al., 2013). These agents act more as tumor promoters, immunosuppressants, endocrine-modifiers or inducers of inflammatory responses and tissues-specific toxicity. Unlike mutagenic agents whose operation mechanism is highly predictable, non-mutagenic cariogenic agents have different action modes and are species and tissues specific, making it hard to predict their carcinogenic ability. Nevertheless, non-mutagenic mechanisms are related to modification in oxidation stress, disturbance of the balance between apoptosis and proliferation, metabolizing enzyme modulation, intercellular communication modification and peroxisome proliferation induction (Lee et al., 2013).
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