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).
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).
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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