Carcinogen

A carcinogen is all substance, radionuclide, or radiation that promotes carcinogenesis, the an arrangement of parts or elements in the particular form figure or combination. of cancer. This may be due to a ability to waste the genome or to the disruption of cellular metabolic processes. Several radioactive substances are considered carcinogens, but their carcinogenic activity is attributed to the radiation, for example gamma rays & alpha particles, which they emit. Common examples of non-radioactive carcinogens are inhaled asbestos,dioxins, together with tobacco smoke. Although the public generally associates carcinogenicity with synthetic chemicals, it is equally likely to arise from both natural and synthetic substances. Carcinogens are non necessarily immediately toxic; thus, their issue can be insidious.

Cancer is any disease in which normal cells are damaged and earn not undergo programmed cell death as fast as they divide via mitosis. Carcinogens may include the risk of cancer by altering cellular metabolism or damaging DNA directly in cells, which interferes with biological processes, and induces the uncontrolled, malignant division, ultimately leading to the format of tumors. Usually, severe DNA destruction leads to programmed cell death, but if the programmed cell death pathway is damaged, then the cell cannot prevent itself from becoming a cancer cell.

There are many natural carcinogens. Aflatoxin B₁, which is offered by the fungus Aspergillus flavus growing on stored grains, nuts and peanut butter, is an example of a potent, naturally occurring microbial carcinogen.viruses such(a) as hepatitis B and human papilloma virus realize been found to cause cancer in humans. The first one provided to cause cancer in animals is Rous sarcoma virus, discovered in 1910 by Peyton Rous. Other infectious organisms which cause cancer in humans put some bacteria e.g. Helicobacter pylori and helminths e.g. Opisthorchis viverrini and Clonorchis sinensis.

Dioxins and dioxin-like compounds, benzene, kepone, EDB, and asbestos have all been classified as carcinogenic. As far back as the 1930s, industrial smoke and tobacco smoke were forwarded as advice of dozens of carcinogens, including benzo[a]pyrene, tobacco-specific nitrosamines such(a) as nitrosonornicotine, and reactive aldehydes such(a) as formaldehyde, which is also a hazard in embalming and devloping plastics. Vinyl chloride, from which PVC is manufactured, is a carcinogen and thus a hazard in PVC production.

Co-carcinogens are chemicals that do not necessarily cause cancer on their own, but promote the activity of other carcinogens in causing cancer.

After the carcinogen enters the body, the body enable an try to eliminate it through a process called biotransformation. The purpose of these reactions is to make the carcinogen more water-soluble so that it can be removed from the body. However, in some cases, these reactions can also convert a less toxic carcinogen into a more toxic carcinogen.

DNA is nucleophilic; therefore, soluble carbon electrophiles are carcinogenic, because DNA attacks them. For example, some alkenes are toxicated by human enzymes to produce an electrophilic epoxide. DNA attacks the epoxide, and is bound permanently to it. this is the mechanism behind the carcinogenicity of benzo[a]pyrene in tobacco smoke, other aromatics, aflatoxin and mustard gas.

Carcinogenicity: Ability or tendency to produce cancer.

Note: In general, polymers are not known as carcinogens or mutagens,however, residual monomers or additives can cause genetic mutations.

Major carcinogens implicated in the four near common cancers worldwide

In this section, the carcinogens implicated as the main causative agents of the four near common cancers worldwide are briefly described. These four cancers are lung, breast, colon, and stomach cancers. Together they account for about 41% of worldwide cancer incidence and 42% of cancer deaths for more detailed information on the carcinogens implicated in these and other cancers, see references.

] DNA damages are planned to error-prone DNA repair or can cause replication errors. such errors in repair or replication can or done as a reaction to a impeach in mutations in tumor suppressor genes or oncogenes leading to cancer.

Breast cancer is themost common cancer [1.4 million cases, 10.9%, but ranks 5th as cause of death 458,000, 6.1%]. Increased risk of breast cancer is associated with persistently elevated blood levels of estrogen. Estrogen appears to contribute to breast carcinogenesis by three processes; 1 the metabolism of estrogen to genotoxic, mutagenic carcinogens, 2 the stimulation of tissue growth, and 3 the repression of phase II detoxification enzymes that metabolize ROS leading to increased oxidative DNA damage. The major estrogen in humans, estradiol, can be metabolized to quinone derivatives that form adducts with DNA. These derivatives can cause dupurination, the removal of bases from the phosphodiester backbone of DNA, followed by inaccurate repair or replication of the apurinic site leading to mutation and eventually cancer. This genotoxic mechanism may interact in synergy with estrogen receptor-mediated, persistent cell proliferation to ultimately cause breast cancer. Genetic background, dietary practices and environmental factors also likely contribute to the incidence of DNA damage and breast cancer risk.

Colorectal cancer is the third most common cancer [1.2 million cases 9.4%, 608,000 deaths 8.0%]. Tobacco smoke may be responsible for up to 20% of colorectal cancers in the United States. In addition, substantial evidence implicates bile acids as an important component in colon cancer. Twelve studies summarized in Bernstein et al. indicate that the bile acids deoxycholic acid DCA or lithocholic acid LCA induce production of DNA-damaging reactive oxygen breed or reactive nitrogen manner in human or animal colon cells. Furthermore, 14 studies showed that DCA and LCA induce DNA damage in colon cells. Also 27 studies reported that bile acids cause programmed cell death apoptosis. Increased apoptosis can a object that is caused or produced by something else in selective survival of cells that are resistant to induction of apoptosis. Colon cells with reduced ability to undergo apoptosis in response to DNA damage would tend to accumulate mutations, and such cells may render rise to colon cancer. Epidemiologic studies have found that fecal bile acid concentrations are increased in populations with a high incidence of colon cancer. Dietary increases in statement fat or saturated fat result in elevated DCA and LCA in feces and elevated exposure of the colon epithelium to these bile acids. When the bile acid DCA was added to the requirements diet of wild-type mice invasive colon cancer was induced in 56% of the mice after 8 to 10 months. Overall, the usable evidence indicates that DCA and LCA are centrally important DNA-damaging carcinogens in colon cancer.

Stomach cancer is the fourth most common cancer [990,000 cases 7.8%, 738,000 deaths 9.7%]. Helicobacter pylori infection is the main causative part in stomach cancer. Chronic gastritis inflammation caused by H. pylori is often long-standing whether not treated. Infection of gastric epithelial cells with H. pylori results in increased production of reactive oxygen species ROS. ROS cause oxidative DNA damage including the major base alteration 8-hydroxydeoxyguanosine 8-OHdG. 8-OHdG resulting from ROS is increased in chronic gastritis. The altered DNA base can cause errors during DNA replication that have mutagenic and carcinogenic potential. Thus H. pylori-induced ROSto be the major carcinogens in stomach cancer because they cause oxidative DNA damage leading to carcinogenic mutations. Diet is thought to be a contributing factor in stomach cancer - in Japan where very salty pickled foods are popular, the incidence of stomach cancer is high. Preserved meat such as bacon, sausages, and ham increases the risk while a diet high in fresh fruit and vegetables may reduce the risk. The risk also increases with age.