Cancer – Food Related Carcinogens And Anticarcinogens
Cancer – Food Related Carcinogens And Anticarcinogens
Okaka, J.C., Enoch, N.T., Antionette N.C. Okaka.
What Is Cancer?
Cancer in humans is a group of over one hundred and fifty related diseases that can arise in nearly any tissue in the body. Archaeological evidences indicate that cancer is as old as man. Today, cancer is considered the most problematic ailment of modern man. To place an order for the Complete Project Material, pay N5,000 to Then text the name of the Project topic, email address and your names to 08060565721.
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To place an order for the Complete Project Material, pay N5,000 to
Then text the name of the Project topic, email address and your names to 08060565721.Cancer is characterized by uncontrolled and disorderly multiplication of abnormally shaped cells in body tissues. The multiplication of these abnormal cells may be locally contained, but if not promptly checked for some types of cancer, the multiplying cells may infiltrate to and destroy adjacent tissues.
Mode O f Operation Of Cancer
Cancer cells may migrate via the lymphatic system and through the veinous blood to other parts of the body where they grow as colonies called Metastasis.
Metastasis can also arise in a few instances from the penetration of cancerous cells through the walls of veinous capillaries into the veinous circulation.
Tumours And Types Of Tumours
Tumours, that is, out growth of cancer cells resulting from the multiplication of activated cells are of two basic types, benign and malignant tumours. Tumours whether they are benign or malignant, are commonly referred to as neoplasms.
Benign tumours (benign neoplasms), are usually encapsulated within the membranes of connective tissues, forming capsules which prevent further spreading i.e. they do not metastasise. Benign tumour cells appear alike when viewed under the microscope.
Malignant tumours on the other hand, are not so-to-speak immobilized by connective tissues or can be transported to other distant organs via an overwhelmed lymphatic system or through the venous capillaries. Cancer-like changes have been reported for all known groups of higher animal forms including homo-sapiens.
Classes Of Cancer
Cancers are classified by pathologists based on type of tissue or cell from which they arise. Cancers may also be looked at from their location in the body. Hence, they may be designated lung, breast, brain or liver cancer.
In the classification of cancers according to their tissue type origin, two most prevalent types are sarcomas and carcinomas. Sarcomas arise from connective tissues associated with muscles, bones, cartilages and fibrous binding tissues. Carcinomas on the other hand, refers to cancers arising from epithelial tissues that cover the external surface of the alimentary tract and other organs derived from the embryo gut (i.e. mucous membranes, liver, pancreas, intestines, prostrate and thyroid).
Mixed tumours, which combine the elements of carcinomas and sarcomas, are known as carcinosarcomas. Other tissue-based classes of cancers are those, which involve exclusively blood forming tissues, nerve tissue and pigment tissue conditions. Lymphomas and leukemias are lympho/blood cancers, while gliomas and melanomas are examples of nerve tissue and pigment tissue cancer respectively.
Based on cell-type from which cancers can arise, they may be classified as basal cell type. For example, a carcinoma that arises from basal cells found in the outermost and innermost surfaces of epithelia of the skin is called a basal-cell carcinoma of the skin.
Some Common Designations Of Cancer Of Some Organs
Skin – Basal cell epitheliomas, squamous cell epitheliomas (epitheliomoid carcinomas)
Breast, Liver – Hepatocellular carcinomas
Pancreas – Adenocarcinomas
Ovary – Serous cystadeno-carcinomas
Lymphoid Tissue – Lymphomas
Prostrate – Adenocarcinomas
Stomach – Adenocarcinomas, Lymphomas, Sarcomas
Oesophagus – Epidemoid, Carcinomas
Epidemiological Studies And Cancer-Diet Trends
Epidemiological studies do not produce direct experiment evidence that prove or pinpoint the presence of specific cancer causing factor. Rather, they provide associative hypothesis or risk factors for further studies. A major epidemiological lead indicating the relationship between diet and breast cancer for example is that, breast cancer is uncommon in developing societies as well as in Japan, but increases among these populations as they migrate to the United States. Another supporting epidemiological trend is that in New York, breast cancer is particularly common among the Jewish women, while in Israel, it is common among Jewish women returning from European Countries, but not common in those returning from Asia or Africa. A common risk factor in those described as high cancer prone and low cancer prone groups is the high fat (especially animal fat) intake by the former group.
Epidemiological methodology has provided very useful information that has helped scientists to consolidate on their current knowledge of their rather complex topic, diet and cancer. Risk factors have now been described for some specific cancers. For example, epidemiological studies, have helped us to know that in parts of China and Japan, salty smoked fish is dominant risk factor for stomach cancer, while in United States and elsewhere, the same types of studies indicate colon cancers correlates with alcohol, total fat intake, and low levels of exercise. In China, Japan, Africa and the United States, liver cancer is correlated with dietary intake of Aflatoxin B, and Chronic hepatitis B or C infection, while risk factors associated with oesophageal cancer in China are alcohol, tobacco, pickled/fermented vegetables and vitamin A supplement intake.
Where specific chemical exposures have been measurable and restricted to known populations, epidemiological studies have been quite helpful in the identification of a number of specific chemical/occupational carcinogens or probable carcinogens for humans. However, these epidemiological studies have not too provided direct evidence that prove that the listed chemical culprits are definite human diet-based carcinogens, except in the case of Aflatoxin B and probably alcohol. Epidemiological studies of cancer differences among nations and populations, among members within groups and between cancer patients and matched controls suggest a strong link between environment and cancer. Environment in this context would include such diverse risk factors as exposure to chemical/occupational hazards, sunlight, alcohol, tobacco and of course diet but excludes the inherent genetic susceptibility of the individual. The incidence of some forms of cancer among different subgroups in especially different countries show a minimum 6-fold difference (ovary, breast and bladder) in countries where they exist and where they are low-keyed. Other cancers like those of the oesophagus, skin, liver and penis may show a difference of up to 100-fold magnitude. These glaring difference in magnitude of cancer incidence for people in different countries tend to suggest that these cancers might be avoidable if their causes are detected and ameliorating factors can be put in place.
Epidemiological data derived from monitoring the cancer rates of ethnic people whose food habits have changed over the decades due to migration to other countries, where they adopted new dietary habits, show that the incidence rate of cancer of the oesophagus, colon, rectum, prostrate, breast and ovary among indigenous Japanese is 3-15 times lower, and that for stomach cancer 3 times higher than those of Hawaiian Caucasians in 1978. Second generation Japanese living in Hawaii show a lower stomach cancer risk, while other cancer risks approach the higher level of Hawaiian Caucasians. These trends suggest that the diet rather than genetic differences may play a dominant role in aetiology of these cancers. Knowledge about the possible links between diet and health has increased within the past two decades and consequently, many Food scientists and Nutritionists hold view that diet plays a significant role in chronic diseases such as cancer.
Sources Of Food Borne Carcinogens
Apart from the number of carcinogens, positively identified as occupational in nature and are associated with industrial and medical environments, experiments involving short term genotoxicity assays and laboratory bioassays have added to the list of known carcinogens, including a wide range of food borne compounds. These compounds found in foods such as fermented vegetables, mouldy grains and nuts and broiled salted fish, promote mutation, transform cell growth characteristics, and increase cancer growth rate in surrogate animal models. Well documented examples of these dietary procarcinogens, which include nitosamines/nitosamides, the mould toxin, aflatoxin B, the polycyclic aromatic hydrocarbons etc. are discussed below.
These compounds are of great human concern, and have been found in a variety of foods, which include:
Cabbage, charcoal grilled meat, spinach, lettuce, tea, lemon, sesame oil, wheat, oat, barley, soybeans, rice, plums, cherries, apples, liver, egg yolk, vegetable oil (cotton seed, linseed, olives, peanut, corn), cycad nut, pigment gland of of cottonseed, spinach, smoked foods, green leafy vegetables, cured flesh foods, pickled vegetables from nitrites in-vivo in stomach, pork, beef, chicken, lamb and fish.
Nitrosamines And Nitrosamides
These two types of N-nitroso compounds are formed from the nitrisation of substituted amines, ureas, carbamates and guanidines. The nitrosamines need enzymatic activation in-vivo to become direct carcinogens. Nitrosamides on the other hand are direct carcinogens since activation in-vivo is nonenzymatic. Direct carcinogens produce lesions at organs of entry while those, which need enzymatic activation, produce their lesion in more distal organs. N-nitroso compounds can be derived from three sources exogenous levels in foods, tobacco smoke and endogenous production in acidic environment of the stomach. Exogenous N-nitoso compounds in food are usually of the amine type since the amides are found to be unstable in foods in which they are formed from secondary and tertiary amines and nitrasating agent which is usually nitrous oxide a by-product of meat curing from nitrite. Endogenous N-nitroso compounds are formed in-vivo in the acidic (meat and cheese) environment of the stomach from substrates such as primary amines (methyl amine in cheese and pickles, tryptamine in meat and cheese), secondary amines (diethylamine in fish and pyrrolidine in many foods), amino acids, aromatic amines (N-methyl aniline in cheese), guanidines (creatine in meat), and urea (citrulline in fruits and vegetables).
The National Academy of Sciences in 1981, estimated that exposure of smokers to volatile nitrosamine through cigarette smoke was 17g/day, two –order magnitude higher than the estimated dietary exposure through foods with very high levels of nitrosamines. Food sources of nitrosamines to humans were ranked lower than that either from nitrosamines inhaled from car interiors (0.5g/day) or from cosmetics (0.4g/day).
Polycyclic Aromatic Hydrocarbons (PAH)
These are fused aromatic ring systems formed from the in complete combustion of organic matter especially from fossil fuels, coals and petroleum. Many members of this group of aromatics are non-carcinogenic. However, the high molecular weight member Benzo (a) pyrene, a five ringed PAH which has been widely studied is a potent carcinogen. PAHs are present in high concentrations (up to 0.2g/kg) in charcoal broiled meats as a result of deposition by the smoke during cooking, levels of PAH on broiled meat are drastically reduced if the meat is held above the fire.
The relative risk to humans of dietary ingestion of PAH is uncertain since oral exposure has not produced cancer in laboratory animals, the skin as topical application of PAHs does. There is increased concern about the inhalation of the polycyclic aromatic hydrocarbon through cigarette smoke since this source of contamination has been correlated with cancer of the respiratory system.
Heterocyclic Aromatic Amines (HAA)
HAA like PAH are recognized mutagens and are formed by in complete combustion or pyrolysis of food. They are produced by the reaction of amino acids, sugars and creatine. Major components of pyrolysis product of these amines include mainly aminopyridines. Deep fat frying and stewing yields much lower levels of the HAAs than pan frying and broiling. Cooking temperature 1500c (rare to medium done) yields lower levels of pyrolysis products than higher temperatures (medium to well done). Nearly all HAAs tested in cancer studies have been found to be carcinogenic in laboratory animals including rats. Although the liver is the principal target organ, lessons have been seen in oral cavity, small and large intestines, clitorial and mammary glands, blood vessel, lung and skin.
These are metabolites produced by a variety of moulds. Aflatoxins are produced by Aspergillus flavus and A. parasiticus. The four major aflatoxins are designated (Aflatoxin B1), AFB1, AFB2, AFG1 and AFG2. Another set of aflatoxins M1 and M2 are breakdown products found in milk of cows consuming feed contaminated with AFB1. The action level of aflatoxin in food commodities in the United States is 0.02g/kg. The action level for AFM1 found in milk of cows fed grains contaminated withAFB1 is 0.0005g/kg milk. The major concern from a human health standpoint arises from the high potency of aflatoxin to produce cancer in laboratory animals and a correlating evidence that AFB1 is a hepatocarcinogen in human populations. Birds, fish and mammals are susceptible to the carcinogenic effect of aflatoxin, but these animals show differences in degree of susceptibility. Aflatoxins are also acute liver toxin intervention by keeping down the level of aflatoxin consumed from contaminated food or feed is popular programme for reducing the risk of cancer from this source.
General Mechanism Of Carcinogens
The majority of special synthetic chemical carcinogens including some food additives of past years and the naturally occurring chemical carcinogens which have been investigated appear to initiate neoplasia only after the compounds (precarcinogens) are metabolized to ultimate carcinogens directly or via their proximate carcinogen intermediates. Ultimate carcinogens are in classical cases strong electrophilic reactants with electron deficient carbon and nitrogen centers. These electrophiles once formed can react covalently with electron rich (nucleophilic) sites in cellular molecules (DNA, RNA and Proteins). Initiation of carcinogenesis proper that with time gives rise to tumour production takes place when electrophilic ultimate carcinogen binds to the informational macromolecules controlling cell replication such as nucleic acids and proteins of target tissue. Whenever it had been possible to bring strong electrophilic forms of chemical carcinogens into contact with DNA in mutagenic tests, they have exhibited mutagenic activity, hence ultimate carcinogens are both elctrophilic and mutagenic in character. The test for mutagenicity provides a simple powerful tool for detection of potential carcinogens in food.
Promotional And Inhibitional Mechanisms In Carcinogenesis
Side by side with carcinogen activation reactions are inactivation reactions and balance between the metabolism to ultimate carcinogen and to non-carcinogen derivatives is an important factor in determining the potency of any known carcinogen. Mechanistically, carcinogens may be segregated nito two groups, those that are capable of disrupting gene structure or function otherwise by directly inducing chromosome breaks or causing mutagenic nucleotide insertions, deletion or single base substitution in the genetic material (genotoxins), and others which promote carcinogenesis by promotional mechanisms which are thought to include stimulations of cell proliferation (mitogenesis), blockage of gap-function communication between normal and mutated cells within the tissue, indirect stimulation of chromosome breakage (clastogenesis), prooxidant DNA damage, interference with protein kinase and other pathways through which proto-oncogens and suppressor gene proteins regulate cell proliferation (non genotoxic carcinogens).
Dietary factors and contaminants such as polychlorinated biphenyls (PBCs) and even high caloric, high fat and protein content of diets appear to be able to increase tumour response to carcinogen treated animal without directly disrupting DNA integrity. The above factors are also known as tumour promoters. Of the listed food related carcinogens, most probable of which are listed as probable human carcinogens, only the aflatoxins are accepted by the International Agency for Research on cancer causing in humans based on direct evidence.
Enzyme Activation/Deactivation Of Carcinogens
The majority of known food related genotoxins are not carcinogens until they are activated by cellular enzymes into highly electrophilic species capable of interacting covalently with informational macromolecules in target organs. Competing side-by-side with this activation mechanisms are detoxification mechanisms that convert genotoxins (precarcinogens) to less carcinogenic, more readily excreted polar metabolites. It is note worthy that the same enzyme system can be an activator and a stimulator of detoxification of a carcinogen under different environments. The enzyme systems implicated in carcinogen metabolism are complex and include gueno reductase, peroxidase, epoxide, hydrolases, sulphotransferases, UDP-glucoronyl transferase, flavin-containing monooxengenases among others in addition to the cytochrome P-450 and glutathione transferases. The potential of any food borne carcinogen is a function of not only the dose of carcinogen but will depend on a number of other factors which include species, organ type, developmental age, genetic disposition, recent history of history of exposure to enzyme inhibitors, inducers and repressors and most of all, the balance between synergistic and competing enzyme pathways. Dietary modulators are known to impose selective enzyme induction and inhibition that alter the balance of these competing enzymatic pathways and so positively influence tumourigenesis. Specific cytochrome P-450 isoenzymes have been demonstrated to have opposing activities with different carcinogenens.
Post Carcinogen And Adduct Repair Mechanisms
Not all carcinogen DNA adducts lead to tumour formation. Damaged DNA molecules must replicate to ’’fix’’ the damage as a mutation in replicons. Several enzymatic pathways exist for the repair of the carcinogen DNA adducts and may restore the damaged sites before replication occurs.
Low Molecular Weight Carcinogen DNA Adduct Repair
The low molecular weight N-nitroso carcinogens such as dimethyl and diethyl nitrosamine (DMN and DEN) respectively produce methyl and ethyl adducts on the DNA as N7-guanyl, 06-guanyl and 04-thymidyl adducts. The 06-guanyl adducts which are strongly carcinogenic can be removed by covalent transfer of the methyl or ethyl group to an alkyl transferase repair protein. However, the alkyl transferase is not recycled and has to be synthesized to cope with additional carcinogen challenge. Thus, susceptibility of the individual organ or cell to small alkylating carcinogens is inversely related to alkyl transferase content and has regulatory implications due to DNA repair system saturation which may result in threshold tumour induction, i.e. at limiting quantities of alkyl transferase.
High Molecular Weight Carcinogen DNA Adduct Repair
Bulky genotoxins such as the mycotoxins, poly aromatic and heterocyclic amines are repaired primarily through an excision repair. This may involve more than a dozen repair proteins. Bulky adducts block the progression of DNA polymerase complex and arrest cell replication. The repair is accomplished through polymerase bypass which leaves a gap in the daughter strand. The gap is subsequently filled by an enzymatic ’’SOS’’ repair system. This emergency repair system is prone to mutations due to insertion of incorrect nucleotide. Another incidence of mutation may occur at N7-guanyl adducts through spontaneous depurination owing to the instability of the positively charged imidazole ring introduced by adduction at position 7.
Proto Oncogenes In Tumourigenesis
Oncogenes are the specific genes identified in animal tumour viruses which lead to tumour development when damaged or deleted. All animal cells are now known to carry analogous gene versions called proto-oncogenes. Where as the viral oncogenes are transforming, cellular protooncogenes code for a variety of growth receptors, and signal transduction proteins that regulate normal cell growth. Recent studies support the premise that mutated proto-oncogenes which are deficient in growth regulation are involved in the cancer process for many human cancers. For example, a family of proto-oncogenes termed KN and H-ras, occur in mutated form in different human tumours. Several laboratories isolated ras genes from human bladder carcinoma cells and discovered that there was a single-point mutation on these ras genes which cause a charge on the 12th amino acid of the ras protein. This mutation was sufficient to cause mouse cells transformed with the mutant gene to become tumourgenic . Several other examples have been identified.
Studies using animal models have shown that food borne carcinogens elicit proto-oncogene mutation in association with their initiation of tumours. Benzo (a) pyrene (BP), a food mutagen is known to induce K-ras codon 12mutations in 100% of mouse lung tumours examined. Diethyl nitrosamine (DEN) induced codon 61 mutation in 24% of mouse liver tumours. Urethane induced these mutations in almost all mouse skin tumours studied. Each carcinogen appears to have a restricted spectrum of oncogene mutations probably due to its unique chemical properties and localized specificity for nucleotide adduction. A brief treatment of juveniles, with AFB1 (aflatoxin B1) produced hepatic tumour in rats and trouts carrying similar ras gene mutations. Similar mutations have not been described in human hepatocellular carcinoma. However, hepatocellular carcinoma patients from Africa and Asia with chronic dietary AFB1 exposure showed point mutations at only one site codon 249, in P55 tumour-supressor gene. These mutations are compatible with the mutational specificity of AFB1 and have not been reported in hepatic tumour from patients exposed to Hepatitis B but not AFB1. A lot is still to be uncovered in the neoplastic process. However, proto-oncogene mutational activation is important in tumourigenesis and some food-related carcinogens are capable of causing these events in higher and lower vertebrate cancers.
Cancer Diagnosis And Detection
Early detection of cancer, when it is still localized and symptomless is the best available approach to prevention of cancer deaths. With the best of modern treatments available, about one third of all cancers are cured. On the other hand, about 50-60% of cell cancer could be successfully treated if identified at an early stage. The more common diagnostic techniques are papanicolau mammography, xerography and thermography. Various techniques have been employed in the detection of cancer at an early stage.
Papanicolaou (’’Pap’’) test is a technique which permits physicians to detect early cervical cancer by examination of the microscopic characteristics of cells naturally secreted by the uterine cervix. Similar techniques are used to detect lung and oral cancer from extruded cells. Cells shed by the bladder into the urine, sometimes indicates the presence of cancerous papillomas and early bladder cancer. Mammography is a simple inexpensive x-ray technique used to detect breast cancers that are too small to be palpated. It reveals cancer as small as 5mm and small calcium deposits that are often indicative of cancer. Xerography is a method that records images by means of dusts that adheres to electrostatically sensitized plates and sheets of paper. It is used to take and interpret x-rays of the female breast for early diagnosis of breast cancer and calcium deposits. Thermography which records heat patterns of the breast allows physicians to note those patterns characteristic of early cancer.
Successful treatment of cancer today requires the complete removal or destruction of all cancerous cells. Where some cells are left, the disease recurs. Currently, surgery and radiation are the most effective forms of treatment. Chemotherapy is helpful in some forms of cancer. The choice of therapy is governed by the type, location and size of the cancer at the time of diagnosis and general condition of the patient. Popular treatment modes include surgery, radiation and chemotherapy.
For surgery to be curative, it must be performed before the cancer spreads into organs and tissues that cannot be safely removed. Radical surgery has become the standard improved techniques and equipment have reduced the risks and improved the rehabilitation of patients. In addition to saving life by eradicating cancer, surgery also improves the remaining months or years of life for persons whose cancers cannot be eradicated, restoring comfort and a sense of usefulness. For example, when severe pains accompany cancers, surgery can bring relief by severing the nerve pathways that carry the painful sensation. Surgery is currently more valuable as a preventive measure in controlling cancer.
Radiation therapy makes use of ionizing radiations namely: x-rays, particles (electrons, neutrons and pimensons) produced by machines and gamma rays from radioactive elements to destroy the cells by injuring their capacity to divide. Although some normal cells are killed during radiation therapy, cells outside the field of radiation usually repair the damage. Some cancers do not respond to radiation therapy. Differences in sensitivities of tumours to irradiation are due to variations in origin of cells of the tumours. Deep-seated tumours can be reached with high energy irradiation instruments which produce energy in the multi-million electron volt range. These instruments are more versatile and precise.
Cancer chemotherapy can produce cures in certain forms of cancer. Two cancers frequently cured by drugs are choriocacinoma , a rare, highly malignant tumour that originates in the placenta and Burkitt’s lympohoma, a cancer common in African children. Treatments with combination of drugs have produced long term disease free remissions in many children with acute leukemia. Multiple carcinomas of the superficial layers of the skin have been eradicated after the application of certain ointments to the skin. Chemotherapy often gives the patient a more comfortable life if not cure. Some cancers are resistant to drugs. Most cancer drugs are limited in their usefulness. This is due to the fact that most cancer drugs destroy only the cell population that is dividing whereas other non-dividing cancer cells are not affected. Furthermore, most cancer drugs do some damage to normal cells as well as cancer cells and some cancer cells may become resistant to the drugs. To help overcome these difficulties, drug combinations are administered simultaneously or in sequence. This allows cancer cells at different stages of division to be killed and cause less damage to normal cells. Special supportive and precautionary measures have been developed and protect cancer patients undergoing chemotherapy. For instance, when a patient’s white blood cells are depleted in leukemia, administration of antibiotics offers protection from many infections.
Diet Control In Cancer Intervention
As many nations progress developmentally, except for a specific population subgroup, who may be afflicted by poverty or specific ailments, nutritional intervention strategies tend to progressively shift from emphasizing the need to combat disease arising from insufficient nutrient intake to emphasizing how to combat the effects of consuming the wrong amount and mix of nutrients and how these affect one’s risk from chronic disease such as cancer. Current research trends indicate that several factors associated with diets e.g. total caloric intake, anticarcinogens in foods, and exposure to carcinogens that occur naturally in foods and induced by food preparation may be relevant variables in the diet-cancer equation. Reports by the United States National Academy of Sciences, National Research Council/Committee on diet and health in 1982 and 1989 resulted in the recommendation in that country that diets be modified to decrease the risk of certain cancers and other chronic diseases by paying attention to the following major issues:
1) Need to reduce fat intake to 30% of total calories.
2) Need to reduce the amount of saturated fat and cholesterol.
3) Moderation in salt and alcohol intake.
4) Need to increase the consumption of fresh fruits and vegetables.
5) Need to increase fibre intake from different food sources.
Evidences abound which show that a variety of natural and symbiotic factors can reduce or completely prevent chemical carcinogenesis in certain protocols in experimental animals. Ascorbic acid (vitamin C) is known to inhibit the endogenous formation of carcinogenic N-nitrosamine in-vivo from dietary nitrite and nitrisable amines even though the role of vitamin C in human cancer is presently not well understood. The list below shows vitamins, trace minerals, plant phytochemicals and protease inhibitors, food additives and processing products, drugs and even the industrial pollutant Aroclor 1254. The role of these compounds in human chemoprevention remains to be established.
This task for epidemiologists is made more difficult by the fact that natural ’’anticarcinogens’’ are consumed not singly, but in variable combinations with unknown efficacy within the diet.
Below are the classifications of experimental anticarcinogens-partial list of chemical categories:
Agents that block initial DNA damage:
Nucleophiles, Organosulphides, Terpenes, Aromatic isothiocyanates, Indoles, Conjugated linoleic acid, Dithiolethones, Cumarins, Phenols, Tannins, Sarcophytols, Dithiocarbamates, Trimethylquinolines, Barbiturates.
Agents that suppress post-initiation processes:
Retinoides, Protease inhibitors, Drugs that inhibit arachidonic acid metabolism, Difluoromethylornithine, Terpenes, Cyanates, Isothiocyanates, Selenium salts, Inositol hexaphosphate.
Many compounds found in food identified as potentially anticarcinogenic are entering human trials as commopreventive supplements and hopefully will provide data that will help in the more concrete evaluation of the potential benefit or otherwise of diet shifts and supplemental nutrition on organo-toxicity, antinutritive effects and possibility to influence tumour promotion. It is now a popular view from animal studies that retinoids including beta-carotene, suppress tumour and progression by mechanisms which include antioxidant arrest of prooxidant promotion. Chlorigenic acid, caffeic acid and ferulic acid found in foods suppress tumour promotion and arachidonic acid metabolism probably through antioxidant activity. Epidemiologic studies sometime supported by animal studies also indicated that people who consume diets rich in plant protease inhibitors (legumes and cereals) have a low risk for colon, breast, prostrate, oral and pharyngeal cancers. Notwithstanding the gaps in our understanding of diet-chronic disease relationships, many persons in the United States and elsewhere in the industrialized nations are embracing these new diet strategies even if on trial basis. The food industries in these countries have also responded to the proposed diet shift by making available many products that are in line with the call for diet modification. It is believed that in about two decades or so, data would become available to effectiveness of these diet shifts in reducing the incidence of cancer in humans. For now, trends are emerging on the relationships between nutrition and risk of certain cancers in specific organs. Fruit and vegetable consumption generally reduce the risk of cancer associated with the oesophagus, lung, stomach, colon, rectum and possibly kidney and thyroid gland. The intake of red meat and processed meat increase risk of cancers of the breast, prostate, colon, and rectum. Alcohol consumption show increased risk of various cancers which include those of the upper digestive tract, mouth, throat and oesophagus, liver, breast and possibly those of the stomach and colon while obesity predisposes postmenopausal breast to higher risk of cancer of the breast and cancer of the endometrium. Physical activity is currently considered a strong risk factor for colo-rectal cancers.
Nutritionists and food scientists in developing countries, while still battling with the issue of inadequate amount of food and nutrients cannot neglect the diet-chronic disease information emanating from industrialized nations. Sometimes, the diet shifts recommended are the same old but gradually disappearing way of eating in primitive societies.
Carcinogenecities of heterocyclic amines in cooked food. Ohgaki, W., Takayama, S. and Sugimura, T. Mut. Research 259:399-410,1991.
DNA repair enzymes. Sancar, A. and Sancar, G.B. Ann. Rev. Biochem 57:29-67,1998.
Epidemiological characteristics of breast cancer in middle and late ages. Hems, G. British J. Cancer 24:226-234,1970.
Chemoprevention of cancer: phenolic antioxidants (BHA, Hocman, G. International J. Biochemistry 20:639-684,1988).
Cancer – Food Related Carcinogens And Anticarcinogens
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