Antinutrients and Phytochemicals in Food - American Chemical Society

Chapter 1

Beneficial Health Effects and Drawbacks of Antinutrients and Phytochemicals in Foods

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An Overview Fereidoon Shahidi Department of Biochemistry, Memorial University of Newfoundland, St. John's, Newfoundland A1B 3X9, Canada Antinutrients in foods are responsible for deleterious effects related to the absorption of nutrients and micronutrients. However, some antinutrients may exert beneficial health effects at low concentrations. The mechanisms by which adverse and beneficial effects of food antinutrients operate are the same. Thus, manipulation of processing conditions and/or removal of certain unwanted components of foods may be required. Antinutrients and phytochemicals found in foods have been categorized as having both adverse and beneficial health effects in humans. These concentration-dependent effects may be manipulated in such away that advantage is taken from their healthrelated benefits so that management of chronic diseases becomes possible. For this purpose, current recommendations suggest that consumption of plant such as grains, fruits and vegetables be increased in order to prevent or possibly cure cardiovascular disease, diabetes and cancer (J, 2). Nonetheless, there is a concern about high intake of foods that are rich in antinutrients due to their increased burden on the body's tolerance to potentially harmful compounds (3, 4). For example, phytic acid, lectins, phenolic compounds and tannins, saponins, enzyme inhibitors, cyanogenic glycosides and glucosinolates have shown to reduce the availability of certain nutrients and impair growth. Some compounds such as phytoestrogens and lignans have also been linked to induction of infertility in humans. Therefore, it is prudent to examine all aspects related to food antinutrients, including their potential health benefits and methods of analyses. When used at low levels, phytic acid, lectins and phenolic compounds as well as enzyme inhibitors and saponins have been shown to reduce the blood glucose and/or plasma cholesterol and triacylglycerols. Meanwhile, phenolic compounds from plant sources, phytic acid, protease inhibitors, saponins, lignans and phytoestrogens have been demonstrated to reduce cancer risks. This monograph intends to cover the occurrence and problems associated with the use of plant food antinutrients, their © 1997 American Chemical Society In Antinutrients and Phytochemicals in Food; Shahidi, F.; ACS Symposium Series; American Chemical Society: Washington, DC, 1997.

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ANTINUTRIENTS AND P H Y T O C H E M I C A L S IN F O O D

removal from foods in order to detoxify them, and changes that occur in them during processing. Potential beneficial health effects of food antinutrients and phytochemicals will also be discussed.


Phenolic Compounds and their Antioxidant Activity in Foods and Biological Systems Phenolic compounds are found in reasonably large quantities and in a variety of chemical forms in plant foods and serve as secondary metabolites that protect plant tissues against injuries and insect and animal attack. Phenolic compounds in plant foods belong to the families of phenolic acids, flavonoids, isoflavonoids, and tocopherols, among others. Phenolic compounds found in foods generally contribute to their astringency and may also reduce the availability of certain minerals such as zinc. During thermal processing, phenolic compounds may undergo oxidation and oxidized phenolics so formed, such as quinones, may combine with amino acids, thus making them nutritionally unavailable. Furthermore, such reaction products are generally highly colored in nature and impart undesirable dark colors to foods. Therefore, in some cases, it might be beneficial to remove phenolics in foods by devising novel processing techniques. The isolated phenolics may then be used in different applications in order to control oxidation of food lipids. The most widely distributed phenolics in plant foods are tocopherols. Both tocopherols (alpha, beta, gamma and delta) and tocotrienols (alpha, beta and gamma) may be present. While the vitamin E activity of a-tocopherol exceeds that of other tocopherols/tocotrienols, its in-vitro activity as an antioxidant is not as good as the other tocopherols (5) and follows the trend given below. a-tocopherol < p-tocopherol * y-tocopherol < 5-tocopherol In general, grains and particularly their oil and oil-rich fractions such as those from the germ provide a good source of compounds with vitamin E activity (6). It should also be noted that grains are a unique source of tocotrienols which are known to inhibit cholesterol synthesis. Phenolic acids are another group of antioxidants found abundantly in whole grains and oilseeds, particularly in the bran layer (7). Phenolic acids in foods, such as those of benzoic and cinnamic acid derivatives occur in the free, esterified/etherified and insoluble-bound forms. The antioxidant activity of phenolic acids in a meat model system was recently reported (8). It has been shown that the in-vitro activity of phenolic acids as antioxidants was in the following order (9). Protocatechuic > Chlorogenic > Caffeic > Vannilic > Syringic > p-Coumaric Flavonoids and isoflavonoids are other groups of phenolic antioxidants found in foods. Green tea is a rich source (25%) of flavonoids of the catechin type. Tea catechins as well as myricetin, another flavonoid found in plat foods, are among the

In Antinutrients and Phytochemicals in Food; Shahidi, F.; ACS Symposium Series; American Chemical Society: Washington, DC, 1997.

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Beneficial Health Effects and Drawbacks of Antinutrients


strongest natural antioxidants found in nature {10). In addition, isoflavonoids, such as those found in soybean in relatively large amounts, also exhibit potent antioxidant activity. The skin of onions contains up to 6% flavonoids, mainly quercetin (77). Since lipid peroxidation is implicated as being a cause of atherosclerosis and many degenerative diseases such as cataract and the aging process, it is anticipated that use of natural antioxidants not only protects foods against rancidity development, it might also augment the body for its antioxidant defense mechanism, particularly in the elderly. Figure 1 shows possible contribution of free radicals in diseases and potential effect of antioxidants in preventing/controlling free radical formation and their deleterious effects. Phytates Phytic acid (/wvo-inositol-l,2,3,4,5,6-hexakis dihydrogen phosphate; PA) is present in foods in varying concentrations of 0.1-6.0% (72, 73). Phytates are found as crystalline globoids inside protein bodies in the cotyledon of legumes and oilseeds or in the bran region of cereal grains {4, 12). Phytic acid, with its highly negatively charged structure, is a very reactive compound and particularly attracts positivelycharged ions such as those of zinc and calcium. Therefore, it is considered as a food antinutrient and its removal during food processing has been considered {14, 15). In addition, P A may also react with charged groups of proteins, either directly or indirectly, via negatively charged groups of proteins mediated by a positively-charged metal ion such as calcium. Interaction of P A with starch molecules, directly via hydrogen bonding with phosphate groups or indirectly through proteins to which it is attached, is also possible. Such bindings may reduce the solubility and digestibility of protein and starch components of food. However, literature data in this area of research are often contradictory {16-18). Potential beneficial effects of P A relate to its ability to lower blood glucose response to starchy foods {19). Removal of P A from navy beans was reported to cause an increase in blood glucose response while addition of P A back to the beans flattened the response {20). The effect of reducing the blood glucose response may be exerted by influencing the rate of starch digestion. Antinutrients such as P A and tannins may lower the rate of starch digestion by the same mechanism that makes them antinutrients (27). Such compounds can bind directly with the amylase enzyme, thus inactivating it. Indirectly, P A and tannins may also bind with calcium which is required for stabilization of amylase activity or possibly with starch in order to affect its gelatinization or accessibility to digestive enzymes {4). Phytic acid has also been implicated as having a significant effect on reducing plasma cholesterol and levels of triacylglycerols (22). The effect is thought to be related to the ability of P A to bind to zinc and thus lower the ratio of plasma zinc to copper which is known to dispose humans to cardiovascular disease (22). The effect may also be related to the ability of P A to reduce the plasma glucose and insulin concentrations which may, in turn, lead to reduced stimulus for hepatic lipid synthesis {21, 24).


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0 , H 0, LH 2

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Formation


Antioxidants

Free Radicals and Oxygen Radical Species Inactivation ^

, H 0 , 'OH, *0 , LOOH, L O \ L \ LOO* 2

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0 , H 0 , L-L, LOH 2

2

Effect Antioxidants

DNA

Protein

Lipids

Antioxidants

Tissue Damage (Cancer, Heart Disease, Cataract, Aging) Figure 1. Formation of free radicals, their effects, and neutralization by antioxidants.



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Another potential beneficial health effect of phytates relates to their protective influence against cancer. When P A was added to rat diet at 0.6-2.0%, a negative relationship was observed between P A concentration and the epithelial cell proliferation in the ascending and the descending colon (25). Furthermore, when P A was added at 1-2% in the drinking water, either one week prior or 2 to 21 weeks after the induction of carcinogen, a significant reduction in the number and size of tumors in the colon of test animals was noted (26, 27). Further details on the beneficial effects of P A on reducing carcinogenesis are provided by Thompson (4). The effect of P A in reducing cancer risk may be exerted by a number of mechanisms. P A may bind iron, a catalyst of lipid peroxidation, and thus may reduce formation offreeradicals and subsequently breakdown of cellular membranes which encourage cell proliferation (28). Alternatively, P A may bind to zinc which is required for D N A synthesis, thus reducing cell proliferation. Furthermore, P A may interact with bacterial enzymes such as (J-glucosidase and mucinase in the colon, therefore reducing the conversion of primary to secondary bile acids which are considered as promoters of tumorogenesis. Involvement of inositol phosphate, produced upon P A hydrolysis, also enhances the activity of the baseline killer cells (29) . Enzyme Inhibitors Protease inhibitors. Protease inhibitors are found in abundance in raw cereals and legumes. Due to their particular protein nature, protease inhibitors may be easily denatured by heat treatment. This class of compounds is abundant in raw cereals and legumes, especially soybean. Due to their particular protein nature, protease inhibitors may be easily denatured by heat processing although some residual activity may still remain in the commercially produced products (30). The antinutrient activity of protease inhibitors is associated with growth inhibition and pancreatic hypertrophy (30) . Trypsin inhibitors in soybean give rise to inactivation and loss of trypsin in the small intestine, thus trigger the release of cholecystokinin and induce pancreatic synthesis of excess trypsin and burden on sulfur-containing amino acids in requirement of the body (37). Potential beneficial effects of protease inhibitors remain unclear, although lower incidences of pancreatic cancer has been observed in populations where the intake of soybean and its products is high (32). This topic is thoroughly discussed in a later chapter. Amylase inhibitors. Amylase inhibitors are also very heat labile and have been reported as having hypoglycemic effects (33). However, instability of this inhibitor under the conditions of the gastrointestinal tract resulted in failure to reduce insulin responses and increase the caloric output of food by using them as starch blocker tablets (34). While protease inhibitors have been linked with pancreatic cancer in animal studies, they may also act as anticarcinogenic agents. The Bowman-Birk inhibitors derived from soybean have been shown to inhibit or prevent the development of chemically-induced cancer of the liver, lung, colon, oral and oesophagus (35-38).


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Saponins Saponins are made of a steroid (or triterpene) group attached to a sugar moiety. These surface-active compounds are found in legumes as well as certain spices and herbs. Saponins are able to lyse erthrocytes due to their interaction with cholesterol in the erythrocyte membrane (39, 40). Saponins, which have a bitter taste, are toxic in high concentrations and may also affect nutrient absorption by inhibition of metabolic and digestive enzymes as well as binding with nutrients such as zinc. Due to their strong surface activity, saponins are of interest for their beneficial biological effects. The hypocholesterolemic effect of saponins is quite strong, especially when fed in the presence of cholesterol (41-43). These topics are discussed in detail in later chapters. Lignans, Phytoestrogen and Other Related Compounds Lignans and phytoestrogens are present in higher plants including cereals, legumes, oilseeds, fruits and vegetables. Lignans are a group of diphenolic compounds with a dibenzylbutane backbone. This group of compound is also present in biological fluids in man and animals produced by the bacterial flora in the colon from plant precursors. Meanwhile, phytoestrogens are present mainly as isoflavones and the coumestans. The most abundant isoflavones are glycosides of genestein and diadzein the 4-methyl ether derivatives formononetin and Biochanin A. The important coumestans include coumestrol, 4 -methoxy coumestrol, sativol, tri-foliol and repensol. Dietary phytoestrogens may cause infertility and liver disease (44-46). Similarly, lignans are thought to have oestrogenic and antifertility effects, however, epidemiological data and biological properties of phytoestrogens and lignans suggest that they may serve as important compounds in the prevention and control of cancer, particularly the hormone-dependent ones. Therefore, vegetarians were found to have a higher urinary excretion of lignans and isoflavonic phytoestrogens than breast cancer patients and omnivores (47). Japanese women on traditional diets were found to have a lower risk of cancer and excreted 14% higher amounts of phytoestrogen than the Finnish women of high risk cancer (48). Strong support for anticarcinogenicity of phytoestrogen comes from studies which showed excellent relationship between cancer risk and soybean intake in the Japanese population as well as between soybean intake and urinary excretion of phytoestrogen (48). Induced mammary tumors by chemicals were also inhibited when soybeans were fed to test subjects (49). A reduction in cell proliferation as well as colon and mammary cancer risks was also observed when diets of rats were supplemented with flaxseed, a known source of mammalian lignan precursors (50-52). The exact mechanism by which these anticarcinogenic activities are exerted is not yet fully understood but several mechanisms have been postulated and detailed in the literature (46, 53-55).


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Lectins and Haemagglutinins Lectins and haemagglutinins are sugar-binding proteins which may bind and agglutinate red blood cells. They occur in most plant foods including those that are often consumed in the raw form (56). Although lectins in soybeans and peanuts are not toxic, thosefromjack beans, winged beans, kidney beans, mung beans, lima beans, and castor beans are all toxic when taken orally (57). The toxicity of lecins arises from their biding with the specific receptor sites on the epithelial cells of the intestinal mucosa with subsequent lesion and abnormal development of microvillae (57). The consumption of lectin-containing foods may lead to endogenous loss of nitrogen and protein utilization. The carbohydrates and proteins that are undigested and unabsorbed in the small intestines reach the colon where they are fermented by the bacterialflorato short-chain fatty acids and gases. These may in turn contribute to some of the gastrointestinal symptoms associated with the intake of raw beans or purified lectins. The lectin-induced disruption of the intestinal mucosa may allow entrance of the bacteria and their endotoxins to the blood stream and cause toxic response (58). Lectins may also be internalized directly and cause systemic effects such as increased protein catabolism and breakdown of stored fat and glycogen, and disturbance in mineral metabolism (57). Literature Cited 1.

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Atwal, A.; Eskin, N.; McDonald, B.; Vaisey-Genser, M. Nutr. Rep. Int. 1980, 21, 257-267. Thompson, L.U.; Sarraino, M. J. Agric. Food Chem. 1986, 34, 468-469. Reinhold, J.; Nasr, K.; Lahimgarzadeh, A.; Hedayati, H. Lancet, 1973, 1, 283-288. Yoon, J.H.; Thompson, L.U.; Jenkins, D.J.A. Am. J. Clin. Nutr. 1983, 38, 835-842. Thompson, L.U.; Button, C.L.; Jenkins, D.J.A. Am. J. Clin. Nutr. 1987, 38, 481-488. Thompson, L.U. Food Technol. 1988, 42 (4), 123-132. Jariwalls, R.J.; Sabin, R.; Lawson, S.; Herman, Z.S. J. Appl. Nutr. 1990, 42, 18-28. Klevay, L.M. Nutr. Rep. Int. 1977, 15, 587-593. Nielson, B.K.; Thomson, L.U.; Bird, R.P. Cancer Lett. 1987, 37, 317-325. Wolever, T.M.S. World Res. Nutr. Diet. 1990, 62, 120-125. Shamsuddin, A.M.; Elsayed, A.M.; Ullah, A. Carcinogenesis 1988, 9, 577580. Shamsuddin, A.M.; Ullah, A.; Chakvarthy, A. Carcinogenesis 1989, 10, 1461-1463. Fraf, E.; Eaton, J.W. Free Rad. Biol. Med. 1990, 8, 61-69. Baten, A.; Ullah, A.; Tomazic, V.J.; Shamsuddin, A.M. Carcinogenesis 1989, 10, 1595-1599. Hathcock, J.N. In Nutrient and Toxicological Consequences of Food Processing, Friedman, M., Ed.; Plenum Press: New York, USA, 1991, pp. 273-279. Liener, I.E.; Kakade, M.L. In Toxic Constituents ofPlant Foodstuffs; Liener, I.E., Ed.; Academic Press: New York, 1980, pp. 7-71. Kennedy, A.R.; Billings, P.C. In Anticarcinogenesis and Radiation Protection, Corutti, P.A.; Nygerard, D.F.; Simic, M.G., Eds.; Plenum Press: New York, USA, 1987, pp. 285-295. Plus, W.; Kemp, N. Diabeblogia 1973, 9, 97-101. Carlson, G.L.; Li, B., Ban, P.; Olsen, W. Science 1983, 219, 393-399. St. Clair, W.H.; Billings, PC.; Kennedy, A.R. Cancer Lett. 1990, 52, 145152. Witschi, H.; Kennedy, A.R. Carcinogenesis 1989, 10, 2275-2277. Messachi, D.V.; Billings, P.; Shklar, G.; Kennedy, A.R. J. Nat. Cancer Inst. 1986, 76, 447-452. Messina, M.; Barnes, S. J. Nat. Cancer Inst. 1991, 83, 541-546. Birk, Y ; Peri, I. In Toxic Constituents of Plant Foodstuffs; Liener, I.E., Ed.; Academic Press: New York, USA, 1980, pp. 161-182. Scott, M.T.; Gross-Sampson, M.; Bomford, R. 1985. Int. Arch. Allergy, Appl. Immunol. 1985, 77, 409-412. Gestener, B.; Assa, Y.; Henis, Y.; Tencer, Y.; Royman, M.; Birk, Y.; Bondi, A. Biochem. Biophys. Acta 1972, 270, 181-187. Sidhu, G.S.; Oakenful, D.G. Br. J. Nutr. 1986, 55, 643-649.


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Antinutrients and Phytochemicals in Food - American Chemical Society

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