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10. Endogenous and exogenous feed toxins

Feedstuffs incorporated in compounded feeds are known to contain a wide variety of toxicants that are endogenous (Table-10) or exogenous in nature and adversely affect the production of egg and meat. Amelioration of these toxicants is absolutely necessary to warrant the health and profitable poultry production. The feed based toxins concerned in poultry feeding are divided into the following groups:

(A) Endogenous toxicants

   

i)

Proteins

-

Haemagglutinns (lectins) and Protease inhibitors

ii)

Glucosides

-

Cyanogenes, Estrogens, Goitrogens and Saponins

iii)

Phenols

-

Gossypol and Tannins

iv)

Others

-

Aliphatic nitro compounds, Anti-vitamins, Erucic acid and other fatty acids, Non-starch polysaccharides, Oxalates and Phytates

(B) Exogenous toxicants

-

Mycotoxins, Argemone, Insecticides and Pesticides

PROTEINS

Protease inhibitors: These are widely distributed in plant kingdom, particularly, the legumes. Raw soybean seeds contain trypsin inhibitors, that cause growth inhibition, hypertrophy of pancreas followed by a stimulation of its secretory activity. These also result in an endogenous loss of the pancreatic enzymes, trypsin and chymotrypsin which are rich in the sulphur-containing amino acids, and thus accentuating the deficiency of methionine, being the first limiting amino acid in soybean.

The soybean has received the most attention with respect to the effect of heat treatment on its trypsin inhibitory activity. Trypsin inhibitor activity of solvent-extracted soybean meal has been reported to be destroyed by exposure to flowing steam for 60 min. or by autoclaving under 5Lb/in2 for 45 min, 10 Lb/in2 for 30 min, 15 Lb/in2 for 20 min. or 20 Lb/in2 for 10 min. Regardless of moisture content (5 and 19%), atmospheric steaming (100C) destroys 95% of trypsin inhibitor content of dehulled and defatted raw soybean flakes within 15 min and protein efficiency is higher at 19% than 5% moisture level.

Phytohaemagglutinins (lectins): Phytohaemagglutinins, present in legume seeds, exhibit the unique phenomenon of being able to combine with glycoprotein component of cell membrane and in case of Red Blood Cells, this is accompanied by haemagglutination, occurs only if the lectin molecule has at least two active groups. Another effect of lectins is a non-specific interference with the absorption of nutrients like protein. This is attributable to the attachment of the lectins to the cells lining of the intestinal wall resulting in disorganization of the main absorption cells. Lectins are among toxic principles responsible for poor growth. Dry heat is not effective in elimination of this toxic component but soaking and cooking is helpful.

Some of phytohaemgglutinins are extremely toxic, such as ricin from castor bean; others, such as kidney beans. Reports of studies on castor meal suggest that autoclaving (1.055 kg/cm2 at 122.2C for 30 min) or water-cooking (addition of caster meal in boiling water 1: 5 w/v and heating for 30 min) reduces the heamagglutinating activity considerably in meal (from 160 to 20 HA unit) when compared with other processing methods viz. water soaking (submerged completely in water 1: 10 w/v and left overnight with stirring, 40 HA unit), ammoniation (addition of 6 M ammonium hydroxide to raw caster 1: 4 w/v and hot air oven drying at 80C for 45 min, 40 HA unit) and hexane extraction (hexaneextraction for 6 hrs, 80 HA unit). These stud is also suggest that castor meal processed either by autoclaving or cooking with water can be included as protein source in broiler diets up to 2.5% level without adversely affecting the performance and general health status of birds.

GLUCOSIDES

Goitrogens: Goitrogenic agents are found in seeds of rape and mustard. The use of these meals has been restricted due to the presence of thioglucosides or glucosinolates, which, upon hydrolysis, release products (2-OH-3 butenyl isothiocynate and 5 -Vinyloxazolidinine-2-thione- goitroin), which are goiterogenic and growth depressant. The predominant glucosinolate of rape and mustard is progoitrinin, which is a deleterious factor. Such goitrogens at dietary levels of 0.03 to 0.42% do not cause any apparent affect on performance or goitrogenicity in chicks. However, glucosinolates may be removed from meal by extraction with hot water, dilute alkali or acetone or decomposed with iron salts or soda ash. The goitrogenic products may be removed by extraction with acetone or water or by steam stripping of volatile isothiocynates.

Cyanogens: Intact glucosides are not toxic, but become toxic when they are hydrolyzed to release free HCN. The enzymes, the glucosidases, when active in plant tissue, may release HCN byautolysis, which is enhanced by moisture. However, in general spontaneous release of HCN from plant depends on the presence of specific glucosidase and water. Auto hydrolysis is enhanced, if plant is soaked in water after crushing. Crushing without soaking, however, will lead to slow release of HCN and it is well recognized that bruised cassava root is not suitable for consumption. A satisfactory method of HCN extraction involves closed steam distillation with hydrochloric acid at 100C for at least three hours. In general, feed ingredients containing cyanogens can be processed by cooking, followed by discard of cooking water or fermented or boiled then dried.

Table 10. Endogenous toxic factors in feeds of plant origin.

Feedstuffs

Toxic factors

Raw soyabean and its meal

Trypsin inhibitor, phytohaemagglutinin, antigens, lipoxygenase, goiterogen, saponin, estrogen, phytic-acid and oligosaccharides (NSPs – 30.3%)

Groundnut and its meal

Trypsin inhibitor, goiterogen, tannins, oligosaccharides and lectins

Mustard or rape seed and its meal

Goiterogens (thioglucosides or glucosinolates), tannic acid, erucic acid, sinapine (cholinester), pectins and oligosaccharides (NSPs - 46.1 %)

Safflower seed and its meal

Estrogenic factor, Two phenolic glucosides (Bitter flavour) and Fibre

Sunflower seed and its meal

Chlorogenic, quinic-acid and Fibre (Tannin like compounds)

Sesame seed and its cake

Phytate (5g/100g) and Oxalates (35 mg/100g)

Linseed and its cake

Linamarin (cyanogenic glucoside), antipyridoxine (Linatin) factor and mucilage (HCN Level → 10-300 mg)

Kapok seed meal (seeds of silk cotton tree)

Tannins, tyrosine and fattyacids with cyclopropene rings

Copra meal (coconut meal)

Fibre (mannans) and Estrogenic factor

Palm kernel meal

Fibre (half of the fibre–NDF high levels of galactomannans β-(1,4)-D mannans) and Sharp shells

Cotton seed and its meals

Gossypol (phenol like compound), cyclopropenoid fatty acids, tannins

Cotton seed and its meals

Gossypol (phenol like compounds) cyclopropenoid fatty acids, tannins

Guar meal (Cyamopsis tetragonoloba)

Guar gum (18-20%), antitrypsin factor and antivitamin E factor

Castor seed and its meal

Ricin (toxalbumin)-Phytohaemagglutinin

Ricinine (Toxic-alkaloid)

Ricinus allergen(Protein Polysaccharide)

Neem seed and its meal (Azadirachta indica)

Bitterness → Limonoids → Triterpenoids

Bitter principles: Protomeliacins, Limonoids, Azadirone, Gedunin, Vilasinin and Secomeliacins

Nonisoprenoid polypenolics-Flavanoids, Tannins and coumarin viz. Nimbin, Salannin and Azadirachtin

Dried seeds – limonoids – 0.001 to 0.1%, Azadirone, 0.45% and Epoxy Azadirone, 0.72%, Azadiradione, 0.7% and Salanin, 0.95%

Mahua cake (Madhuca latifolia)

Mowrin (Saponin) and Tannins

Karanja cake (Pongamia glabra)

Fat bound toxic factors – Karajnjin and Pongamol (Flavanoids) (NSPs – 38%)

Lupin meal

Quinolizidine alkaloids, pectins, oligosaccharides, high manganese, saponin.

Peas

Protease inhibitors, tannins, Lipoxygenase and lectins

Rubber seed meal

Hydrocyanic-acid (20-40mg/kg)

Maize

Selenoamino acids (seleniferous)

Estrogen (mouldy)

Trypsin inhibitor

Wheat

Tyramine, Trypsin-inhibitor, NSPs (11.4%)

Rice

Estrogen and haemagglutinins

Rye

Amylase and protease inhibitor and NSPs (13.2%)

Oats

Amylase inhibitor and estrogens

Triticale

Trypsin and chymotrypsin inhibitor (NSPs)

Some varieties of barley

β - glucan (NSPs – 16.7%)

Some varieties of sorghum

Tannins

Rice-polish and rice bran

Trypsin inhibitor and antithiamine factor

Chunies

Antitryptic factor

Sal seed and its meal

Tannic – acid (tannins)

Tapioca meal (Cassava)

Cyanogenic glucoside (HCN – 1000 – 3000 mg/kg DM)

Fish meal and meat meal (prepared from spoiled or putrefied material)

Gizzerosine and histamine (Biogenic amines)

The main cause of HCN toxicity is the inhibition of cytochrome oxidase, the cell respiration-regulating enzyme. The level of HCN lethal to living organisms is in the range of several milligrams/kg body weights and death occurs with in a few seconds. The signs of HCN poisoning are nervousness, abnormal respiration, trembling, blue colouration of mucous membranes, staggering and convulsions.

Saponins: Most of the biological activities of saponins arise from the surface activity and their ability to form complexes with sterols and proteins. In view of the ability to form stable complexes with cholesterol, it has been found possible to reduce liver and serum cholesterol by using dietary saponins.

Approximately 20% alfalfa in chick ration (equivalent to 0.37% saponin) depresses the growth rate. However, the growth of quails remains unaffected by 2% alfalfa top saponins but by 5% alfalfa root saponins depress growth. Saponins can be extracted with hot water followed extraction with ethanol or methanol.

Estrogens: A number of isoflavones having estrogenic activity have been reported to be present in soybeans. One of these genistein (4, 5, 7-trihydro-xyisoflavone), in addition to estrogenic activity can cause growth inhibition, elevated levels of zinc in the Iiver and bones and increased deposition of calcium, phosphorus, manganese in bones. Solvent extracted soybeans do not contain sufficient amount of estrogen to cause any adverse effect in chickens. Dry or moist heat treatment or solvent extraction can achieve inactivation of estrogens.

PHENOLS

Gossypol: Gossypol is phenol like compound (polyphenolic binaphthalene derivative) indentified in cottonseeds, its meal and oil. More than 0.06% free gossypol in the diet depresses growth in chicks. The depression is severe when the level increases to 1.2%. In laying hens, 0.024% reduces egg production and hatchability. A comparatively low level of gossypol (more than 0.005%) in the diet causes an olive green discoloration of the yolk. Dietary levels of 0.015% or less free gossypol is believed to be safe when cotton seed meal is used as protein supplement in balanced diet of poultry.

The cake after hydraulic pressing, screw pressing and solvent extraction, contains 0.04-0.1%, 0.02-0.05% and 0.02-0.03% free gossypol, respectively. The heat generated during the commercial production of cotton seed meal helps to bind 80 to 90% gossypol with protein rendering it non-toxic. Higher levels of gossypol can be tolerated, if iron salts are added to diet @ 1 to 2 ppm iron for every 1 ppm of free gossypol. Solid substrate fermentation involving certain fungi is capable of reducing 90% of free gossypol of cottonseed and eliminating its toxicity in chicks.

Tannins: Another group of phenolic compounds is termed as tannins and is widely distributed in nature. Rapeseed or mustard residue appears to contain 2.85 to 3.7% tannins. The published reports reveal a wide variation (3.5 to 13.3%) in the tannin contents in deoiled salseed meals. The tannin content of sorghum grain may range from 0.25 to 2.5%. Tannins at 0.5% level and above in diet cause reduction in growth and available energy value of feed, decreased availability of protein and severe mortality at higher levels (4% and above). They also inhibit enzyme activities (trypsin, amylase and lipase) or enzyme systems.

Attempts have been also made for removal of tannins from deoiled salseed meal. These methods include cold water processing, boil water processing, treatment with acids 0.1 N, HCI (1:10 w/v), 2.5% HCI), alkalies (0.01 N, NaOH, 0.1 N, NaHCO3, 0.05-5% Ca(OH)2), Salt (3% NaCI), extraction with either acetone (30%) or ethanol (4%) or methanol and autoclaving with tannin removal of 36-58, 42-80, 13-65, 12-68, 43-57, 41-49, 31-100, 38-53, 63-72, 33-38 and 17-100%, respectively.

OTHER ENDOGENOUS TOXICANTS

Erucic acid and other fatty acids: Erucic acid appears to be a major factor affecting the utilization of mustard oil cake or rapeseed meal by poultry. Solvent-extracted mustard oil cake might be useful substitute to groundnut oil cake, if diets are otherwise comparable. Residual oil present in these meals contains about 40-50% erucic acid.

A diet constraining 0.6% erucic acid (as contained in 10% mustard oil cake) does not cause any adverse effect on performance of birds. However, erucic acid at levels beyond 0.605% in diet is known to cause growth depression, reduction in feed intake and efficiency in growing chicks.

Polyenoic fatty acids present in the fish oil impart fishy flavour to meat and eggs. A level of 4% of these marine polyenoic fatty acids in carcass fat is sufficient for detection of off flavours.

Non-starch polysaccharides (NSP): Cereal grains are very rich in carbohydrates including sugars, starch and cell wall polysaccharides. The use of many cereals (oats, barley, bajra, ragi etc.) is limited in poultry because of the presence of non-starch polysaccharides. Poultry birds lack enzymes needed to digest -Iinkages of -glucans present in barley and oats and pentosans of rye, wheat and triticale which limit their utilization. Efforts have been made to render such substances to advantage through processing which include water soaking to mobilize native enzymes to action, application of heat and milling to expose cell wall contents and enzyme supplementation to hydrolyze the substrate or development of non-waxy cultivars to contain less or negligible soluble -glucans or pentosans. Water treatment also removes water soluble NSP of the cereal. In enzyme supplementation, hydrolysis of pentosans and -glucans into simpler polymers, alter the ability of these polysac- charides to form highly viscous solutions, which inhibit nutrient diffusion and transport and thus improve their utilization. Other methods like gamma irradiation, acid treatment and milling are also reported to increase utilization of cereals.

Phytates: Phytates (salts of phytic acid), are formed due to combination of six phosphate molecule with inositol, a cyclic alcohol with six hydroxy radicals similar to hexose sugar. The availability of phytin P is influenced by alimentary tract pH and the level of vitamin D3, calcium, Ca to P ratio and Zn. Supplementation with adequate minerals, which are affected by phytates, is usually practiced. At present, dietary supplementation of phytase enzyme (250-500 units/kg) is practiced to enhance the utilization of phytate P in poultry. Autoclaving soya bean meal can reverse the increased requirement of metals. Cottonseed meal can be treated with phytase enzyme prepared from (Aspergillus ficcum or niger). In both, vegetable and animal kingdom oxalic acid is found as free and in salt form.

Antivitamins: Raw soybean contains an enzyme Iypoxygenase which catalyses oxidation of carotene, the precursor of vitamin A and can be destroyed by heating soybeans for 15 min at atmospheric pressure. Autoclaving of soybean protein or supplementation with vitamin D3 for about 8-10 times can eliminate the rachitogenic activity. Raw kidney beans contain anti-vitamin E activity that is eliminated by autoclaving. The dicumarol in sweet clover produces severe hemorrhages due to reduced prothrombin levels in the blood interfering with the blood clotting mechanism. The effect is due to the reduction of vitamin K utilization needed for the production of prothrombin in liver. An antagonist of pyridoxine from linseed has been identified as 1-amino-D proline and occurs naturally in combination with glutamic acid as a peptide, which is known as linatine. The nutritive value of linseed meal for chicks can be considerably improved after extracting the meal with water and autoclaving and supplementing with pyridoxine hydrochloride.

EXOGENOUS TOXICANTS

Mycotoxins: Some of the important mycotoxins are aflatoxins, Ochratoxin A, T-2 toxin, rubratoxin B and citrin. Aflatoxin B1 is most pathogenic to poultry as compared to other aflatoxins viz. B2, G1 and G2. Aflatoxin toxicity (aflatoxicosis) has been reported to cause serious health hazard to poultry and other avian species. Aflatoxicosis in chicken is characterized by listlessness, anorexia, poor pigmentation, jaundice and dehydration of combs and shanks. Sensitivity or resistance to aflatoxins is inherited as distinctive characteristics of breed and strain. The adverse effect of aflatoxins on performance of chicken is also dose and time related. This toxin is primarily a hepatotoxin in young broiler chicken. One effect that is used as a diagnosis of aflatoxicosis in poultry is an enlarged, fatty, yellow and friable liver that occurs in broilers when they consume aflatoxins contaminated feed. This mycotoxin is also a nephrotoxin and some kidney pathology does results during aflatoxicosis. Aflatoxins affect the commercial poultry production in many ways: (a) reduce body weight gain; (b) make birds more susceptible to brushing; (c) decrease egg production, egg weight and hatchability; (d) suppress the immune system of poultry making them more susceptible to diseases; (e) disrupt bone development causing a rachitic type problem and (f) can cause nutritional problems through its effect on nutrient absorption and metabolism.

Aflatoxin inhibits fat digestion with a consequent streatorrhoea by decreasing enzymes and bile acids resulting into high faecal fat and liver fat content. Aflatoxin causes reduction in nutrient retention, changes in haematological values and bio-chemical parameters. This toxin causes low or heavy mortality depending upon level and duration of intake of contaminated feed. Reduction in size of bursa of Fabricious is observed in growing chicks during aflatoxicosis.

Ochratoxin A is primarily a nephrotoxin in poultry but it does have some secondary hepatotoxicity. The major diagnostic lesion of this mycotoxin is pale and enlarged kidneys. Ochratoxin like aflatoxin can affect poultry in number of ways: it i) depresses growth of poultry; ii) acts as an immuno-suppressant making birds more susceptible to diseases and brushing and iii) can affect nutrient absorption and metabolism. It is important to note that ochratoxin is three times more toxic than aflatoxins to broiler chicken. This toxin is produced by certain Pencillium (P.Verrucosum) and Aspergillus (A.Ochraceus and A.alutaceus) species. It has been implicated in total human disease Balkan Endemic Nephropathy.

T-2 toxin is produced by fungus Fusarium tricincutum. T-2 toxin is another mycotoxin that can produce severe adverse effects on broiler chicken. T-2 toxin is a radiomimetic toxin, which means that the toxicity of T-2 toxin is very similar to the effects of radiation. The principle presumptive lesion caused by T-2 toxin is a crusty lesion in the mouth of poultry on lower and upper mandible. T-2 toxin can limit poultry production by a number of methods: 1) decreasing body weight, 2) acting as immuno-suppressant and 3) altering nutrient absorption and causing nutritional disease.

Rubratoxin B causes reduction in growth, atrophy of bursa hypertrophy of liver. Tremortirn A affects central nervous system and causes tremors. One of the symptoms of citrinin toxicity in poultry is a dramatic increase in the amount of water consumed and excreted which helps in diagnosing its toxicosis.

There are a number of ways in which feeds can become multiple mycotoxin contaminated. Several analytical laboratories have found that most mycotoxin contaminated samples contain more than just a single mycotoxin. When aflatoxin and Ochratoxin are co-contaminants of poultry feed, these interact in a synergistic manner. During dual exposure of these toxins, ochratoxin prevents the major effect of aflatoxin (i.e. fatty, yellow, enlarged and friable liver). This confuses the ability to diagnose aflatoxicosis in the field. The target organ in this interaction appears to be the kidney. Citrinin is a nephrotoxin similar to ochratoxin and is produced by some of the fungi that also produce ochratoxin. The interaction is characterized as antagonistic. During co-toxicity ochratoxin prevents the very important diagnostic index of citrinin (increase in the amount of water consumption and excretion) which would make it very difficult to diagnose citrinin in the field based upon symptoms, if ochratoxin was also a contaminant. Aflatoxin and T2 toxin combination is like interaction between aflatoxin and ochratoxin and exhibit synergistic toxicity. The tolerance level of aflatoxin B1, dietary additive to protect broilers from aflatoxin B1 toxicity and physico- chemical treatments for inactivation of preformed aflatoxin B1 in feeds have been depicted in Tables 7, 8 and 9.

Table 7. Tolerance levels (ppb) of dietary aflatoxin in different poultry birds.

Cross-bred broilers

-

400

Pure bred broiler chicks

-

200

White Leghorn chicks

-

150

Quail chicks

-

300

Quail layers

-

300

Guinea fowl keets

-

1500

Layers

-

600

Table 8. Dietary additives and their dietary inclusion levels for protection to broilers against dietary aflatoxins

Detoxifying agents

g/qtl. Feed

Activated charcoal

100 - 200

Hydrated sodium calcium aluminosilicate (HSCAS)

100 - 200

Esterified glucomannan (EGM)

50 - 100

Herbal mixture (Acacia catechu. 25%, Phyllanthus niruri, 400%, Andrographis paniculata, 25%, base 10%)

50 - 75

Butylated hydroxyanisole

50 - 100

Dl-methionine*

100 - 200

Selenium**

0.200 - 0.300

Butylated hydroxy toluene*

50 -150

L-lysine HCI

150

Water soluble vitamins*

Double of the requirements

Increase the dietary protein level

Upto 26 to 28%

*Growth sparing effect.

**Alleviation of toxicity due to low levels of aflatoxins; growth and mortality effects at higher levels of aflatoxins.

Table 9. The physico-chemical treatments for inactivation of preformed aflatoxins in contaminated maize and groundnut cake.

i.

Raising the moisture level upto 20%. Autoclaving at 5 PSI for one hour followed by drying in an oven at 80C.

ii.

Adding sodium hydroxide (15 g/kg) and mixing. Raising the moisture content upto 20%, autoclaving at 5 PSI for one hour and drying in an oven.

iii.

Agitation of one kilogram of feedstuff with 20 g Ca(OH)2 followed by addition and mixing of formaldehyde to raise the moisture content upto 15%. Autoclaving at 15 PSI for an hour and drying.

iv.

Addition of liquor ammonia to yield 6% concentration. Raising of moisture content upto 20%. Storing airtight for 20 days. Heating at 35C and drying in an oven.

Pesticides and other industrial chemicals: Pesticide/insecticide residues also pose a health hazard to livestock including poultry. These compounds of diverse chemical nature may be categorized into (a) the chlorinated hydrocarbon i.e. organochlorine (OC), such as DDT, BHC, aldrin, endrin, dieldrin, methoxychlor, chlordane, texaphene, mirex, etc., which are of persistent nature but harmless, if used correctly; (b) the organophosphorus compounds (OP), such as parathion, malathion, sumithion, dimelthoate, diazinon, etc.; (c) the carbonate compounds, such as carbaryl, pyrolan, etc. and (d) the synthetic pyrethroids, such as permehrin, cypermethrin, deltamehrin, allethrin, fenvalerate, etc.

The organochlorine insecticides are much less toxic and yet are dangerous because of their persistence and cumulative character in the body tissues. The poultry and other livestock products, viz. milk, meat, eggs obtained from the animals and birds, which are being exposed to the residues of such persistent insecticides, could be also harmful for human consumers.

Acute oral LD50 of malathion has been reported to be 524.80 mg/kg body weight for desi poultry birds. Exposure to some organophosphorus esters causes organophosphorus -induced delayed neurotoxicity (OPIDN) in adult poultry characterized by degeneration of axons and followed by myelin in the peripheral and central nervous systems.

DDT, sprayed on litters, feeders, roofs or nests in poultry houses, could be detected in the fatty tissues of birds and eggs within the same week. Feeding of the measured doses of DDT at 15 ppm level causes no detrimental effect on egg production although residual DDT persisted in egg yolk and abdominal fat as long as 17 and 13 weeks. No significant level of the residue could be detected in eggs at a feeding level of 0.1 - 0.15 ppm. A build up of 0.05 ppm residue in 7 days and 0.14 ppm in 8 weeks in eggs could be detected on a diet containing less than 0.1 ppm DDT. Fertility, hatchability of eggs or progressive growth was not significantly affected even at 5, 15 and 50 ppm levels in the diet.

Exposure of laying hens to technical DDT at a level of 100 ppm for 40-50 days was found to cause disorders in eggshell formation reducing its thickness and strength. Sperm production could be greatly reduced by incorporating 0.1 - 0.3% DDT is diet of domestic fowl. Broilers may retain more residues since they are forming new tissues rapidly and their feed consumption is also higher. A recent report on the effect of dietary fenvalerate (FEN) and methyl parathion (MPA) in broilers revealed that FEN and MPA adversely affected the performance beyond dietary levels of 100 ppm and 25 ppm, respectively. Zeolite + activated charcoal (13.75:1) at rate of 2 kg/ton had a beneficial role in protecting birds from lower levels of insecticidal toxicity.

Argemone contamination: Argemona maxicana is a yellow flowered poppy belonging to the family Papaveraceae and genera, Argemona. Due to its high oil content and cheap availability seeds are used as adulterant with mustard seed and its cake in oil extraction. The toxic effect of this was identified as back as 1910 wherein odema was noticed in human beings. It also caused glaucoma, cancer, swelling of leg, diarrhoea, increased intraoccular tension and atrophy of optic nerve in animals including chickens. However, it has been observed that heating of this oil to 240C for 15 minutes makes innocuous.

The feed ingredients must be processed properly before incorporating in poultry diets. Incorporation of non-conventional feed ingredients in diets has been possible only due to the development of suitable technologies to eliminate the most toxic factors. Now suitable processing techniques to detoxify "potential" feed ingredients have to be developed so that full nutritional potential may be exploited. Better processing methods are required for improving the nutritive value or maximizing the utilization of conventional feeds in poultry. Mycotoxins and pesticides contaminating poultry feed pose a great risk to poultry industry .It is important that toxic hazards of such residues are understood and necessary control measures should be practiced.

Future strategies for undertaking poultry nutrition research

Research in poultry nutrition in future will be governed by many factors viz. consumer’s demand for egg and meat with desirable characteristics such as types and content of fatty acids, increased antioxidant content of products to improve quality and shelf-life and use of additives to enhance nutrients availability and alleviation of anti-nutritional factors. Thus, nutrition research has to be diverted towards optimization of meat and egg production, dietary manipulation for quality eggs and meat, interaction between nutrition and health, feed processing, search for newer feedstuffs and use of genetically modify food grains, oilseeds and their byproducts.

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