Minerals in this group include calcium, phosphorus, magnesium, potassium, sodium, chlorine and sulfur.
Ca and P, which make up 70% of the total amount of minerals in the body, are usually examined together. 99% of Ca and 80% of P in the organism are found in bones and teeth. Major absorption of calcium takes place in the duodenum. It is under the influence of factors such as absorption and form of Ca, content pH, vitamin D, Ca/P ratio, excessive intake of other minerals (Fe, Al, Mn), excess fat in the ration. When Ca is insufficient in the diet, most of the absorbed mineral is actively transported. In other words, in animals, Ca is absorbed from the intestines as needed. Absorption efficiency varies according to the need. A significant part of the absorbed Ca is excreted in the urine and stool. Calcium, along with phosphorus, participates in the formation of bones and teeth. Since the amount of Ca in the bones of newborn animals is limited, a significant amount of Ca is needed for the development and calcification of bones during development. Calcium also has duties in vital metabolic events. Controlling the blood Ca level by the hormones secreted from the parathyroid and adrenal glands is an indicator of physiological importance. When the mineral is needed, it is used from the stores in the bones. When the Ca level in the blood rises, the excess mineral accumulates in the stores to be used when needed. In addition, some of it is excreted through the kidney or with the stool. Ca and P are critical minerals required in rations for growth, egg and milk production. Ca is also needed for the elimination of bone disorders. Egg and milk production requires significant amounts of Ca. When chickens are fed with Ca below their needs, they produce thin and soft-shelled eggs. As long as there is insufficient Ca in the rations, the total egg and reproductive efficiency decreases. Cows react to this situation by reducing their milk yield. One of the main functions of Blood Ca is to regulate the heartbeat. P, Na, K, Mg and some of the other minerals are also effective in determining the rate of heartbeat. An increase in blood Ca level causes the heartbeat to accelerate. This mineral also plays a role in controlling muscle and nerve impulses. As the Ca-ion concentration increases, muscle and nerve stimulations decrease. Calcium also has a function in blood coagulation. The most obvious consequences of calcium and P deficiencies are observed in bone development. In the absence of these minerals, bones continue to develop; however, it cannot gain hardness due to insufficient calcification. As a result, rickets, which are characterized by visible bone disorder, occur in the young and osteomalacia in the elderly. This phenomenon also occurs in vitamin D deficiency, which is necessary for Ca and P metabolism. In animals exposed to rickets, the joints are enlarged in the long bones. Gait disturbance is inevitable as there is swelling in the joints. Inadequate intake of Ca in chickens causes significant reductions in egg production and quality, and skeletal disorders. At the same time, feed consumption and feed efficiency are adversely affected by this situation. In case of excessive consumption, excess Ca accumulates in soft tissues as well as bones. The amounts of the mineral above the need cause the deterioration of P, Mg, Zn metabolism. Likewise, Co, Mn, Fe and I are also affected by this situation. In ruminants that consume legume roughage in free amounts, a part of their Ca need can be met, along with the survival rate. The addition of Ca to the rations is obligatory in poultry fed with mixed feed. In carnivores that feed on bone and meat, all the need for Ca can be met. On the other hand, cats and dogs fed bone-free diets should be given appropriate Ca sources. Limestone, DCP, fluorinated phosphate, mussel shell are Ca sources that can be used in animal feeding.
Phosphorus, which is sensitive to many factors affecting the absorption of calcium, can be absorbed in organic and inorganic forms. The source of P used, intestinal pH, age of the animal, other minerals (Ca, Fe, Al, Mn, K and Mg) taken with the feed are the main factors affecting the absorption. Since P found in plant sources is in the form of phytic acid, the degree of benefit of poultry from it is very low. P, which is effective on bone formation and metabolism together with calcium, also has specific functions in the body. It is involved in keeping the blood Ca level at optimal limits, in carbohydrate metabolism, in the structure of phosphoproteins that provide cell membrane permeability with nucleic acids, and energy-rich phosphates such as hexophosphate, adenophosphate, and creatine phosphate. It also enters the structure of phospholipids, which are vital for the transport and metabolism of fats and cell membranes. It functions in energy metabolism. They are components of RNA and DNA that are necessary for cell formation and therefore play a role in protein synthesis. Apart from this, it is also included in the structure of various enzymes. P deficiency is a common problem for animals of all kinds in every region of the world. The first sign of this mineral deficiency is a general symptom of decreased appetite. Loss of appetite, weakening and death in laying hens occur within 10-12 days following severe deficiency. In cases of moderate disability, there is rickets and growth retardation. The problems that occur in the bones as a result of this mineral deficiency are similar to the symptoms due to Ca deficiency. Likewise, reductions in egg production and quality are observed. Depending on its role in the metabolism of nutrients, P deficiency causes reductions in all kinds of yield performance, including fertility, and general condition disorders. In cases where phosphorus is taken insufficiently, urinary tract disorders, pica cases, which are characterized by ingestion of non-feed materials such as wood, bone and sacks in ruminants, occur. With the limitation of microbial activity, cellulose digestion decreases, protein and RNA synthesis decreases. Excessive consumption of this mineral reduces the absorption of various nutrients, especially Ca. On the contrary, the absorption of P decreases in excess intake of Ca and Mg. Vitamin D is necessary for the evaluation of phosphorus. For the effective use of both Ca and P, there must be an appropriate ratio between the two minerals. If P is taken more than calcium, urinary tract stones are formed, especially in ruminants. It is obligatory to add P to the rations both in poultry and monogastric animals that cannot benefit from plant-based phosphorus sufficiently and in ruminants fed with roughage based rations. Feeds generally contain P in certain proportions. Phosphorus content of roughage depends on the mineral status of the soil. Cereal grain feeds, milling by-products, all protein feeds, especially animal origin, are rich in P. Clean disease-free bone meal, fluorinated phosphate rocks, especially dicalcium phosphate (DCP) are suitable P sources.
Ca/P ratio and vitamin D: Three factors are effective in the optimum evaluation of Ca and P in animals. These:
1) Providing minerals in evaluable form and in appropriate amounts, 2) Finding the appropriate ratio between both minerals, 3) Providing adequate amounts of vitamin D, which regulates the metabolism of both minerals. Along with Vitamin D, calcitonin and parathormone are involved in the metabolism of both minerals. These are effective in maintaining normal levels of Ca and P in the blood. The Ca/P ratio is generally recommended as 1-2/1. However, in animals other than ruminants, a ratio between 1/1 and 2/1 is acceptable. This ratio for laying hens is 3.5-4/1; It is reported that it can be between 1/1 and 7/1 in ruminants.
Half of the magnesium (Mg) found in many tissues in the body is in the bones, and the other half is in the soft tissues and body fluids. Mg performs its function in bone formation together with Ca. Absorption of this mineral occurs through the digestive tract. Especially the small intestine is the most suitable place for absorption. The higher the amount of Mg in the diet, the lower the absorption. High levels of Ca and P in the feed adversely affect the absorption of minerals. In particular, P forms insoluble salts with Mg. It has been reported that animal fats increase the Mg requirement in chicks, and the addition of high fatty acids reduces the absorption of the mineral in dairy cows. When Ca and P levels are increased in the diet, the amount of Mg should also be increased. Mg has many physiological functions. Mg in the skeleton participates in the formation of bones and teeth. Mg is the second element found in intracellular fluids. Therefore, it is an essential mineral for cell metabolism. Approximately 1% of the total mineral is found extracellularly. Oxidative phosphorylation is significantly reduced in the deficiency of Mg, which acts as an active component of many enzymes. Magnesium plays a role in carbohydrate and lipid metabolism as well as in protein synthesis. Symptoms such as delayed growth, hypersensitivity, tetany, peripheral vasodilation, decreased appetite, and muscle coordination disorder are the obvious consequences of Mg deficiency. Diets generally contain Mg at the level required for optimal growth. This is an exception for grazing ruminants and especially for adult dairy cows. They are sensitive to Mg deficiency. In the case called meadow (grass) tetany, which is a result of Mg deficiency, the blood mineral level, normally 2.5 mg/100 ml, drops rapidly. On the other hand, there is no literature finding on this mineral excess. However, intravenous injections of Mg salts cause cardiac disorders that result in death. Most of the feeds contain Mg to meet the needs of animals. However, certain amounts of Mg are added to mineral mixtures in order to secure the need. 15% of Mg in the structure of roughage and 30-40% of that in grains and concentrates can be used. Unlike most minerals, the amount of Mg increases as the plant ages. Fertilizing with excessive N and K affects negatively. Magnesium oxide and magnesium sulfate can be used as a mineral source.
This mineral is the major cation of intracellular fluids. Unlike sodium (Na), it is found in limited amounts in intercellular fluids. It is the most abundant mineral in the body after Ca and P. The amount of Na in the blood is higher than potassium (K). On the other hand, the amount of K found in muscle tissue and milk is several times higher than Na. The main absorption site of the mineral is the small intestine, and the main excretion route of absorbed K is the kidneys. It is the main cation of intracellular fluids and plays a role in regulating osmotic pressure and maintaining acid-base balance. It is necessary for the activity of muscles and enzyme reactions related to creatine. It is a mineral that affects carbohydrate metabolism. Although potassium deficiency is a rare phenomenon, it may occur in beef cattle fed with highly concentrated feeds. In these cases, growth retardation, general weakening of the muscles, shaky gait, pica, diarrhea, abdominal distension, weakening and subsequent death are observed. On the other hand, excess of this mineral impairs the absorption and utilization of Mg. Toxicities related to excessive consumption are not very common. However, it can occur in cases of limitation of water consumption or salt water or kidney dysfunction. Forages of plant origin, especially forages rich in K.
Sodium and Chlorine
Salt consisting of both minerals is quite common in nature. The animal body contains about 0.21% sodium (Na). Some of it is in the insoluble form in the skeleton, while a large portion is found in the extracellular fluids and plays a very active role. Unlike Na, Cl is found inside and outside the cells of body tissues. Both minerals are easily absorbed in the upper part of the small intestine. About 80% of the Na and Cl entering the digestive system in animals occurs in saliva, gastric juice, bile, and pancreatic fluid. Both minerals are excreted as salts, mostly in the urine and a small amount in the feces. Another way in which Na is excreted in significant amounts is through vomiting, diarrhea and sweating. Along with potassium, Na (cation) and Cl (anion) in body fluids play a role in maintaining osmotic pressure and maintaining acid-base balance. Sodium plays a role in transporting nutrients to cells, removing metabolic wastes, and maintaining water balance between tissues. Chlorine is the major anion of gastric juice and combines with the H ion to form hydrochloric acid. In sodium deficiency, the evaluation of feed decreases in developing animals, yield decreases in dairy cows, and live weight loss in adults. On the other hand, fertility disorders, which are characterized by infertility in male animals and delayed sexual maturity in females, occur. Decreased productivity, weight loss and cannibalism in laying hens are signs of Na deficiency. In chlorine deficiency, decrease in growth rate and nervous symptoms occur in the face of sudden noise in chicks. On the other hand, salt toxicity, which usually occurs when water is limited, is easily seen in animals other than ruminants. Leg cramps, blindness and other nervous disorders are the results of excess sodium. The main and readily available source of sodium and chlorine for animals is salt. The amount of salt needed is affected by the growth period of the animal, the yield level, the composition of the ration and the ambient temperature. Cats and dogs fed animal diets require less salt than those fed on plant-based diets.
The amount and form of Sulfur (S) to be given to animals varies greatly depending on the species. Non-ruminant animals can utilize sulfur from amino acids. On the other hand, they cannot use elemental sulfur in amino acid synthesis. Ruminants, on the other hand, utilize elemental sulfur and sulfates for amino acid synthesis by rumen microorganisms. In some animals, organic sulfur is more easily absorbed than the inorganic form. Sulfur, which is found in organic form in cells, is the building material of amino acids such as cystine, cysteine and methionine. Sulfur is supplied from proteins rich in these amino acids. Sulfur is found in the structure of vitamins such as thiamine and biotin and the hormone insulin. This mineral is found in a large part of body tissues, especially in hair, fleece and feathers. It is 4% in the form of cystine in the fleece. It plays a role in fat metabolism because it is in the structure of biotin. On the other hand, due to the inclusion of thiamine in its composition, it plays a role in carbohydrate metabolism. The inclusion of insulin and glutathione, which are described as regulators of energy metabolism, also adds a special importance to the mineral. In case of deficiency of S, which is effective in protein synthesis, growth regression occurs. At the same time, there are negativities in the growth of the fleece and shedding in the fleece. On the other hand, sulfur toxicity that occurs in excess sulfur is practically insignificant. To meet the sulfur requirement, monogastric animals and poultry should be given amino acids containing S. Ruminants can benefit from S in the structure of proteins through rumen microorganisms. In case of using urea, which is one of the non-protein nitrogen compounds, additional S should be given. Sulfate form or elemental S can be used in ruminants and horses.
Microminerals (trace elements)
Minerals in this group include Iron, Copper, Zinc, Manganese, Iodine, Selenium, Cobalt, Molybdenum, Fluorine, Chromium, Silicium, Aluminum, Arsenic, Cadmium, Lead and Mercury.
More than half of the Fe in the animal body is found in the structure of hemoglobin and myoglobin. The rest is located in the liver, spleen, kidney, bone marrow and muscles. The amount of Fe in the body varies from birth to puberty. The absorption of iron is quite low and absorption takes place in the small intestine. The absorption of this mineral is under the control of the mucosal blockade system in the intestines. Fe is absorbed after converting from the ferritin+++ form to ferro++. Animals have a limited capacity to remove Fe from the body. Fe homeostasis in the body is largely controlled by absorption. Iron absorption is affected by the age of the animal, Fe status and health, conditions of the digestive tract, the physical form of Fe consumed, and the amount of other compounds in the feed. Iron (Fe) plays a key role in many biochemical reactions. With electron transport (cytochromes), it enters the structure of enzymes responsible for the activation of oxygen and hemoglobin and myoglobulin, which undertakes the transport of oxygen to the tissues. While 60% of the total body Fe is found in hemoglobin, the amount of Fe in myoglobulin is 3-7%. In iron deficiency, many systems are adversely affected, as oxygen will decrease in the tissues due to the decrease in hemoglobin concentration. In this context, symptoms such as decreased body weight gain, apathy, loss of appetite, and susceptibility to infections occur, as well as anemia and the blood changes that occur as a result. Fe deficiency can be seen in young and growing animals that cannot get enough minerals with milk or feed. Animal-based feeds such as meat meal and fish meal are richer in Fe than plant-based feeds. Fe in simple iron salts is better absorbed than the mineral found in feedstuffs. The presence of high levels of P and phytate in the feed reduces the absorption of the mineral by forming iron phosphate and iron phytate. Inorganic Fe sources can be used in animal nutrition. It is reported that iron carbonate and ferrous sulfate have a high degree of bioavailability, whereas iron oxide is underestimated. In studies conducted to determine bioavailability in ruminants, when the bioavailability for iron sulfate was 0, this value was found to be 60% for iron carbonate and as iron oxide.
The amount of copper (Cu), which is essential for life, in the animal body is about 2 ppm. It is very poorly absorbed in most animal species. The chemical form affects the absorption of the mineral. While it is the absorption rate of Cu in the ration in adult animals, this value is -30 in young animals. It has been reported that absorption is at the level of 1-3% in ruminants, absorption occurs in lambs and calves with undeveloped rumen as much as monogastric and a higher value is obtained than in adults. It has been observed that Cu is evaluated differently in animals of the same age, breed and physiological condition, or even raised under the same environmental conditions. The main storage organ of copper is the liver. In mammals, 90% of Cu in plasma is in the form of ceruloplasmin, a metalloprotein. In most animal species, a large part of the ingested Cu is found in feces, and this is a non-absorbable mineral. The active excretion pathway of copper is bile. Apart from that, it is excreted through urine, milk and intestines. There is a reciprocal relationship between copper, molybdenum (Mo) and sulfur. In the presence of sulfur, especially Mo decreases the storage of Cu in the organs and the synthesis of ceruloplasmin, as a result less mineral is excreted with bile, but the amount excreted in the urine increases. High dietary Cu intake reduces the amount of Mo stored in the liver. As the sulfur level increases, the amount of Mo excreted in the urine increases, so the storage of the mineral is adversely affected. Copper is an essential mineral for cellular respiration, bone formation, connective tissue development, keratinization, and tissue pigmentation. Copper, which plays a role in the formation of hemoglobin, is effective in the evaluation of Fe. In cases where copper is not sufficient, Fe is assimilated; However, it cannot be converted to hemoglobin. Copper also enters into the structure of metalloenzymes with important physiological functions such as cytochromoxidase, lysyl oxidase, tyrosinase. Depending on iron deficiency, besides anemia and diarrhea, bone, fertility, nervous and cardiovascular system disorders, loss of pigment in hair and wool (acromotrichia), insufficient keratinization in wool, hair and nails, suppression of immune system are observed. In addition, growth below the optimum level and decreased appetite are among the general symptoms seen in Cu deficiency. In poultry, the general symptom of copper deficiency is anemia. Internal bleeding due to vascular defects can lead to death before severe anemia occurs. In young birds fed with diets deficient in Cu, lameness occurs and the bones become easily brittle. As a result of severe copper deficiency (0.7-0.9 ppm) in laying hens, yield decreases, and Cu levels in plasma, liver and eggs decrease. In breeder chickens, hatchability can drop rapidly and reach zero in 14 days. Embryos taken from chickens fed with insufficient copper have anemia and growth retardation. Nervous system disorders such as neonatal ataxia (swayback) occur in lambs. There are two types of these cases. The first is the acute form seen in newborn lambs, and the other is the delayed form that occurs a few weeks and months later. In both forms, paralysis, coordination disorder in the legs, and convulsions may occur. Lambs are born weak and may die because they cannot suckle milk. The most obvious criterion of copper deficiency in ruminants is the loss of pigment in hair and fleece. Pigmentation in sheep is very sensitive to changes in copper consumption. Black hair and fleece formation occurs 2 days after copper deficiency or excess Mo and SO4. Particularly, brittleness of long bones and lameness are the symptoms seen in ruminants as a result of Cu deficiency. Fertility disorders, characterized by delayed estrus and abortions, may occur in cattle and sheep grazing on pastures that are insufficient in copper. Copper is also closely related to other minerals. The negative effects of excess Mo intake with sulfate can be treated with Cu application. Cu consumption over 250 ppm can cause poisoning. Excess copper is stored in the liver and causes death. Cu level to be given to horses and cattle fed in regions with high Mo levels should be increased to 5 times the normal level. Chronic copper poisoning observed in ruminants is not observed in monogastric animals. The reason for these cases, which occur in grazing ruminants, is excessive Cu consumption as well as very low intake of molybdenum and sulfate. The presence of high levels of zinc in the diet prevents Cu poisoning. Cu content generally decreases as plants age, and those grown in alkaline soils contain low levels of Cu. The amount of Cu in cereal grains is low compared to oil seeds. Animal feeds, especially liver meal, are rich in Cu. Among the copper preparations, from highest to lowest bioavailability, copper sulfate, copper carbonate.
Unlike other microminerals, zinc (Zn) shows a suitable distribution in the animal body according to the tissues. However, the Zn concentration is higher in epidermal tissues such as skin, hair, feathers, and fleece. The main absorption site of zinc in monogastric animals is the small intestine. In studies conducted on sheep, the absorption of the mineral from the rumen was higher than in the small intestine. Zinc absorption is adversely affected by compounds such as phytate, Ca-phytate, cellulose, P, Cu, chromium in the diet. Chelates such as EDTA and casein and fish meal increase Zn absorption. The most important factor affecting absorption is the amount of Zn in the diet. The main excretion route of zinc is feces, and a small amount is excreted in the urine. Zinc plays a role as an activator in the structure of enzymes. The carbonic anhydrase enzyme, which it enters into its structure, contains 0.3% Zn. In mineral deficiency, plasma alkaline phosphatase activity, liver, retina and testicular alcohol dehydrogenase decrease. This mineral is necessary for protein synthesis and metabolism, nucleic acid and carbohydrate metabolisms. More than 200 Zn proteins are known today. It is a microelement that plays a role in hair and bone formation. Zinc also interacts with hormones biologically. It plays a role in the production, storage and release of hormones. Zinc is essential for the integrity of the immune system. Apart from all these, zinc is effective in protecting membranes, prostaglandin and lipid metabolism and growth of rumen microorganisms by showing antioxidant effect. It is also reported that zinc is effective in maintaining plasma vitamin A concentration and functions in the normal function of ovarian epithelium. Zinc deficiency can be observed very commonly in practice in poultry. The age of the animal, the amount of Zn in the ration and its bioavailability, the compounds with which it has an antagonistic relationship in the ration play a role in the formation of mineral deficiency. Decreased growth, shortening and thickening of leg bones, enlargement of joints occur in chick mineral deficiency. It has been reported that Zn deficiency in poultry also causes severe dermatitis around the feet, legs and beaks, hyperkeratinization of the skin, epidermal thickening and poor feathering. In chickens fed with rations containing insufficient amount of Zn, hatchability declines rapidly and decreases to zero in about two months. Early symptoms of zinc deficiency are decreased feed consumption, growth rate and feed efficiency. In animals consuming insufficient Zn, feed passes more slowly through the digestive tract. Zn deficiency in ruminants can cause inflammations characterized by submucous bleeding around the mouth and nose, coarse hair and shedding of fleece. In severe zinc deficiency in these animals, parakeratosis occurs in the skin as a clinical sign. Parakeratosis is observed around the sucrotum, head, feet, nose and neck in calves, and in the udder in dairy cows. These cases also occur in the rumen papillae and esophageal mucosa. Marginal deficiencies observed in grazing cattle and sheep cause significant economic losses by decreasing growth and fertility without any clinical symptoms. In these cases, serum Zn level decreases. Apart from all these, when we look at zinc deficiency in general, the production and release of testosterone, insulin and adrenal corticosteroid hormones decrease. It adversely affects spermatogenesis, primary and secondary sex organs in males and all processes related to fertility in females. In mineral deficiency, DNA, RNA and protein synthesis regress. The Zn content of plants varies considerably. Leguminous plants have higher Zn content than meadows. It is reported that the usefulness of Zn in feeds grown in the tropics is low. Inorganic Zn source must be present in feeds. Animal protein feeds are richer in Zn than vegetable protein sources. In addition, the bioavailability of the mineral in the structure of these feeds is high. In most cases, it is sufficient to add 50-60 ppm Zn to the ration dry matter. This amount affects the ration Ca and phytate status. Likewise, since zinc has an antagonistic relationship with Cu, the Zn level in the diet should be increased in case of excess copper intake. The sources of Zn used in the feed industry are sulfate, oxide and carbonate forms. Among these, sulfate and oxide forms are important. When the bioavailability of the sulfate form in poultry is accepted as 0, this value is 44% for the oxide form. The oxide to be used for this purpose should not contain more than 0.05% lead, 0.03% arsenic and 0.001% cadmium. In studies with dairy cows, it has been determined that organic sources such as Zn methionine increase milk yield, somatic cell count is lower in the milk obtained, and hoof quality is higher.
Manganese (Mn) is found in low concentration but widely in the body. Bone, liver, kidney and pancreas are the organs with the highest amounts. It is absorbed from the small intestine. In all animal species, Mn shows low absorption ability, this event takes place in the small intestine. Ca, P and Fe affect the absorption of the mineral. High levels of Fe intake in chickens negatively affect the absorption of manganese and increase the emergence of perosis cases. Estrogenic hormones increase the absorption of Mn. Like other micro minerals, Mn also acts as an enzyme activator. The enzymes arginase, pyruvate carboxylase and Mnsuperoxide dismutase contain Mn. The enzymes that the mineral enters into are involved in oxidative phosphorylation, amino acid metabolism, fatty acid synthesis and cholesterol metabolism. Manganese is an essential mineral for growth and fertility. Mn, which is vital for normal bone growth, plays an essential role in the development of the organic matrix of bones. Defects that cannot be corrected occur in chicks in manganese deficiency. Poultry are more susceptible to Mn deficiency than mammals. Perosis is the most important disease caused by this mineral deficiency in chickens. It leads to the formation of nutritional chondrodystrophy, which is characterized by enlargement, malformation and rotation in the joints. In Mn deficiency, nervous symptoms in chicks, decrease in egg production in layer and breeder chickens, decrease in hatchability, and formation of thin-shelled or unshelled eggs are observed. Fertility disorders caused by Mn deficiency are of great importance. Testicular degeneration is observed in males and ovulation defects in females. Irregularity of estrus is the symptoms seen in cattle. Manganese oxide and sulfate are the main sources used in animal feed. The oxide form to be used in the feed industry should not contain more than 100 ppm of lead. Studies have shown that the bioavailability of the sulfate form is highest in chicks, followed by oxide and carbonate forms. When the bioavailability of the sulfate form is accepted as 0, this value is 62-77% for oxide and 32-36% for carbonate. In bioavailability studies with sheep, when the bioavailability of manganese sulfate form was taken as 0, MnO was 57.7%, MnO2 32.9% and MnCO2 27.8%.
Cobalt (Co), which is widely found in the animal body, is in high concentration in liver, bone and kidney. 43% of the Co in the body is in the muscles and the other in the bones. It is found at high levels (0.15 and 0.25 ppm on a dry matter basis, respectively) in the liver and kidney. The absorption of Co in ruminants is quite low compared to monogastric animals. In ruminants using cobalt in the synthesis of vitamin B12, 3% of the mineral is converted to vitamin. This rate depends on the amount of cobalt consumed, and in the studies conducted, it was determined that the conversion rate was .5 in sheep fed with insufficient rations in terms of Co, while it was 3% in those who received sufficient Co. In ruminants, the main route of excretion of Co is stool (87%). Apart from this, it is also excreted with urine (1%) and milk (). Cobalt is a component of vitamin B12 and this vitamin contains 4.5% Co. Vitamin B12 enters the structure of many enzymes with various metabolic functions. Therefore, the functions of Co in metabolism are identical to the functions of vitamin B12. It plays a role in vitamin, nucleic acid and protein metabolism, purine and pyrimidine synthesis, methyl group transfer, protein synthesis from amino acids, carbohydrate and fat synthesis. Rumen microorganisms use Co in the synthesis of vitamin B12 and for their own growth. The symptoms of Co deficiency in cattle and sheep are similar to the symptoms of vitamin B12 deficiency. Ruminants grazing on mineral-deficient pastures experience loss of appetite, growth retardation and weight loss, anemia and ultimately death. Non-specific symptoms such as decrease in live weight and feed consumption and decrease in feed conversion ratio occur in poultry. Incubation yield is affected and embryo death may occur on day 17 of incubation. Liver, kidney, meat, fish, milk and eggs are good sources of vitamin B12 from foods of animal origin, and the level in these foods depends on the amount of vitamin B12 and Co taken with the feed. The form used as a Co source in feeds is cobalt carbonate and contains 40% mineral. However, carbonate, sulfate and oxide forms can be used for this purpose. The oxide form has lower bioavailability than carbonate and sulfate.
Iodine (I) is found in the thyroid at a rate of 70-80%. Apart from that, the ovaries, salivary glands and secretions contain high levels of I. The thyroid gland has a significant mineral storage capacity. Soils in various parts of the world are poor in terms of I. It is found in inorganic form in feed and water. The mineral is absorbed from the digestive tract and transported bound to plasma proteins. In addition to the I in the feed, the I in the saliva and other intestinal fluids and the iodine-containing hormones are broken down and the resulting mineral is reabsorbed in the digestive tract. In ruminants, 70-80% of I is absorbed daily directly from the rumen and u from the abomasum. A significant part of I is excreted in the urine. It is known that iodine plays a role in the synthesis of thyroid hormones such as thyroxine and triiodotronin. Thyroxine contains 65% I. This hormone plays a role in thermoregulation, intermediate metabolism, fertility, growth and development, circulation, muscle function, and control of the oxidation rate of cells. In goiter cases characterized by insufficient function of the thyroid, energy exchange, the amount of heat released by the tissues decreases and the metabolic rate decreases. Insufficient thyroid hormones in poultry cause growth retardation, decrease in egg production and size. In breeding chickens, there is a decrease in hatchability and thyroid enlargement in the embryo. I deficiency in young ruminants causes general weakening and calves being born blind, hairless and stillborn. There is deterioration in the quantity and quality of fleece in sheep. Irregular estrus and abortions are observed in breeding animals. Long-term deficiency in cattle leads to a decrease in feed consumption, milk fat and yield. At the same time, it is observed that animals are vulnerable to stress and the frequency of ketosis formation increases. The amount of I in feeds varies considerably. When the feeds are ranked in terms of I content, animal origin feeds take the first place, followed by oilseed meals and grain feeds. For ruminants, sources such as potassium iodide, sodium iodide and calcium iodate have equal bioavailability. It is recommended to use stabilized forms in order to prevent mineral loss. On the other hand, horses are the animals most susceptible to I excess compared to sheep, cattle and poultry. Tolerable I level is 50 ppm in cattle and sheep, 300 ppm in poultry, and 5 ppm in horses. Symptoms of poisoning in cattle occur between 50-300 ppm. Young animals are more susceptible than lactating animals.
Selenium (Se) is similar to sulfur in terms of chemical structure. It is found in plants as amino acid analogues with Se sulphur, together with proteins. When sufficient levels of Se are taken with the feed, the mineral density in the kidney is at the highest level. This is followed by the liver, spleen and pancreas. As the amount of Se in the diet increases, the amount of minerals accumulated in the liver increases. The main site of absorption of selenium is the small intestine. Absorption is lower in ruminants than in monogastrics. The reason for the low absorption in sheep is the conversion of selenite into compounds that do not dissolve in the rumen. The main excretion route of Se ingested with feed is urine. Selenium is found in the structure of the enzyme glutathione peroxidase, which protects cells from oxidative damage. In other words, this enzyme performs its antioxidant function in animal tissues. As a component of glutathione peroxidase, Se breaks down peroxides without damaging cell membranes. Peroxidation of lipids causes disruption of the integrity of cells and adversely affects metabolism. Vitamin E in cell membranes is the first line of protection against peroxidation of vital phospholipids. Even with the presence of vitamins, some peroxide may form. Glutathione peroxidase, which Se enters into its structure, creates the second line of protection and breaks down these peroxides before they have any harmful effects. Vitamin E, Se and sulphur-containing amino acids are effective in preventing the same nutritional disorders. It has been determined that Vitamin E and Se have a saving effect on each other. Vitamin E shows this effect by keeping the Se in the body in an active form and by preventing the breakdown of membrane lipids in the first stage, allowing less Se to be used for this purpose in the second stage. In Se, it maintains the integrity of the pancreas, increasing fat digestion and the absorption of vitamin E. Likewise, Se saves the amount of vitamin E used to prevent lipid peroxidation. Selenium plays a specific role in the synthesis of prostaglandins and the metabolism of essential fatty acids. Se and vitamin E are necessary for an adequate immune response, and they also provide protection against heavy metal (mercury, cadmium, silver, arsenic, lead) poisoning. Selenium deficiency is effective in the emergence of 3 diseases called exudative diathesis, pancreatic dystrophy and nutritional muscular dystrophy in chicks. The first two of these can be prevented by adding Se to the ration. For the prevention of the third disease, vitamin E and amino acids containing S should be administered together. Exudative diathesis, known as the increase in the permeability of the capillary vessel walls, is also prevented by vitamin E. Mineral deficiency in young ruminants leads to white muscle disease, which is characterized by muscle degeneration. Selenium excess as well as selenium deficiency is an important issue in animal nutrition. Selenium poisoning can be seen in animals fed with roughage and concentrates grown in soils rich in selenium. Hair loss, nail loss, anemia, excessive salivation, blindness, paralysis and death are the symptoms of Se poisoning, and the case with these symptoms is defined as alkaline disease. Excessive intake of Se in poultry leads to a decrease in egg and hatching yields and embryonic deformations. Diets containing high levels of protein are effective in preventing Se poisoning. Among the sources of Se that can be added to feeds are Na-selenite and Na-selenate. Of these, selenite is easily reduced to elemental Se, which forms insoluble compounds with other metals. Therefore, selenate is preferred. However, it has been reported that high stability Na-selenite, which is premixed using carriers such as wheat bran, flaxseed meal, glucose monohydrate and soy protein, and stored in a cool and dry environment, can be used in poultry. In recent years, there have been reports that selenium provided in this form may have a carcinogenic effect, and that the healthiest form is its organic form.
Fluorine (F) is a very toxic mineral. Some animal species require very little F. Consumed F is rapidly absorbed and passes into the blood, and as a result of its reaction with Ca, calcium fluoride is formed. This form of the mineral accumulates in hard tissues. Even if large amounts of minerals are taken in soft tissues and fluids, excessive accumulation does not occur. Fluorine is excreted mainly in the urine. Milk F concentration is limitedly affected by ration mineral content. Fluorine prevents tooth decay in children and possibly some animals. Tooth decay in farm animals does not pose a health problem. The excess Ca in the diet prevents the accumulation of F in the bones. The toxic effect of fluorine occurs as a result of an accumulation, so in some cases, poisoning may not be seen. The first signs of fluorine poisoning (fluorosis) are observed in the bones and teeth. In these cases, the bones become soft and spots occur on the bones. In addition, the bristles become coarse. Feed conversion rate decreases in F poisoning. In order to prevent fluorosis, the amount of F in phosphates with drinking water should be controlled. Animals should not be given water containing high levels of F.
Molybdenum (Mo) was found to be essential, and it was established in 1953 when it was determined that it was included in the structure of the xanthine oxidase enzyme. Mo shows very easy and fast absorption ability. The type and age of the animal affect the absorption and the amount of mineral in the ration. It is generally stored at a very low level. Liver and bone are the places where it is stored at the highest level. The amount of protein, Fe, Zn, lead, ascorbic acid and α-tocopherol in the ration affect the Mo level in the tissues. Mo is also excreted from the body very quickly in the urine. Molybdenum is a component of the xanthine oxidase enzyme necessary for the formation of uric acid in poultry. Apart from this, it is also included in the structure of enzymes such as aldehyde oxidase, which plays a role in niacin metabolism, and sulfide oxidase, which oxidizes sulfite to sulfate. It stimulates the activity of rumen microorganisms. In animal nutrition, too much of molybdenum is important than its deficiency. Excessive Mo consumption affects Cu deficiency, in other words, it impairs Cu metabolism. Animals other than ruminants are highly resistant to Mo poisoning under normal feeding conditions.
Chromium (Cr) is absorbed better if it is organically bound. Since the absorption of chromium (Cr) is limited in animals, it is also found in tissues at very low levels. Its organic form is more effective than inorganic forms and strengthens insulin activity. Since it forms the core of Glucose Tolerance Factor (GTF), it is reported to be effective in glucose metabolism in humans and mice. As a matter of fact, insufficient Cr intake in humans has a detrimental effect on glucose and insulin metabolisms. Under normal conditions, there is no information on the benefit of adding Cr to the ration in animals; however, there is evidence that the addition of chromium to the diet under high temperature will improve growth performance. In chronic Cr poisoning in animals, dermatitis, irritation in the respiratory system, ulceration of the nasal septum and lung cancer are observed.
Silicon (Si) content in soil and plants is quite high. Cereal grains contain less Si than the leaves and branches of the plant. It is necessary for growth and skeletal development in chicks. In a study, it was shown that Si is important in maximizing prolyl hydrolase enzyme activity, which is a measure in determining the rate of collagen biosynthesis.
Aluminum, Arsenic, Cadmium, Lead and Mercury
These minerals are studied for their toxic effects. Lead (Pb) and arsenic (As) can cause poisoning in ruminants. On the other hand, animal feeds contain low levels of aluminum (Al). There is no evidence that this mineral is essential in animals. Al is reported to increase growth rate in birds by inhibiting the absorption of high levels of F. Arsenic (As) in the structure of feeds is easily absorbed. Organic compounds of As, such as arsenylic acid, which is used as a growth stimulant in pigs and poultry, are easily absorbed and are excreted with manure. Although As. poisoning occurs rarely, the symptoms of chronic poisoning in cattle can be listed as weight loss, changes in hair, diarrhea, inflammation in the eyes and respiratory tract mucosa. Sudden death occurs in acute poisoning. As. is essential for pigs, chicks and humans. The mineral is necessary for the formation of compounds such as cystine and taurine from methionine. The absorption of cadmium (Kd) in feed is limited. Absorbed Kd accumulates in the liver, then goes to the kidney. This mineral has a toxic effect for all systems in animals. In cases of poisoning, decrease in feed consumption, retardation in growth, infertility, delay in testicular development or degeneration, abortion, damage to liver and kidney, anemia and death are observed. This mineral is in antagonistic relationship with Cu, Zn and Fe. Lead (Pb) can be taken into the body by absorption, inhalation and skin. Absorption is quite high in young people. Absorbed Pb accumulates in the liver and kidney. It has been reported that Fe, Zn, S and vitamin E have a protective effect against lead poisoning. Mercury (Hg), which has a toxic effect, is not essential. It is easily absorbed by digestion and respiratory tract. Methylmercury is more harmful than inorganic mercury. Symptoms such as diarrhea, stomach inflammation, salivation occur as a result of poisoning. Deaths due to mercury poisoning are attributed to kidney failure.