Distribution and Metabolism of Iodine in Animals
1.1 Distribution of iodine in animals
The average content of iodine in animals is 50-200ug/kg, but this value varies widely, mainly depending on the content of iodine in the diet. Under normal feeding conditions, the distribution of iodine in the animal body is: 70%-80% of the thyroid gland, 3%-4% of the muscle, 3% of the bone cheese, and 5%-10% of other organs and tissues. Iodine in the blood exists in the form of thyroxine, which is mainly bound to plasma proteins, and a small amount is free in the plasma.
1.2 Metabolism of iodine
Iodine enters the animal body along with the feed and drinking water. Most of the iodine in the feed is inorganic iodine compounds, which can be directly absorbed in various parts of the digestive tract, and the digestion and absorption rate is particularly high. Organic forms of iodine are also particularly well absorbed, but at a slower rate. The main site of absorption in monogastric animals is the small intestine, followed by the stomach; the main site of absorption in ruminants is the rumen.
The iodine absorbed through the digestive tract exists in the form of I-1 after entering the blood, and about 60%-70% is taken up by the thyroid gland. In the thyroid gland, it is first oxidized to I2 and then combined with the tyrosine residues in thyroglobulin to form iodide thyroglobulin, which is stored in the thyroid gland and can be hydrolyzed under the action of proteolytic enzymes in the lysosome to release triglycerides with hormone activity. Iodothyronine (T3) and thyroxine (T4) enter other tissues and organs of the body through blood circulation to play a role. 80% of the thyroxine entering the tissues and organs is decomposed by deiodinase, and the released iodine circulates to the thyroid gland for reuse. The turnover metabolism of inorganic iodine in the body is faster, while the turnover metabolism of organic iodine is slower.
Iodine is mainly excreted with urine through the kidneys, and a small part is excreted with saliva, gastric juice, bile and feces through the gastrointestinal tract. The endogenous fecal iodine of monogastric animals and dairy calves is mainly excreted with bile, while that of adult ruminants is excreted with bile in saliva, and part of it is excreted in the form of iodine-containing pyruvic acid derivatives. In addition, iodine can also be excreted through the lungs and skin, and in producing animals through animal products.
2 Nutritional Physiological Functions of Iodine
2.1 Regulate metabolism and maintain body heat balance
An appropriate amount of thyroxine can increase the activity of nuclear RNA polymerase, increase the synthesis of the whole RNA, and thus indirectly promote the synthesis of protein; the activity of other enzymes involved in substance metabolism can also be improved.
Thyroxine can act on the link between material metabolism and energy metabolism, that is, the process of oxidative phosphorylation, and promote the biological oxidation process in the triphosphate cycle. An appropriate dose of thyroxine can promote the biological oxidation of sugar and fat, coordinate oxidation and phosphorylation, and store part of the released energy in adenosine triphosphate (ATP), while the rest can be maintained in the form of heat or released outside the body.
2.2 Affect the growth and development of animals
Thyroxine has a regulatory effect on the development of the central nervous system, skeletal system, cardiovascular system and digestive system, and can promote tissue differentiation and growth, thereby promoting young growth and development, increasing basal metabolic rate and oxygen consumption. Iodine deficiency in young animals can be manifested as stunted growth and development, decreased vitality, resulting in "cretinism".
2.3 Affect animal reproductive performance
Iodine is an essential trace element to maintain good reproductive performance of animals. Iodine deficiency can cause animal reproductive disorders, abnormal or inhibited, and even infertility. Severe iodine deficiency can also affect offspring, causing growth stagnation and hypoplasia in offspring. Iodine deficiency in male animals can lead to decreased, poor quality. Iodine deficiency in female animals can lead to decreased conception rate, miscarriage, weak fetus and postpartum retained placenta. Iodine deficiency in breeders can lead to decreased hatchability, yolk sac absorption disorder, and prolonged incubation time. In addition, iodine deficiency in animals can also lead to lower iodine content in their products.
2.4 Affecting the coat condition of animals
Iodine deficiency will affect the normal growth of animal fur, resulting in dry and dirty coat skin, slow growth, hair loss or even whole body hair loss, thickened skin, loss of luster in hair and feathers, and fibrosis of coat all over the body.
3 Iodine deficiency and poisoning in animals
3.1 Iodine deficiency
There are two types of iodine deficiency in animals, one is primary iodine deficiency, which is mainly due to insufficient iodine content in feed. This deficiency is generally endemic. For example, iodine deficiency in local soil and drinking water can lead to insufficient iodine content in local feed materials and agricultural products, and easily cause iodine deficiency in local residents and livestock. Another type of iodine deficiency is secondary iodine deficiency, mainly because the feed contains substances that antagonize the absorption and utilization of iodine, such as thiocyanate, glucose isothiocyanate, glycoside arachidonoside and cyanogenic glycosides, etc. . The goiter-producing substances such as thiometazol and thiourea, which are more abundant in the feed, can also lead to iodine deficiency in animals. In addition, the concentration of potassium ions in the feed is too high, which can promote the excretion of iodine and cause iodine deficiency in animals.
3.2 Iodine poisoning
Excessive iodine consumption can also lead to hyperiodine goiter and animal poisoning. Zhang Sufang and others reported that drinking water with 0.2% KI prevents acute death of chicks caused by mycosis. More than 10 hours after drinking, food loss, wilting, eyes closing, neck shrinkage, napping, unsteady gait, increased oral mucus, loose stools, dyspnea, and paroxysmal angular arch. Pulmonary edema, congestion, increased tracheal mucus, duodenal hemorrhage, hepatic and renal enlargement and congestion, ileocecal effusion, and mild brain edema were seen at autopsy.
4 Disease prevention and treatment
Supplementing iodine is the most fundamental and effective control measure, but the dosage should be strictly controlled to avoid overdose poisoning.
Oral iodized salt is a common method for the treatment of iodine deficiency. Adult cattle 100-150mg/d, adult sheep 20-50mg/d, lamb 5-10mg/d. Add 0.25% potassium iodide to the chicken feed diet, or add 0.023% potassium iodide to ordinary saline, and let it drink freely. Oral compound iodine solution (5% I, 10% KI), 10-20 drops/d for cattle, 5-10 drops/d for adult sheep, 1-3 drops/d for lambs, 20 days as a course of treatment, every 2-3 months Repeat the course one more time. When the goiter is enlarged and solid, iodine ointment can be applied; after the gland is suppurated, the surgical incision is rinsed with dilute iodine solution.
To prevent this disease, attention should be paid to the iodine content in the diet to meet the needs of animals. Use iodine-containing salt bricks to allow animals to lick freely, or add seaweed, seaweed and other substances to the feed, or mix iodine into mineral supplements, usually potassium iodide or potassium iodate is mixed with stearic acid, mixed with Put it into feed or salt bricks to prevent iodine volatilization, the concentration is 0.01%, and it has a good effect of preventing iodine deficiency.
