28101054
Iodine toxicity in ruminants
e inadequate intake of iodine is still a topical problem, because it contributes to a reduction in performance through the disturbed health of adult animals and their offspring. e necessity of iodine is frequently described in association with hypothyroidal state. In our work we want to assign the hidden risk of prolonged iodine feeding in ruminants. We discuss the possible sources of iodine intoxication, the clinical signs of the intoxication, its effects on production, reproduction, and thyroid functions; animal susceptibility to intoxication; laboratory and necropsy findings; diagnostic, and therapeutic possibilities.
36339399
Iodine deficiency disorders: contemporary scientific issues.
Iodine deficiency is the leading cause of preventable intellectual impairment and is associated with a spectrum of neurologic and developmental pathology. More than one billion people are at risk. The developing fetus, newborn, and young child are the most susceptible to the effects of an iodine-deficient diet. If intervention is not initiated in a timely fashion, the pathophysiologic abnormalities become resistant to treatment and permanent intellectual, neurologic, and somatic deficits result. The technology of iodine deficiency intervention is well established. Iodized salt, the preferred method, is easy to produce, administer in physiologic doses, and is cost effective. The distribution of iodized salt and social marketing are key to a successful iodine deficiency elimination program. In remote regions, iodized oil is a useful interim intervention. However, it is clear that technology is not enough. Any national effort to eliminate iodine deficiency must extend far beyond the Ministry of Health. The program will require the full participation of a range of national government ministries and agencies and the full support and participation of local or regional governments.
23807638
The effects of iodine deficiency on ewe fertility and perinatal lamb mortality.
AIMS
To substantiate a previous report of improved fertility and perinatal lamb mortality rate following iodine supplementation in a Manawatu Romney ewe flock. To contribute data which might be used to predict a response to iodine supplementation.


METHODS
A controlled iodine supplementation trial was performed over 2 successive years. The possible confounding factor of different lambing paddocks on perinatal lamb mortality was removed by the reversal of the paddocks used by the supplemented and control ewes during the second year.


RESULTS
During 2 successive years, iodine supplementation resulted in improved reproductive performance in a Manawatu Romney flock with 21% and 14% more lambs born to supplemented than to control mixed-age ewes in 1996 and 1997 respectively. Supplementation also resulted in improved perinatal lamb survival, although this effect was greater during the wetter 1996 Lambing season. Despite the production response during both years, a difference in lamb thyroid:bodyweight ratio was only noted following the drier 1997 winter. Ewe thyroid hormone concentrations before mating and during mid-pregnancy were poor indices of deficiency.


CONCLUSIONS
Iodine deficiency should be included in the list of differential diagnoses for poor reproductive performance in ewes and in the investigation of high perinatal lamb mortality rates.


CLINICAL SIGNIFICANCE
The annual cost associated with iodine deficiency in this Manawatu Romney flock is conservatively estimated at dollar 6.00 per ewe. This economic loss is considerably greater than the annual cost of iodine supplementation using iodised oil.
68106452
Iodine in the Food Chain
The incorporation of iodine into the food chain of soil and water on the one hand and of animals and humans on the other is of decisive importance for meeting human iodine requirements.
43782220
Utilisation of iodine from different sources in pigs
Balance experiments have demonstrated that growing pigs fed a ration consisting of wheat, barley, extracted soya meal, dicalciumphosphate, and iodine‐free feeding salt utilised 48.8% of the received iodine. The tested supplementary iodine sources included potassium iodide (KI), ethylenediamine dihydroiodide (EDDI), iodine humate (HUI) prepared from iodine acid (HIO3), and the product P containing 0.004% iodine in an oil base (P). The amount of the supplemented iodine was in all cases 1 mg per 1 kg feed. The utilisation of iodine from the supplements reached 93.6, 92.6, 90.7, and 67.9% for KI, EDDI, P, and HUI, respectively. The values were significantly higher compared with controls (P < 0.01). Compared with KI and EDDI, the utilisation of iodine from HUI was significantly lower (P < 0.01). The lower availability of iodine from HUI was probably due to the high binding capacity of humate. The amount of urinary iodine excreted by control pigs receiving in the non‐supplemented ration 147.5 μg iodine per day, was 40.3 μg per day (27.3%). In the pigs receiving in the supplemented ration 1647.5 μg iodine per day, the amount of urinary iodine reached 734.9 to 805.0 μg per day (44.6 to 48.9%). The corresponding values of faecal excretion were 75.6 μg iodine per day (51.2%) for the control pigs and 106.2 to 121.1 μg iodine per day (6.45 to 7.35%) for the pigs fed the supplemented rations. A high amount of 528.6 μg iodine per day (32.1%) was excreted in the faeces by pigs of the group HUI.
34636110
Iodine concentrations in porcine blood, urine, and tissues after a single dose of iodised oil
Experimental groups of pigs were treated orally with 120 mg (Group O 120), or 480 mg (Group O 480) of iodine per animal, or intramuscularly with 240 mg (Group I 240) of iodine per animal. Iodine was administered in the form of iodised fatty acid esters (IFAE). The treatment resulted in significantly increased iodine concentrations in tissues and a single dose was sufficient to meet the requirement for the whole fattening period (180 days). Urinary iodine concentrations in all the experi- mental groups were higher than in the control group C receiving iodine only from conventional feed. Urinary excretion of iodine between days 2 and 5 was more distinctive in orally treated than in intramuscularly treated animals (Figure 1). Iodine concen- trations at the end of the fattening period (day 180) were higher in the treated than in the control groups. The treatment effect was more marked in Groups O 480 and I 240 than in Group O 120. The dynamics of blood serum iodine concentrations was similar to urinary concentrations (Figure 2). Mean thyroid gland weights in the groups O 120, O 480, I 240, and C were 9.19, 8.51, 7.10, and 12.01 g, respectively. An opposite tendency was observed for iodine concentrations in thyroid gland dry matter (Figure 3). No effects of any of the treatments on total protein, albumin, total lipids, or cholesterol concentrations in blood serum were observed. Group C showed lower tissue iodine concentrations than any of the experimental groups. The only exception was hepatic tissue in which approximately the same iodine concentrations were found in all the groups. Data ob- tained in Groups O 120, O 480, and I 240 indicate that decisive for tissue concentrations was rather the dose of iodine than the route of administration. Iodine is stored above all in the thyroid gland and adipose tissue. As can be seen in Figure 4, its concentration was higher in muscles with a higher proportion of fat (neck) than in lean muscles (ham). For free full paper in pdf format see http://www.vri.cz/vetmed.asp
21536196
Serum thyrotropin, thyroxine, and tri-iodothyronine in dairy cows fed varying amounts of iodine.
The objective was to determine whether dairy cows fed supplemental iodine daily at 2.5 or 5.0 mg per kg body weight for 49 wk had altered thyroid status relative to controls fed no supplemental iodine. Average daily dose of iodine was 1.6 and 3.3 g. Iodine as ethylene diamine dihydriodide was fed to Holstein cows beginning at 8 to 10 wk of lactation, for the remainder of that lactation, through the dry period, and into the next lactation. On day 341 after onset of iodine feeding, each cow was injected intravenously with 15 microgram thyrotropin releasing hormone per 100 kg body weight. Thyrotropin in jugular blood collected before injection of releasing hormone averaged 7.6, 6.1, and 8.2 ng/ml for cows given 0, 2.5, and 5.0 mg iodine/kg body weight; there were no differences between means. Releasing hormone increased thyrotropin, thyroxine, and tri-iodothyronine in serum of all cows, but increases were not affected by quantity of dietary iodine.
24212442
Chronic iodine toxicity in dairy cattle: blood chemistry, leukocytes, and milk iodide.
Preliminary data from farm herds fed excessive dietary iodide and displaying signs of iodism indicated hyperglycemia, hypocholesterolemia, and a neutrophilic-lymphopenic shift in blood leukocytes. Subsequently blood, milk, and urine were analyzed from 90 cows in 10 herds fed normal (average 16 mg/cow daily) or high (average 164 mg) iodide as ethylenediamine dihydriodide for prophylactic purposes and from one herd fed iodinated casein for 3 wk. Glucose, area nitrogen, and neutrophils were higher while cholesterol and lymphocytes were lower in blood from cows fed high iodide. Milk iodide averaged .37 +/- .03 ppm from normal and 2.16 +/- .25 from herds fed high iodide. Neutrophils, glucose, protein, and globulin of serum increased while lymphocytes, cholesterol, and thyroxine decreased as iodide in milk and urine increased. Signs of iodism included lacrimation, coryza, conjunctivitis, coughing, hair loss, and exophthalmus. These findings corroborate other reports that excessive iodide alters metabolism and is toxic to immune mechanisms, suggesting that dietary iodide should be limited to nutritional requirements and prolonged prophylactic or therapeutic use should be avoided.
7720785
Iodine toxicosis in six herds of dairy cattle.
Daily iodine intake estimated to range from greater than 68 to 600 mg/animal/day was associated with signs referable to iodine intoxication in adult cows in 6 herds of dairy cattle. Signs were reversed by lowering supplemental intake to less than 12 mg/animal/day. Results of biochemical tests other than those for serum and milk iodine were not diagnostic. Serum iodine concentrations were 2.6 to 6.9 times the mean iodine concentration found in 12 control cows, each receiving 12 mg of iodine/day. Milk iodine concentrations were 3.6 to 13.6 times milk iodine concentrations in the control cows.
130933474
The value of iodine for livestock in central Pennsylvania.
By E. B. FoKBEs, Director^ Institute of Animal Nutrition, Pennsylvania State College; GEO. M. KARNS, Senior Industrial Felloiv, Mellon Institute of Industrial Research; S. I. BECHDEL, Professor of Dairy Production, P. S. WILLIAMS, Associate Professor of Dairy Husbandry, T. B. KEITH, Assistant in Animal Husbandry, E. W. CALLENBACH, Associate Professor of Poultry Husbandry, and R. R. MURPHY, Graduate Assistant in Poultry Husbandry, Pennsylvania State College INTRODUCTION
22359149
Iodine Deficiency in Europe
Iodine is a trace element present in the human body in minute amounts (15-20 mg in adults, i.e. 0.0285 x 10(-3)% of body weight). The only confirmed function of iodine is to constitute an essential substrate for the synthesis of thyroid hormones, tetraiodothyronine, thyroxine or T4 and triiodothyronine, T3 (1). In thyroxine, iodine is 60% by weight. Thyroid hormones, in turn, play a decisive role in the metabolism of all cells of the organism (2) and in the process of early growth and development of most organs, especially of the brain (3). Brain development in humans occurs from fetal life up to the third postnatal year (4). Consequently, a deficit in iodine and/or in thyroid hormones occurring during this critical period of life will result not only in the slowing down of the metabolic activities of all the cells of the organism but also in irreversible alterations in the development of the brain. The clinical consequence will be mental retardation (5). When the physiological requirements of iodine are not met in a given population, a series of functional and developmental abnormalities occur (Table 1), including thyroid function abnormalities and, when iodine deficiency is severe, endemic goiter and cretinism, endemic mental retardation, decreased fertility rate, increased perinatal death, and infant mortality. These complications, which constitute an hindrance to the development of the affected population, are grouped under the general heading of Iodine Deficiency Disorders, IDD (6). Broad geographic areas exist in which the population is affected by IDD.(ABSTRACT TRUNCATED AT 250 WORDS)
84985821
Severe experimental hyperthyroidism in the ruminant. I. Metabolic effects
1. Metabolism experiments have been made with five sheep fed iodinated casein in doses sufficient to give symptoms of hyperthyroidism, ranging from moderate to severe. Two comparable sheep were included to serve as controls. 2. The same ration was used throughout each experiment, and it was found that the digestibility of its dry matter and of its crude protein content declined when the sheep were made hyperthyroid. This was due to increased peristalsis. 3. The treated sheep lost body N when iodinated casein was given, the loss being proportional to dosage. Calculations indicated increases in the endogenous catabolism by up to 120%, and also increases in deamination. 4. There was an increased excretion of urea and ammonia during hyperthyroidism, the latter being associated with a decrease in the plasma carbon dioxide combining capacity. 5. Purine catabolism was accelerated by more than 50% in some sheep. Starvation of one sheep did not depress nucleoprotein catabolism as it does in the normal sheep.
1789130
Effects of excessive intakes of iodine upon growth and thyroid function of growing Holstein heifers.
Thirty Holstein heifer calves averaging 120 days of age and 102 kg of body weight were allocated to one control and four treatment groups of six each. Iodine, as ethylenediamine dihydriodide, was mixed 1:9 with dextrose and administered once daily atop feed at .625, 1.25, 2.5, or 5.0 mg iodine per kilogram body weight. Calves were housed individually in unheated, well-ventilated barns and fed complete mixed feeds containing less than 1 ppm iodine. Feed intakes were recorded daily and body weights weekly. Jugular venous blood was collected from iodine treated calves at 0, 4, 8, and 12 wk of the experiment and analyzed for iodine, thyroxine, and triiodothyronine of plasma. Feed intake per unit body weight and per unit gain were not significantly different between treated and control calves. However, daily feed intake and average daily gain decreased slightly at the highest iodine intake. Thyroxine and triiodothyronine were not different among treatments. Thyroxine declined in all calves from 0 to 12 wk. Thyroxine of calves fed 5.0 mg of iodine per kilogram body weight decreased more than of calves fed less iodine. Iodine intake as high as 5.0 mg/kg body weight was tolerated without morbidity, although a minor effect on performance and thyroid activity was indicated.
1298268
Serum thyrotropin and thyroxine after thyrotropin releasing hormone in dairy cows fed varying amounts of iodine.
Abstract The objective was to determine whether dairy cows fed relatively large amounts of iodine had altered thyroid status. In addition, polarographic analysis for determination of iodine and bromine in milk and urine is described. Five dairy herds fed an average of 16mg iodine/head per day (range 11 to 25) and five fed 164mg iodine/head per day (range 74 to 402) were identified. Iodine fed was estimated from minimal guaranteed iodine content of concentrates, iodized salt, minerals, liquid supplements, and silage topdressing. Iodine from other dietary sources was considered negligible. Each dairyman selected three cows each in early ( 120 days) lactation. Blood was collected from each cow selected; then 150 μ g thyrotropin releasing hormone were given. Iodine in milk ( μ g/ml) and urine ( μ g/mg creatinine) were 2.2 and 65 for cows in high iodine herds, more than that (.37 and 20) in low iodine herds. At resting (ng/ml) serum thyroxine was 33 and 32 and thyrotropin was 7.4 and 7.9. Serum thyroxine and thyrotropin concentrations were increased following releasing hormone; however, increase was not affected by quantity of dietary iodine. Thyroxine in serum at resting (ng/ml) was less for cows in early lactation (25.9) than for those in middle (36.1) or late (35.5) lactation.
28398150
Iodine toxicity. Physiological effects of elevated dietary iodine on calves.
A guitar soundboard assembly is comprised a plurality of internal braces attached to an inner side of a soundboard for resisting warping. The soundboard is relatively thick for a longer useful life. The braces include two cantilever braces extending between opposite sides of the soundboard. Each cantilever brace is comprised of an elongated bar supported in a spaced position behind the soundboard by a pair of mounting blocks at its ends. Although the soundboard is relatively thick, the portions between the mounting blocks of the cantilever braces are free to vibrate, so that it can vibrate as much as a thinner conventional soundboard. The bases of the mounting blocks of the cantilever braces are slightly angled relative to each other to arch the soundboard forwardly for further increasing stiffness and resisting cave in. The cantilever braces are each thinner on the treble side of the soundboard than on the bass side to reduce rigidity on the treble side and compensate for the lower tension of the treble strings. Additional braces are attached to the soundboard for supporting other positions.
33297719
The toxicology of potassium and sodium iodates: acute toxicity in mice.
Single-dose, acute toxicity experiments, carried out with white Swiss mice, using potassium and sodium iodates and the corresponding iodides, led to the following conclusions: Administered in sufficient quantities, the iodates cause intoxication and death. In some instances, death is attributed to renal damage with retention of non-protein nitrogen. Hemolytic effects are evidenced by hemoglobinuria and, histologically, by hemoglobin casts and hemosiderin deposits in the kidneys. Fatty visceral changes, non-specific in nature, appear within 24 hours after ingestion of iodates or iodides. Similar changes occur in fasted animals. Oral administration of iodates, at levels of 140 to 500 mgm./kgm., often increase the pH of the gastric contents. This is frequently accompanie by degenerative changes in the parietal cells. The damage is transient, as evidenced by restoration to normal in histological appearance of the gastric mucosa and in the pH values after 24 hours. Intraperitoneal and intravenous injections of iodates have little effect on the gastric pH. The toxicity of potassium iodate varies greatly with the route of administration; the oral LD 50 for mice fasted on sawdust overnight is six times that of the intraperitoneal LD 50 . Potassium iodate and sodium iodate have nearly identical oral toxicities and similar intraperitoneal toxicities; the oral toxicity of the potassium compound is nearly the same for heavy and light mice and for both sexes, and is not increased in weanling animals. Similarly, the relative toxicities of iodates and iodides depend on route of administration and on previous treatment of the mice.
22177985
Immunologic effects of experimental iodine toxicosis in young cattle.
A study was designed to evaluate effects of 4 dosage levels (0, 50, 250, or 1,250 mg) of daily iodine supplementation on cell-mediated and humoral immune mechanisms in 40 calves, 10 per group, for a 6-month period. Immune and inflammatory responses were measured by titers to brucella, leptospira, and infectious bovine rhinotracheitis virus vaccinations, by stimulation of lymphocyte mitoses with poke-weed, phytohemagglutinin (PHA), and conconavalin A mitogens, by intradermal PHA responses, by in vitro phagocytosis of Candida albicans by WBC, and by total WBC counts. Calves given 1,250 mg of iodine daily had significant (P = less than 0.05) decreases in persistence of antibody titers to brucella and leptospira organisms, in lymphocyte mitotic activity, in PHA injection induration, in phagocytosis by WBC, and in WBC counts. Calves fed iodine at 50 or 250 mg daily tended to have decreased leptospiral titers, lymphocyte mitoses, PHA injection induration, and in vitro phagocytosis by WBC compared with responses of controls. Seemingly, large amounts of dietary iodine interfere with titer maintenance to some antigens, with lymphocyte DNA synthesis, and with phagocytic activity of WBC.