Toleration of high concentrations of dietary zinc by mink

Adult and kit male and female natural dark ranch mink (Mustela vison) were fed a conventional diet supplemented with 0, 500, 1,000, or 1,500 ppm zinc, as ZnSO4.7H2O, for 144 days. No marked adverse effects were observed in feed consumption, body weight gains, hematologic parameters, fur quality, or survival. Zinc concentrations in liver, kidney, and pancreas of the mink increased in direct proportion to the zinc content of the diet. Histopathologic examination of the livers, kidneys, and pancreata revealed no lesions indicative of zinc toxicosis. The results indicate that mink can tolerate at least 1,500 ppm dietary zinc, as ZnSO4.7H2O, for several months without apparent adverse effects.     

Chronic corneal edema in aged ranch mink

Chronic corneal edema occurred in 53% of 116 ranch mink (Mustela vison) 8 to 11 years old. Most were royal pastel females, the main group at risk. Bilateral in 46 of 66 affected mink studied, the edema evolved over a month or so until the cornea became opaque, diffusely pale blue-gray or white, and greatly thickened. The swollen cornea did not become ulcerated, pigmented, or vascularized, even after it had been severely edematous for a year or two. The edema supervened as a consequence of spontaneous deterioration of the corneal endothelium. Attenuation and loss of the endothelial monolayer were the most common light microscopic changes. Other changes included discrete excrescences (guttata) along the posterior surface of the thickened Descemet's membrane and a subendothelial fibrillar or fibrocellular layer (posterior collagenous layer) often apposed to the excrescences. Likened to the primary endothelial dystrophies of man and the dog, this endothelial disorder of mink is regarded as an abiotrophic degeneration with its own distinguishing features in this species.     

Overt signs of toxicity to dogs and cats of dietary deoxynivalenol

Studies were conducted to determine the dietary amounts of deoxynivalenol (DON; vomitoxin) in dog and cat food that are required to produce overt signs of toxicity (e.g., vomiting or reduced food intake). Wheat naturally contaminated with 37 mg of DON/kg was used to manufacture pet foods containing 0, 1, 2, 4, 6, 8, and 10 mg of DON/kg. Deoxynivalenol concentration in pet food following manufacture was unchanged, indicating that the toxin was stable during conventional extrusion processing. Dogs previously fed DON-contaminated food were able to preferentially select uncontaminated food. Dogs not previously exposed to DON-contaminated food consumed equal quantities of contaminated and uncontaminated food. There was no effect of 6 mg of DON/kg on dog food digestibility. Food intake of dogs was significantly reduced by DON concentrations greater than 4.5 +/- 1.7 mg/kg, and DON greater than 7.7 +/- 1.1 mg/kg reduced cat food intake. Vomiting by dogs and cats was commonly observed at the 8 and 10 mg DON levels.     

板芪口服液急性毒性及长期毒性试验研究

探讨新兽药板芪口服液的急性毒性与长期毒性,评价其安全性。小鼠灌服板芪口服液进行急性毒性预试验,未获得动物的半数致死量,遂以最大给药剂量(270 g生药·kg~(-1)体重)进行急性毒性试验。将80只大鼠随机分为板芪口服液低、中、高剂量组和空白对照组,每组20只,雌雄各半,进行长期毒性试验。分别以10 g生药·kg~(-1)体重(猪临床推荐剂量的20倍)、20 g生药·kg~(-1)体重(猪临床推荐剂量的40倍)、40 g生药·kg~(-1)体重(猪临床推荐剂量的80倍)给大鼠灌服,对照组灌服等体积蒸馏水,给药容积为1 m L·100 g~(-1)体重,每天1次,连续给药30 d,期间观察大鼠外观体征及行为活动。停止给药24 h和15 d后进行剖检、血液生化检查和病理组织切片观察。结果显示,板芪口服液急性毒性试验评价为无毒,长期毒性试验中各剂量组大鼠的观察指标和测定指标与空白对照组相比均无显著差异,表明板芪口服液安全无毒,可用于临床试验。     

壳聚糖对饲料镉致罗非鱼急性毒性的影响

通过两个试验研究了壳聚糖对饲料中镉致罗非鱼急性毒性的影响。试验1将360尾罗非鱼随机分为两个处理(对照组和试验组),每个处理3个重复,比较壳聚糖添加后饲料镉致罗非鱼96 h半致死剂量的变化情况。对照组一次性投喂镉水平分别为0.00%、0.10%、0.25%、0.50%、1.00%和2.00%的6种对照饲料;试验组饲料镉含量与对照组相同,并加入10%壳聚糖,同法进行饲料镉对罗非鱼的急性毒性试验。试验2将160尾罗非鱼随机分为两个处理,每个处理4个重复,分别投喂镉含量为0.50%的对照组和试验组饲料,研究饲料中添加壳聚糖对镉致罗非鱼半致死时间的影响。试验结果为:两个试验中试验组鱼的死亡率均低于对照组;对照组96 h半致死剂量(LD50)和半致死时间(LT50)分别为(49.67±6.11)mg/kg.BW和(47.76±3.03)h,试验组96 h LD50和LT50分别为(86.05±6.11)mg/kg.BW和(65.20±6.09)h,试验组96 h LD50和LT50与对照组相比差异极显著(P<0.01),表明壳聚糖能够缓解饲料中镉对罗非鱼的急性毒性。     

鸡阿奇霉素的慢性毒性实验研究

本试验采用固定剂量(1/20LD50,1/40LD50,1/80LD50)连续染毒法让大发乌骨蛋鸡120d连续摄入阿奇霉素。雏鸡生长缓慢。尸体剖检主要见肝脏体积肿大,呈黄色或浅黄色,胆囊肿大,胆汁淤滞;肠系膜点状出血。组织学变化以肝脏、肾脏、肠黏膜等组织器官的实质性细胞变性甚至坏死为特征。血液病理学变化主要是血清总蛋白含量前期降低,后期升高;白蛋白含量降低;球蛋白、总胆固醇、血糖含量和丙氨酸氨基转移酶、天门冬氨酸氨基转移酶、乳酸脱氢酶及碱性磷酸酶活性升高。     

Effect of dietary fluorine on growth, blood and bone characteristics of growing-finishing pigs

Three hundred eighty-four growing-finishing pigs were used in two experiments to determine the effect of dietary fluorine (F) on growth, blood and bone physical characteristics. Fourteen dietary treatments were formulated by supplementing F (as NaF) to a milo-soybean meal basal diet (7 ppm F) to provide levels of 7, 132, 257, 382, 507 and 632 ppm F for Exp. 1, and 7, 25, 43, 61, 79, 97, 115 and 133 ppm F for Exp. 2. Average daily gain (ADG) and average daily feed intake (ADFI) were not affected (P greater than .09) when F was fed at levels between 7 and approximately 132 ppm. Average daily gain and ADFI were reduced (P less than .0001) for pigs consuming diets with F concentrations greater than 132 ppm (Exp. 1). Feed conversion was not affected (P greater than .17) by any level of F fed. Serum F and alkaline phosphatase concentrations increased (P less than .01) with increasing dietary F levels. Serum and bone Ca and P concentrations were not affected (P greater than .13) by dietary F levels (Exp. 1). In Exp. 1 and 2, bone F increased (P less than .0001) and metatarsal stress and modulus of elasticity decreased (P less than .0001) as level of F increased in the diet. Bone thickness decreased quadratically (P less than .02) in Exp. 1 and linearly (P less than .0007) in Exp. 2 with increased dietary F levels. Scanning electron microscopy showed an increase in porosity of bones from pigs fed the higher levels of F. Growing-finishing pigs were able to tolerate approximately 132 ppm F for growth, but all of the F levels (greater than or equal to 7 ppm) fed in these two experiments affected bone integrity.     

Subacute toxicity of dietary 3-acetyldeoxynivalenol in mice.

3-Acetyldeoxynivalenol was incorporated into a semisynthetic diet at levels of 2.5, 5, 10 or 20 ppm and fed to mice for up to 48 days. Body weights and feed consumption were determined, and blood samples for hematological evaluation were taken. Selected tissues were examined microscopically and the humoral immune response was assessed using the Jerne plaque assay. 3-Acetyldeoxynivalenol caused a dose-related depressed feed consumption within the first seven days and reduced body weight until day 14 when fed at levels up to 10 ppm. When fed at a level of 20 ppm, an initial depression in body weight gain and a general malaise were followed by a return to normal. At necropsy, no macroscopic or microscopic lesions could be found. The immune response was not significantly affected after seven or 14 days, but at 21 days, a dose-dependent enhanced response was observed. The findings indicate that, after an initial period of reduced feed intake, animals are apparently able to overcome the toxic effects of 3-acetyldeoxynivalenol.     

Chronic copper toxicity in a dairy herd

The addition of excessive copper to a commercially prepared dairy ration caused chronic copper toxicity in a dairy herd. A formulation error by a feed company resulted in copper levels of 800 to 1,000 mg/kg in the “as fed concentrate,” amounting to about 400-500 mg copper/kg of the whole ration. Five animals died with typical signs of acute copper toxicity, including intravascular hemolysis and methemoglobinemia. A further 39 cows died on the farm from a combination of debilitation and secondary infectious causes, and 215 were sent to slaughter because of debilitation and poor milk production. The mortality of calves born to dams that had been fed the toxic concentrate was approximately 50%.

We postulate that dairy cows, particularly pregnant cows, may be more susceptible to copper toxicity than other cattle, and suggest reexamination of the presently allowable maximum levels of copper supplementation of diets for dairy cattle.

     

Chronic copper toxicity in a dairy cow

A three year old Holstein dairy cow fed a ration containing a copper supplement died of chronic copper poisoning. The concentration of copper in the liver was 331 ppm (wet weight). The typical lesions of chronic copper toxicity including icterus, hepatic fibrosis and hemoglobinemic nephrosis were found at necropsy. The chronic copper toxicity was not considered to be a herd problem since the liver copper concentration in a slaughtered cull animal and blood samples taken from five animals in the same herd were within normal limits.     

Effects of dry dietary protein on digestibility,nitrogen-balance and growth performance of young male mink

The experiment was to study the nutrient digestibility and metabolism performance of male minks,which were fed different protein level diets during growth period. Effects of protein quantity on growth and development of minks and feed conversion ratio(FCR) were also investigated. Sixty healthy male minks of 45 d were randomly allocated into six groups with ten replicates, which was one sable for each replicate. The minks in six groups were fed diets in which protein levels were 28, 30,32, 34, 36 and 38%,respectively. The six groups were denoted as P28, P30, P32, P34, P36 and P38. After 2 wk, all minks were weighed, average daily gains(ADG) were calculated, and the digestibility values of nutrients were determined. The results indicated that digestibility of calcium, nitrogen of fence, nitrogen deposition, net protein utilization(NPU), and biological value of protein(BV) were similar(P 0.05), however, nitrogen intake greatly varied among groups(P 0.01). Compared with group P28, groups of P34, P36 and P38 showed significant difference(P 0.01) in ADG and FCR. In conclusion, it was recommended that adding34% protein to mink diet would optimize production parameters including ADG, digestibility of nutrition,and FCR, and negative result was observed when diet protein was lower than 28%.     

Pathogenesis of aleutian mink disease. VII. Chronic hepatitis with bile duct proliferation]

Aleutian disease is a chronic persistent viral infection of mink characterized by hypergammaglobulinema, generalized plasmacytosis, sclerosing glomerulonephritis, polyarteritis, and plasma cell hepatitis with bile duct proliferation. The development of hepatic lesions was studied both light- and electron-microscopically in mink experimentally infected with Aleutian disease virus. Fifteen normal and 99 mink experimentally infected with Aleutian disease virus were used. Experimental mink were killed in intervals from 3 weeks to 23 months after infection, and liver sections were processed for both light- and electron-microscopic studies. Experimentally infected mink developed portal and intralobular lymphocytic and plasmacytic infiltrates in the liver 3 weeks after infection. Four to five weeks after infection there was evidence of early bile duct proliferation that began as an outgrowth of the portal bile ducts. Three to five months after infection a marked bile duct proliferation was present in some of the portal triads and adjacent liver lobules; but there was no tendency of these lesions to progress into biliary cirrhosis. Ultrastructural characteristics of proliferating bile duct cells were marked deformation, formation of multiple cell layers, reduction in the number of microvilli and desmosomes, and infiltration of the epithelial cells by lymphoid cells and plasmacytes. The hepatic lesions either develop by direct virus stimulation or by the deposition of virus-antibody complexes.     

Chronic effects of moniliformin in broiler and turkeys fed dietary treatments to market age

Floor pen studies were conducted, with broilers from 1 to 7 wk of age and with turkeys from 1 to 14 wk of age, to evaluate the chronic effects of moniliformin (M). Fusarium fujikuroi (M-1214) culture material was added to typical corn-soybean basal diets to supply 0, 25, or 50 mg M/kg diet (broilers) or 0, 12.5, 25, 37.5, or 50 mg M/kg diet (turkeys). Compared with controls, chicks fed diets containing 50 mg M/kg consumed more feed, had lower body weight gain, were less efficient in converting feed to body weight gain, and had increased relative heart and proventriculus weights. Chicks fed the diet containing 50 mg M/kg also had significantly higher mortality and decreased mean corpuscular volumes compared with controls. Broilers fed 25 and 50 mg M/kg also had increased serum gamma glutamyltransferase activities. Feed intake, body weight gain, and feed conversion of turkeys fed dietary M were not affected. At 6 and 14 wk, turkeys fed 25, 37.5, or 50 mg M/kg diet had increased (P < 0.05) relative heart weights when compared with controls. At week 14, turkeys fed diets containing 37.5 or 50 mg M/kg also had increased (P < 0.05) relative liver weights compared with turkeys fed 0, 12.5, or 25 mg M/kg diet. Lesions, observed only in the hearts of broilers and turkeys fed 50 mg M/kg, were loss of cardiomyocyte cross striations, increased cardiomyocyte nuclear size, and an increased number of cardiomyocyte mitotic figures (turkeys only). Results indicate that > or = 37.5 mg M/kg is hepatoxic and > or = 25 mg M/kg is cardiotoxic to turkeys and 50 mg M/kg diet is toxic to broilers fed to market age.     

Incidence of nursing sickness and biochemical observations in lactating mink with and without dietary salt supplementation.

The impact of dietary sodium on the incidence of nursing sickness in mink dams and on the average litter biomass of 28 and 42 day old kits was studied. One group (n = 115 including 12 barren females) was given a standard feed mixture with a natural content of 0.53 g NaCl/MJ and another group (n = 115 including 8 barren females) was given the same feed mixture supplemented with NaCl to a final content of 1.00 g/MJ. The average dam weight at weaning was significantly lower (P < 0.001) and the incidence of nursing sickness during the last part of the lactation period 3 times higher in the nonsupplemented group. The average litter biomass at weaning did not differ between the 2 experimental groups. A number of biochemical markers of preclinical nursing sickness, e.g. plasma aldosterone and osmolality, Na+ and Cl concentrations in plasma and urine, were studied during the last part of the lactation period and at weaning in 20 dams of the nonsupplemented group, in 10 dams of the salt supplemented group and, for comparison, in 5 + 5 barren females on the day corresponding to day 34 after parturition in nursing mink. The nonsupplemented group had significantly lower concentrations of sodium and chloride in plasma and urine and a significantly higher concentration of plasma aldosterone as compared to the salt supplemented group. Distinct signs of relative salt deficiency and preclinical nursing sickness thus characterized the nonsupplemented group throughout this period, while more blurred hints of electrolyte imbalances were noticed in the sodium chloride supplemented group at weaning. A beneficial effect of salt supplementation on the incidence of nursing sickness was shown; however, it remains unclear whether salt deficiency can cause nursing sickness or whether salt acts as an appetite stimulant preventing inanition and the development of the disorder.     

微胶囊化儿茶素的慢性毒性试验研究

儿茶素是从茶叶中提取的多酚基次生代谢物,具有抗氧化、降血脂、抗动脉粥样硬化、抗衰老、抑制癌细胞等多种功能,但儿茶素在非保护状态下生物利用率不高,利用微胶囊化儿茶素可提高儿茶素的生物学效应.为了给微胶囊化儿茶素的临床安全利用提供依据,笔者等观察了微胶囊化儿茶素的慢性毒理学特性.现将结果报告如下.