Influence of dietary lead and calcium on tissue lead accumulation and depletion, lead metabolism and tissue mineral composition in sheep

Two experiments were conducted to study the metabolism and tissue accumulation and depletion of dietary Pb in sheep. In Exp. 1, a feeding trial, 33 wethers, 56 kg initially, were assigned randomly to two dietary treatments: .25% Ca plus 1,000 ppm Pb or .50% Ca plus 1,000 ppm Pb. Supplemental Ca and Pb were supplied as reagent grade calcium carbonate or reagent grade lead acetate. The experiment was divided into two phases of 75 and 180 d; during the first phase, diets contained 1,000 ppm supplemental Pb and during the second phase, diets contained 3 ppm Pb. Calcium level remained constant within treatments throughout both phases. Sheep were slaughtered at various intervals during both phases and tissue samples taken. Lead increased in all tissues during the accumulation period and decreased during the depletion period; however, kidney was the only tissue in which Pb concentration declined to control values by 180 d. Dietary Ca reduced (P less than .05) the concentration of Pb deposited in liver, but not in other tissues. Interactions of dietary Ca and Pb on tissue concentration of various minerals occurred. In Exp. 2, a balance trial, 27 wethers, 53 kg initially, were allotted randomly to four treatments in a 2 X 2 factorial arrangement. Diets contained either 0 or 1,000 ppm supplemental Pb as reagent grade lead acetate and .25 or .50% total Ca with supplemental Ca from calcium carbonate. Increasing dietary Pb increased (P less than .05) percentage of Pb retained and increased (P less than .01) whole blood Pb concentration (1.0 vs 1.42 micrograms/ml).     

铅胁迫对禾本科牧草生长、生理及Pb2+富集转运的影响

采用苗期盆栽试验,对14份禾本科牧草种质材料进行不同浓度(0,10,50,100,200,300 mg/kg)铅(Pb)胁迫处理,通过对株高、分蘖数、地上/地下生物量、脯氨酸含量、抗氧化酶(SOD、POD、CAT)活性、地上部与根中Pb²⁺含量等指标的测定与分析,探究Pb胁迫对禾草生长生理以及Pb²⁺富集转运的影响。结果表明,随着Pb浓度的增加,14份材料的株高、分蘖数、地上生物量均呈先上升后下降的趋势,地下生物量则逐渐降低,通过综合评价,来自土耳其的长穗冰草G₅具有较强的耐Pb性。随着Pb浓度的增加,地上部与根中Pb²⁺含量逐渐升高,富集系数逐渐降低,转移系数逐渐降低(披碱草G₇与G₈除外),根中Pb²⁺含量显著高于地上部,为Pb²⁺的主要富集器官,披碱草地上部Pb²⁺含量高于其他材料,具有较强的Pb富集转运能力。7份材料的生理指标测定结果表明,随着Pb浓度的增加,7份材料的脯氨酸含量逐渐上升,CAT活性逐渐下降,POD和SOD活性则呈先上升后下降的趋势。     

Acute lead poisoning in cows due to feeding of lead contaminated ash residue

In a dairy herd of 21 cows which were on pasture during the day at the end of May 2002, four eight years old cows were suddenly inappetent and showed severe diarrhoea consisting of black discolorate feces. A few days after the onset of the disease, three affected cows exhibited neurological disorders. These cows were admitted to the IInd Medical Clinic of the University for Veterinary Medicine in Vienna. Following clinical signs were observed: circulatory weakness, anorexia, atony of the rumen, diarrhoea and in accordance with acute lead poisoning typical signs of the central nervous system. One cow died and the other two animals were euthanized. Results of blood testing were anaemia, basophil spotting of erythrocytes, increase of liver enzymes and CK, hypocalcaemia, decrease of potassium and phosphate. The cerebrospinal fluid of two cows showed increased CK-, LDH- and AST-values. The lead contents of whole blood samples were between 0.486 and 0.928 mg/kg, of liver samples 13.3 to 114.4 mg/kg, of kidney samples 172.2 to 448 mg/kg and of rumen content 59 mg/kg fresh matter. At necropsy, enteritis, liver fluke disease and severe interstitial and alveolar pulmonary emphysema were found. Pathohistologically typical ischaemic necrosis of neurons predominantly at the tips of the gyri, disseminated petechial hemorrhages and moderate diffuse neovascularisation, but no acid-fast intranucleolar inclusion bodies in the renal tubules were observed. As causative agent of the acute lead poisoning a residue on combustion, taken up by the cows on the pasture, was confirmed. The ash residue was formed by combustion of three tires which contained 450 g heavy weights of 96.5% lead for wheel balance. The lead content of the ash residue was between 2.9 and 28 g/kg dry matter.     

Blood lead and urinary delta aminolevolonic acid (U-ALA) in the diagnosis of lead toxicosis of dogs

A comparative evaluation of the usefulness of blood lead and urinary delta aminolevolonic acid estimations in the diagnosis of canine lead poisoning was made in 2 dogs which were given increasing quantities of lead by mouth for extended periods. In both lead administered dogs the blood lead levels remained elevated throughout the experimental period of 18 weeks. This contrasted with the results of U-ALA determinations in which elevated levels were detected only infrequently and at erratic intervals lacking relationship to lead exposure.     

Long-term follow-up of blood lead levels and haematological and biochemical parameters in heifers that survived an accidental lead poisoning episode

Four of 10 heifers that survived an episode of lead poisoning caused by an old broken battery in the pasture were periodically monitored from days 14 to 205 after the episode, with the aim of (i) determining the time-course of lead clearance from blood; and (ii) assessing whether the exposed cattle showed changes in haematological parameters or serum markers of hepatic and renal function (e.g. serum creatinine level) that might be useful as indicators of subclinical toxicity. On the first sampling day, lead levels in blood varied between 0.478 and 0.758 mg/l. The half-life of lead in blood was rather variable, ranging from 68 to 266 days. Despite the high blood lead levels, no significant changes were detected in haematological parameters or hepatic/renal markers, all of which remained within normal ranges. In conclusion, these cattle that survived an episode of lead poisoning may constitute a risk for human consumers, but do not appear to have suffered severe health consequences themselves.     

铅镉与细胞凋亡研究最新进展

1引言 铅、镉是不可降解的环境污染物,在环境中可长期蓄积,并通过食物链、土壤、水和空气进入人畜体内,对人和动物机体造成长期的慢性损伤及严重的生态问题.铅、镉与必需金属元素结构相似,可以激活和抑制由必需金属离子调控的细胞进程.     

The effects of thiamin on lead metabolism: organ distribution of lead 203.

The effect of thiamin on the organ distribution of lead was evaluated in CD-1 mice exposed intragastrically or intraperitoneally to a single dose of lead acetate (100 micrograms) containing 100 microCi lead 203. They were treated with either thiamin (25 or 50 mg/kg body weight), calcium ethylenediaminetetraacetic acid (CaEDTA) (50 mg/kg body weight), or combinations of thiamin and CaEDTA. The whole body retention and the organ distribution of lead 203 varied depending upon the route of lead administration, dose of thiamin and the specific treatment combination. Thiamin (25 or 50 mg/kg) treatment increased the whole body retention of both intragastric and intraperitoneal lead by approximately 10% in each instance. Calcium ethylenediaminetetraacetic acid, either alone or in combination with thiamin (50 mg/kg) reduced the whole body retention of lead by as much as 14% regardless of route of lead exposure. The relative retention of lead by the liver, kidney and spleen was greater in mice exposed to lead by the intragastric route. Regardless of route, CaEDTA in the combined treatment reduced the relative retention of lead in both the liver and kidney, whereas thiamin alone only reduced the retention of lead in the kidney. The results of this study indicate that thiamin in combination with CaEDTA alters the distribution and retention of lead in a manner which may have therapeutic application as it relates to chelation therapy.     

Chronic lead poisoning in horses

Lead acetate was fed to 4 groups of 2 horses each to study chronic lead intoxication. A 5th group of 3 horses was maintained as controls. The leas was fed in capsules, with the minimum dosage of 6.25 mg/kg/day of lead as lead acetate (group I). The dose was increased from group I through group IV in an approximate geometric series, with each group being given about 125% of the dose given the previous group. These doses were given for 105 days, a period designated as phase 1. Since clinical signs were not observed after 105 days, the doses were increased and fed for an additional 190 days (days 106 to 295). This period was designated phase 2. The smallest daily dose in phase 2 was set at about 125% of the largest daily dose in phase 1. The doses in each group was increased by about 125% of that of the previous group, as was done in phase 1. Seven horses died or were euthanatized after 18 to 190 days of phase 2 (123 to 295 days after the 1st dose). One horse in group I did not develop any clinical signs of intoxication. Dose-related responses were unnoticed with doses larger than 15.3 mg/kg/day. All horses given lead had increased blood lead and serum iron concentrations. During phase 2, the hematocrit (erythrocyte volume) and hemoglobin contents were depressed. The lead concentration in kidney, liver, spleen, pancreas, brain, bone, and heart was increased in the treated horses. The dose level required to produce lead intoxication was greater than that reported for cattle and that estimated in epizootiologic studies of horses.     

Blood lead concentrations in rabbits

Blood lead concentrations in 68 healthy rabbits from laboratory (n = 15), meat production (n = 45), and home environments (n = 8) were determined. The median blood lead concentration of this heterogeneous population was 8 micrograms/dl (range = 2 to 27 micrograms/dl).     

Experimental lead toxicosis in swine

Thirty pigs, weighing 17 to 24 kg, were exposed to lead or sodium acetate orally or intraperitoneally (IP) 6 days each week for 13 weeks. These pigs were extremely tolerant of lead. Only mild clinical signs of lead toxicosis were observed in orally lead-exposed pigs despite blood lead concentrations of up to 290 micrograms/dl. Four IP lead-exposed pigs died, but eight other IP lead-exposed pigs survived the exposure period despite blood lead concentrations up to 14,300 micrograms/dl. Lead exposure caused marked decreases in blood delta-aminolevulinic acid dehydratase activities of all pigs and moderate decreases of blood hemoglobin concentrations, hematocrit percentages, mean corpuscular volumes, mean corpuscular hemoglobin concentrations, and mean corpuscular hemoglobins in IP lead-exposed, but not in orally lead-exposed pigs. Basophilic stippling was observed in erythrocytes of lead-exposed pigs, but not in those of control pigs.