BSO、GSH、VC和DMPS对汞肾毒性影响的实验研究

目的探讨一次染汞的肾脏毒性作用并观察2氨基4(S丁基磺酰亚氨)丁酸(BSO)、还原型谷胱甘肽(GSH)、维生素C(VC)和二巯基丙磺酸钠(DMPS)预处理对汞肾脏毒性的影响。方法Wistar大鼠64只,随机分成8组。第1组为对照组,第2～4组为低、中、高剂量染汞组,分别皮下注射0.75、1.5和2.5mg kg的氯化汞溶液,第5～8组为预处理干预组。BSO预处理组先腹腔注射BSO0.5mmol kgbw,4h后皮下注射0.75mg kgHgCl2溶液。其他3个预处理组中,先分别腹腔注射GSH3mmol kg,VC4mmol kg或DMPS200μmol kgbw,2h后皮下注射2.5mg kgHgCl2溶液。注射容量均为5ml kgbw。对照组皮下注射生理盐水。注射12h后收集大鼠12h尿液,采集血液,分离血清,切取肝脏和肾皮质样品。测定肝脏、肾皮质和尿中汞含量;尿NAG、ALP、LDH活性和尿蛋白,血清尿素氮(BUN)含量。结果染汞后肝、肾皮质和尿汞含量随染汞剂量加大而逐渐增加。肾皮质汞含量有明显的剂量-效应关系,高剂量组肝汞含量显著高于中低剂量组和对照组。中高剂量组尿汞含量显著高于对照组。BSO预处理组和单纯0.75mg kgHgCl2组比,使肝汞含量增加,肾皮质和尿汞含量降低。GSH、VC和DMPS预处理组肝汞含量显著低于单纯2.5mg kgHgCl2组。尿NAG、ALP、LDH活性和尿蛋白、BUN含量随染汞剂量加大而升高,且2.5mg kgHgCl2组显著高于对照组、0.75和1.5mg kg HgCl2组。BSO预处理组尿NAG、ALP活性和尿蛋白、BUN含量显著高于单纯0.75mg kgHgCl2组和对照组。GSH、VC和DMPS预处理组和单纯2.5mg kgHgCl2组相比,尿NAG、ALP、LDH活性和尿蛋白、BUN含量显著降低。结论随着染汞剂量增加,肝脏、肾皮质和尿汞含量也增加。BSO预处理可增强汞的肾脏毒性作用,而GSH、VC和DMPS预处理则对汞的肾脏毒性具有一定的拮抗作用。     

Effects of BSO, GSH, Vit-C and DMPS on the nephrotoxicity of mercury

OBJECTIVE: To study the effects of BSO, GSH, Vit-C and DMPS on the nephrotoxicity of mercury. METHODS: The rats in groups 1, 2 and 3 were sc injected with 0.75, 1.5 and 2.5 mg/kg HgCl2, respectively. Fourth group rats were ip injected with 0.5 mmol/kg BSO and 4h later sc administrated with 0.75 mg/kg HgCl2. The rats in groups 5, 6 and 7 were ip injected with 3 mmol/kg GSH, 4 mmol/kg Vit-C, 200 micromol/kg DMPS, respectively, and 2 h later sc administrated with 2.5 mg/kg HgCl2. Eighth group rats were sc injected with saline as a control. Mercury concentrations in the liver, renal cortex and urine, urinary NAG, ALP, LDH activities, protein and BUN contents were determined. RESULTS: Urinary NAG, ALP activities, protein and BUN contents in the rats of BSO pretreatment group were significantly higher than that of 0.75 mg/kg HgCl2 alone group and control group. As compared with 2.5 mg/kg HgCl2 alone group, urinary NAG, ALP, LDH activities, urinary protein and BUN contents decreased significantly. CONCLUSION: BSO pretreatment could enhance the renal toxicity of mercury and GSH, Vit-C and DMPS pretreatment had antagonistic effects on nephrotoxicity of mercury.     

Trace metal interactions in vivo: inorganic cobalt enhances urinary copper excretion without producing an associated zincuresis in rats

The effects of cobalt chloride on copper and zinc metabolism in male Sprague-Dawley rats were examined. These effects were compared with those of penicillamine, a chelating agent utilized in the therapy of the genetic abnormality of copper metabolism in humans, Wilson's disease. Cobalt elicited an increased (approximately 4-fold) urinary excretion of copper lasting through 72 h following a single cobalt dose. In contrast to the marked increase in urinary zinc excretion produced by penicillamine, cobalt greatly reduced (approximately 75%) zinc output in urine. Tissue copper and zinc concentrations were measured after treatment with cobalt at doses ranging from 12 to 60 mg/kg body weight. Substantially reduced (approximately 25%) renal copper concentration was observed at 1 and 3 d after cobalt administration. In addition, cobalt produced a concurrent dose-dependent elevation (up to 1.6-fold) in hepatic zinc concentration. Cytosolic zinc was eluted from a Sephadex G-75 column in the molecular weight region associated with metallothionein. Time-dependent induction of metallothionein concentration (10-fold) in liver by cobalt was confirmed by the cadmium/hemoglobin affinity assay. The ability of inorganic cobalt to elevate zinc concentration in liver and produce increased urinary copper excretion without the zincuresis that normally accompanies penicillamine administration represents a newly defined biological property of this essential trace metal.     

Iron supplementation increases gentamicin nephrotoxicity in rats

Gentamicin (GM), an aminoglycoside antibiotic, can cause acute renal failure in humans and experimental animals. It has been proposed that lipid peroxidation may play a role in GM nephrotoxicity. Nutrients such as copper, selenium or iron that influence lipid peroxidation may also be a factor in toxicity. This study investigated the effect of supplemental dietary iron on the nephrotoxicity of GM. Weanling male Sprague-Dawley rats were fed control [0.75 mmol (42 mg) iron/kg] or iron-supplemented [4.32 mmol (242 mg) iron/kg] diets for 3 wk. Rats were subsequently injected intraperitoneally with GM (50 or 100 mg.kg body wt-1.d-1) or saline for 8 d. High dietary iron resulted in greater sensitivity to GM (100 mg/kg body wt) toxicity in terms of elevated urinary excretion of n-acetyl-beta-glucosaminidase (NAG) and increased mineralization, casts and megalocytes in renal tubules. After GM treatment was terminated, NAG excretion decreased with both dietary treatments. However, renal tubular cell damage, due to GM, remained higher than in saline-treated controls in rats fed 4.32 mmol iron/kg diet.     

谷胱甘肽和牛磺酸对汞急性肾毒性影响的实验研究

目的 探讨预先投予GSH和牛磺酸对汞急性肾毒性的影响。方法 将32只Wistar大鼠随机分为对照、HgCl2染毒、GSH HgCl2和牛磺酸 HgCl2 4组。对照组皮下注射0．9％的生理盐水,汞染毒组皮下注射2．5mg／kg的HgCl2溶液,注射容量为5ml／kg。GSH和牛磺酸组于注射相同剂量Hg口2前2h分别腹腔注射3mmoL/kg的GSH溶液和4mmol／kg的牛磺酸溶液。测定尿N-Z乙酰-β-D氨基葡萄糖苷酶(NAG)、碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)活性,尿蛋白和尿肌酐含量,血清尿素氮(BUN)以及尿汞和肾汞含量。结果 与对照组比较,HgCl2染毒组尿NAG、ALP、LDH活性显著升高,尿蛋白、BUN、尿汞、肾汞含量明显增加。预先投予GSH和牛磺酸后,可使汞染毒大鼠尿NAG和ALP活性、尿蛋白和BUN含量均较HgCl2染毒组显著减低;GSH组尿汞显著低于单纯染汞组,而牛磺酸组尿汞、肾汞与汞染毒组比较差异则无显著性。结论 GSH和牛磺酸对汞致急性肾损伤有一定的保护作用。     

Essential elements as early indicators of hexavalent chromium nephrotoxicity

The kidney is the appropriate critical organ for indicating chronic exposure to chromium compounds. The present work investigates the effect of dose-dependent hexavalent chromium concentration in various tissues of rats, the disturbances in metabolism of zinc and copper in liver and kidney, and histopathological changes in kidneys. White Wistar rats were used. Animals were injected intraperitoneally at a dose of 0.5 and 5 mg Cr/kg as K2CrO4. The animals were sacrificed after single and repeated doses at 24 h after the last injection. Disturbances in the metabolism of zinc and copper in the kidney of rats occur when the concentration of chromium in this organ attains about 30 microg Cr/g. An increase in urinary output of these essential metals is a more sensitive indicator of nephrotoxicity than ultrastructural damage of kidney.     

Native and induced rat kidney metallothioneins and their relation to cadmium toxicity

The concentrations of zinc, copper, iron, manganese, magnesium, and phosphorus in the kidneys were determined for control female rats of five different ages (4, 8, 12, 16, and 20 weeks old). The concentration of copper increased with age and it was attributed to three metallothionein peaks on a SW 3000 column. Parenteral administration of Cd-thionein caused swelling of kidneys to different degrees, depending on the age of the rats; the youngest rats were affected most. The concentrations of cadmium and the six metals in the kidneys at 12 hr and 7 days after injection were determined and compared with controls. The distribution among protein fractions of cadmium, zinc, and copper, which are related to metallothionein, were examined by gel permeation chromatography. The elution profiles of the three metals changed not only with the ages of the rats but also with time after injection. The changes were correlated with the copper content in the metallothioneins and with swelling of the kidneys. The changes also correlated with native metallothionein levels.     

Contribution of the cecum and colon to zinc absorption in rats

We examined the role of the large intestine in zinc absorption in rats in three separate experiments. In the first experiment, we examined apparent zinc absorption in rats fed diets containing graded levels of zinc carbonate (0.015-0.535 mmol Zn/kg diet) and evaluated zinc status on the basis of the zinc concentrations in serum and several tissues. The zinc absorption and the serum zinc concentration increased with the zinc content of the diet up to 0. 153 mmol Zn/kg diet. Femoral and pancreatic zinc levels increased linearly up to 0.229 mmol Zn/kg diet. In the second experiment, a zinc carbonate suspension was administered into the cecum via an implanted cannula or into the stomach via an orogastric tube, and the rats were fed diets with or without a highly fermentable fiber, guar gum hydrolysate (GGH, 50 g/kg diet), with coprophagy prevention. The amount of instilled zinc corresponded to the amount of zinc ingested as a component of the diet by the rats of a control group, 0.229 mmol Zn/kg diet. Apparent absorption of cecally instilled zinc was approximately half that observed when zinc was administered into the stomach in both diet groups. Serum and femur zinc concentrations in the cecum-administered groups were approximately 50 and 25% lower, respectively, than those in rats administered zinc into the stomach. The results demonstrate that, in vivo, the absorptive efficiency in the large intestine is not sufficient to satisfy the rat's zinc requirement and does not change when the luminal environment is substantially altered by feeding GGH. In Experiment 3, the effects of cecocolonectomy on zinc absorption were examined in rats with gastric acid suppression. In the cecocolonectomized groups, serum zinc concentration was lower as a result of treatment with a proton pump inhibitor, omeprazole, than in vehicle-treated rats, but not in sham-operated groups. These findings suggest that the cecum and colon contribute to zinc absorption when absorption in the small intestine is impaired.     

Renal and immunological effects of occupational exposure to inorganic mercury.

Seven parameters of renal dysfunction (urinary excretion of albumin, orosomucoid, beta 2-microglobulin, N-acetyl-beta-glucosaminidase (NAG), and copper; serum creatinine concentration, and relative clearance of beta 2-microglobulin) were examined in a group of chloralkali workers exposed to mercury vapour (n = 89) and in an unexposed control group (n = 75). Serum concentrations of immunoglobulins (IgA, IgG, IgM) and auto-antibodies towards glomeruli and other tissues were also determined. The parameters examined were compared between the two groups and related to different exposure parameters. In the chloralkali group median blood mercury concentration (B-Hg) was 55 nmol/l, serum mercury (S-Hg) 45 nmol/l, and urine mercury concentration (U-Hg) 14.3 nmol/mmol creatinine (25.4 micrograms/g creatinine). Corresponding concentrations for the control group were 15 nmol/l, 4 nmol/l, and 1.1 nmol/mmol creatinine (1.9 micrograms/g creatinine) respectively. None of the parameters of renal dysfunction differed significantly between the two groups, but there was a tendency to increased excretion of NAG in the exposed group compared with the controls. Also, a statistically significant relation existed between U-Hg and U-NAG (p less than 0.001). Serum immunoglobulin concentrations did not differ between the groups, and serum titres of autoantibodies (including antiglomerular basement membrane and antilaminin antibodies) were low in both groups. Thus the results gave no evidence of glomerular damage or of a tubular reabsorption defect at the current relatively low exposures. The findings still indicate slight, dose related tubular cell damage in the mercury exposed group. There were no signs of a mercury induced effect on the immune system.     

Renal and immunological effects of occupational exposure to inorganic mercury.

Seven parameters of renal dysfunction (urinary excretion of albumin, orosomucoid, beta 2-microglobulin, N-acetyl-beta-glucosaminidase (NAG), and copper; serum creatinine concentration, and relative clearance of beta 2-microglobulin) were examined in a group of chloralkali workers exposed to mercury vapour (n = 89) and in an unexposed control group (n = 75). Serum concentrations of immunoglobulins (IgA, IgG, IgM) and auto-antibodies towards glomeruli and other tissues were also determined. The parameters examined were compared between the two groups and related to different exposure parameters. In the chloralkali group median blood mercury concentration (B-Hg) was 55 nmol/l, serum mercury (S-Hg) 45 nmol/l, and urine mercury concentration (U-Hg) 14.3 nmol/mmol creatinine (25.4 micrograms/g creatinine). Corresponding concentrations for the control group were 15 nmol/l, 4 nmol/l, and 1.1 nmol/mmol creatinine (1.9 micrograms/g creatinine) respectively. None of the parameters of renal dysfunction differed significantly between the two groups, but there was a tendency to increased excretion of NAG in the exposed group compared with the controls. Also, a statistically significant relation existed between U-Hg and U-NAG (p less than 0.001). Serum immunoglobulin concentrations did not differ between the groups, and serum titres of autoantibodies (including antiglomerular basement membrane and antilaminin antibodies) were low in both groups. Thus the results gave no evidence of glomerular damage or of a tubular reabsorption defect at the current relatively low exposures. The findings still indicate slight, dose related tubular cell damage in the mercury exposed group. There were no signs of a mercury induced effect on the immune system.     

Enzymuria in a population living near a cadmium battery plant.

OBJECTIVES--To study the body burden of cadmium and signs of tubular dysfunction in a rural population living near a closed nickel cadmium battery plant. METHODS--Cadmium and N-acetyl-beta-glucosaminidase (NAG) in urine were measured in 72 subjects who lived close to the plant. RESULTS--Residents living close to the plant had higher median urinary cadmium concentrations than those living farther away (1.01 v 0.46 nmol/mmol creatinine) and than a control group (0.2 nmol/mmol creatinine). There was a significant correlation between urinary cadmium and the excretion of NAG in urine as well as signs of tubular dysfunction in residents who excreted urinary cadmium above 0.5 nmol/mmol creatinine. CONCLUSION--Tubular dysfunction may appear in environmentally exposed subjects at lower cadmium body burdens than previously anticipated.     

Copper and zinc levels in serum and urine of cadmium-exposed people with special reference to renal tubular damage

Urinary copper and zinc concentrations and their serum levels were determined in women environmentally exposed to cadmium, including “itai-itai” disease patients and suspected patients, for evaluating the effect of cadmium exposure on metabolism of such essential metals as copper and zinc in human beings. Copper concentrations in the urine of cadmium-exposed women, especially “itai-itai” patients and suspected patients, were much higher than those of nonexposed women. Zinc concentrations in the urine of cadmium-exposed women, however, were not different from those of nonexposed women. Zinc levels in the serum of the “itai-itai” patients were somewhat lower than those of the nonexposed women. On the other hand, serum copper was almost equal in the cadmium-exposed and the nonexposed women. The correlation coefficient between β₂-microglobulin amounts and copper concentrations in the urine of all women examined was as high as 0.95. It is concluded that exposure to cadmium will cause an increase in the excretion of copper in urine, which is attributable to renal tubular damage due to the cadmium exposure, and that urinary zinc excretion is not increased by cadmium exposure, even in the patients who suffer from severe renal tubular damage.     

Zinc anc copper status of Polynesian residents in the Tokelau Islands

Analyses for zinc and copper were performed in samples of serum, hair, toenails, and a 24-hr urine from Polynesian men and women resident in the Tokelau Islands. Selection of subjects was according to rank of systolic blood pressure obtained in a previous survey. The only difference in zinc anc copper values between the men and the women was a higher hair zinc concentration observed for the men. Rank of blood pressure had no influence on the measurements for zinc or copper, although within blood pressure ranks the men again had a higher hair zinc concentration than the women. Analysis of Tokelauan foods showed that most contained very low concentrations of zinc anc also low concentrations of copper. Octopus was one of the few rich sources of zinc and copper. Estimated daily dietary intakes (excluding water) were 4.5 mg Zn and 1.5 mg Cu. The reliability of measurements in serum, urine, hair, and toenails for assessing zinc and copper status is questioned.     

Effects of changes in dietary zinc, copper and selenium supply and of endotoxin administration on metallothionein I concentrations in blood cells and urine in the rat

These studies were designed to investigate the effects of low dietary zinc, copper or selenium intake of certain types of stress and of injection of zinc, copper or cadmium on metallothionein I (MT-I) concentrations in the blood and urine of rats. The aim was to establish whether such measurements could be of value in the diagnosis of zinc deficiency. Marginal zinc deficiency rapidly caused a major decrease in MT-I levels in the blood cells and to a lesser extent in urine. Injection of zinc and also of cadmium and copper had the opposite effect and increased MT-I concentrations in both samples, although the effects of zinc on blood cells and urine were relatively transient. The MT-I in the blood cells was associated mainly with the erythrocytes. No changes in blood or urine MT-I levels were found in copper- and selenium-deficient rats. Neither cold stress nor restriction of food intake for 24 h had any significant effect on MT-I levels in the blood cells or urine. Endotoxin injection increased urinary MT-I excretion in both zinc-adequate and zinc-deficient rats but did not affect blood cell MT-I levels in either group of animals. It appears therefore that assay of erythrocyte MT levels could be of particular value in the diagnosis of zinc deficiency, especially when it is accompanied by stress or infection.     

Endotoxin-induced changes in copper and zinc metabolism in the Syrian hamster

The temporal response of zinc and copper metabolism to endotoxin administration was examined in Syrian hamsters over a 144-hour period. Serum copper was significantly elevated at 12, 24 and 72 hours after endotoxin, whereas serum zinc was reduced 4-48 hours after treatment. A brief elevation (8 hours) in liver copper concentration and a sustained (72 hours) increase in liver zinc concentration were also observed. The amount of zinc associated with liver metallothionein (MT) progressively increased with time, to a plateau by 24 hours and persisted at the elevated level until 72 hours after endotoxin treatment. In vitro translation of poly (A)+ RNA from liver polyribosomes showed that following endotoxin treatment MTmRNA activity was maximally elevated 6 hours after endotoxin administration and remained elevated 24 and 48 hours thereafter. Slab gel electrophoresis of serum proteins indicated changes in a stainable protein comigrating with purified ceruloplasmin after endotoxin administration. Pooled gingival tissue from endotoxin-treated hamsters demonstrated a consistently elevated copper content 12-144 hours after treatment. Endotoxin isolated from Bacteroides melaninogenicus was more effective in elevating gingival and serum copper and gingival zinc than Escherichia coli endotoxin. It was concluded that endotoxin administration elicits responses that result in enhanced metaollthionein mRNA activity. In addition, Cu and Zn concentrations in serum, liver and gingival tissue are influenced by different endotoxins to different degrees.     

Cadmium turnover and changes of zinc and copper body status of rats continuously exposed to cadmium and ethanol

The effects of continuous exposure to cadmium (Cd) and ethanol on Cd turnover and zinc (Zn) and copper (Cu) body status of male Wistar rats were studied. The animals received an aqueous solution of 10% (w/v) ethanol and/or 50 mg Cd/l as the only drinking fluid for 12 weeks. The concentrations of Zn, Cu and Cd in the serum (or blood), liver, kidneys, spleen, brain, heart, femoral muscle and femur as well as in 24-h urine and faeces specimens were assessed by atomic absorption spectrometry (AAS). Ethanol alone had no effect on Cd accumulation or excretion. By contrast, co-administration of ethanol with Cd influenced the turnover of this toxic metal. Long-term consumption of ethanol alone caused a decrease in femur Zn and liver Cu concentrations. Moreover, the urinary loss of both bioelements decreased, whereas their faecal excretion was increased. Exposure to Cd resulted in an increase in liver and kidney and in a decrease in femur and 24-h urine Zn concentrations. An increase in Cu concentration in the kidney and a decrease in the brain were also noted. Moreover, Cd increased the total pool of Zn in organs (kidneys, liver, spleen, heart and brain), but did not influence that of Cu. Zn concentration in the liver, kidney and spleen of rats co-exposed to Cd and ethanol were increased, but were decreased in the brain and femur, compared to controls. The concentrations of Cu in livers and brains of these rats were decreased, whereas those in kidney, spleen and heart were increased. The urinary excretion of the elements was decreased, whereas their faecal excretion was increased. Moreover, the total amount of Cu in organs decreased below the control value and that of Zn was in the normal range. These changes in Zn and Cu levels could be explained by different effects of both toxic substances, differences in bioelement intakes (due to reduced consumption of drinking solutions and food), and the modifying effect of ethanol on Cd turnover. Our results suggest that alcoholics may be more susceptible to Cd accumulation and its effects on body Zn and Cu.     

Renal impairment caused by chronic occupational chromate exposure

Purpose

To determine the nephritic toxicity of chromate after chronic occupational exposure.

Methods

The environmental contamination was assessed by measuring the chromium (Cr) in 8-h airborne sampler. The integrated level of Cr was determined by Cr concentrations in the whole blood (WB-Cr) and the urine (U-Cr). The renal glomerular and tubule impairment was evaluated by determination of cystatin C (Cys-C) in the serum and microalbumin (mALB), urinary beta₂-microglobulin (??₂M), N-acetyl-beta-d-glucosaminidase (NAG) activity in the urine.

Results

The mean occupational exposure time to Cr was 12.86?years with average daily air level of 27.13???g/m³ comparing to 0.11???g/m³ of the background level. The WB-Cr and U-Cr were 23.49???g/L and 17.41???g/g creatinine (Cre), respectively in the chromate-exposed workers comparing to 3.32???g/L and 1.52???g/g Cre in the controls. The serum Cys-C and urinary mALB were significantly increased in the chromate-exposed workers. Exposure to Cr seems to induce an enhanced level of urinary NAG activity and ??₂M concentration. The increased serum Cys-C concentration was positively correlated with the level of serum Cre. The U-Cr was positively correlated to the concentrations of urinary mALB, ??₂M, and the activity of NAG.

Conclusions

Chronic occupational exposure to chromate causes comprehensive renal impairment though more severity could occur in the tubule than in the glomeruler.     

Optimal protein level is required for normalization of taste sensitivity in rats

The influence of levels of dietary protein on taste sensitivity for sodium chloride and zinc status was studied in rats. Animals were given free access to one of seven graded levels of purified egg protein (PEP) diets for 28 days. Preference tests for the solution of sodium chloride (0.86 and 8.56 mmol/L) versus deionized water were conducted on days 19 and 21. Feces, urine and blood were collected for assay of zinc concentrations. Only the rats fed the 8% PEP diet discriminated low concentration of 0.86 mmol/L sodium chloride solution. The rats fed another diets discriminated only high concentration of 8.56 mmol/L sodium chloride solution. Twenty percent PEP diet-fed group did not discriminate both concentrations of sodium chloride. Zinc in serum concentration (r=0.89, p<0.001) and balance (r=0.78, p<0.001) was correlated with dietary protein intake. Serum zinc concentrations of the rats fed the 8 and 10% PEP diets were within the normal range. Retained zinc levels remained constant within the range of 4–8% PEP diets. The present study indicates that 8% PEP is optimal dietary protein level to normalize taste sensitivity for sodium chloride.     

Lead and zinc concentrations in plasma, erythrocytes, and urine in relation to ALA-D activity after intravenous infusion of Ca-EDTA.

Lead and zinc concentrations in plasma, erythrocytes, and urine, urinary ALA concentration, and ALA-D activity in blood were studied for four hours in two male lead workers during and after a one hour infusion of Ca-EDTA 2Na. Urinary and plasma lead concentrations increased as a result of administering Ca-EDTA 2Na, and the ratios of lead concentrations in plasma to those in urine were greatly increased. The increase of plasma lead concentration was not due to the haemolytic effect of Ca-EDTA 2Na but was mobilised lead, rapidly excreted in the urine. ALA-D activity in blood increased at the end of the experiment with a transient decrease during the infusion of Ca-EDTA 2Na. As zinc concentrations in erythrocytes and plasma did not decrease during the infusion despite an increase in the urinary excretion of zinc, the transient decrease of ALA-D activity was not due to a loss of zinc caused by Ca-EDTA 2Na. From the results of additional experiments in vitro, this transient decrease could be related neither to Ca-EDTA 2Na nor to lead in the blood.     

Lead and zinc concentrations in plasma, erythrocytes, and urine in relation to ALA-D activity after intravenous infusion of Ca-EDTA

Lead and zinc concentrations in plasma, erythrocytes, and urine, urinary ALA concentration, and ALA-D activity in blood were studied for four hours in two male lead workers during and after a one hour infusion of Ca-EDTA 2Na. Urinary and plasma lead concentrations increased as a result of administering Ca-EDTA 2Na, and the ratios of lead concentrations in plasma to those in urine were greatly increased. The increase of plasma lead concentration was not due to the haemolytic effect of Ca-EDTA 2Na but was mobilised lead, rapidly excreted in the urine. ALA-D activity in blood increased at the end of the experiment with a transient decrease during the infusion of Ca-EDTA 2Na. As zinc concentrations in erythrocytes and plasma did not decrease during the infusion despite an increase in the urinary excretion of zinc, the transient decrease of ALA-D activity was not due to a loss of zinc caused by Ca-EDTA 2Na. From the results of additional experiments in vitro, this transient decrease could be related neither to Ca-EDTA 2Na nor to lead in the blood.