The measurement of mercury excretion in urine

The determination of mercury in urine using cold atomic absorption spectrometry according to Gage and Warren is used after slight modification as standard method for the exposure test in persons exposed to its vapours in industry in Czechoslovakia. Within the concentration range between 100 and 600 nmol X l-1 of urine the relative standard deviation was lower than 4%. In workers exposed to mercury in the production of thermometers, fluctuation of urinary mercury concentration due to variations in diuresis could be greatly reduced by adjustment for endogenous creatinine. After the intake of 2.2 or 2.5 l of liquids the concentration of mercury in urine dropped considerably, but returned again to its initial value within 4 hours after fluid intake. The mercury half-life in the organism is estimated at about 30 days, but may be longer at mercury concentrations of 1 mumol X l-1. Contradictory to the original expectation, the Araki's coefficient b that is recommended for suppressing the effect of the volume of excreted urine on the concentration of urinary substances was found to be concentration-dependent: at 500 nmol X l-1 its value shifted towards 1 (0.85), at 100 nmol X l-1 towards zero (0.2-0.3). It is believed that mercury urinalysis data adjusted for endogenous creatinine are sufficiently reliable to be used for assessing the risk of human exposure to mercury.     

Elimination of mercury from amalgam in rats.

The aim of this study was to measure the urinary mercury excretion in rats exposed to amalgam over a two months period. Animals were either exposed to mercury from 4 dental amalgams or fed the diet containing powdered amalgams. The results showed significantly higher mercury amount in urine of both exposed groups than in control. Even two months after the amalgam had been placed in rats teeth, the amount of mercury in the urine remained 4-5 times higher than in control, and 4 times higher than in rats exposed to diet containing powdered amalgam. The elevated urinary Hg amount was accompanied by an increased level of total protein in urine. In the same exposure period the excretion of total protein in urine of rats with amalgam fillings was 2 times higher than in control and 1.5 times higher than in rats exposed to amalgam through diet. Concentrations of mercury in the sera of all groups were below the detection limit of the method. The results show that amount of mercury and protein in the urine of rats were related to the mercury release from dental malgam.     

Automatic method for quantitation of mercury in blood, plasma and urine.

Here we report our experience of quantification of mercury in blood, plasma and urine by using modifications of a procedure for cold vapour atomic absorption. We have tried: (1) modifications of the instrumentation including the tower, the cell and apparatus for measurement; (2) to increase the volume of sample, avoiding problems caused by foaming and background to arrive at a reliable method with low detection limit. Blood and plasma samples were digested overnight in a mixture of nitric acid and perchloric acid (1:5). Recovery of known additions of mercury was close to 100%. Coefficients of variation (CV) within runs and between runs was for B-Hg 4.7 and 9.5, respectively at 20 nmol/l, and for U-Hg 1.8 and 5.2, respectively at 57 nmol/l. The same detection limit of 5 nmol/l was obtained with blood, plasma and urine. This is in the lower range of non-occupationally exposed normal subjects. The results, including those obtained in sample exchange with other laboratories and with reference materials, indicate that the accuracy of this method for quantification of mercury is good.     

The impact of long-term past exposure to elemental mercury on antioxidative capacity and lipid peroxidation in mercury miners

Limited information is available on the effects of chronic mercury exposure in relation to the risk of cardiovascular disease (CVD). It is known from in vitro and in vivo studies that Hg can promote lipid peroxidation through promotion of free radical generation, and interaction with antioxidative enzymes and reduction of bioavailable selenium. The objective of the study was to test the hypothesis that long-term past occupational exposure to elemental Hg (Hg⁰) can modify antioxidative capacity and promote lipid peroxidation in miners.

The study population comprised 54 mercury miners and 58 workers as the control group. The miners were examined in the post-exposure period. We evaluated their previous exposure to Hg⁰, the putative appearance of certain nonspecific symptoms and signs of micromercurialism, as well as the main behavioural and biological risk factors for CVD, and determined: 1) Hg and Se levels in blood and urine, 2) antioxidative enzymes, Cu/Zn superoxide dismutase (CuZn-SOD), catalase (CAT), and selenoenzyme glutathione peroxidase (GSH-Px) activity in erythrocytes as indirect indices of free radical activity, 3) pineal hormone melationin (MEL) in blood and urine, and 4) lipid hydroperoxides (LOOHs) and malondialdehyde (MDA) as lipid peroxidation products.

The mercury miners were intermittently exposed to Hg⁰ for periods of 7 to 31 years. The total number of exposure periods varied from 13 to 119. The cumulative U-Hg peak level varied from 794-11,365 μg/L. The current blood and urine Hg concentrations were practically on the same level in miners and controls. Miners showed some neurotoxic and nephrotoxic sequels of micromercurialism. No significant differences in behavioural and biological risk factors for CVD were found between miners and controls. A weak correlation (r = 0.36, p < 0.01) between systolic blood pressure and average past exposure U-Hg level was found. The mean P-Se in miners (71.4 μg/L) was significantly lower (p < 0.05) than in the controls (77.3 μg/L), while the mean U-Se tended to be higher (p < 0.05) in miners (16.5 μg/g creatinine) than in the controls (14.0 μg/g creatinine). Among antioxidative enzyme activities, only CAT in erythrocytes was significantly higher (p < 0.01) in miners (3.14 MU/g Hb) than in the controls (2.65 MU/g Hb). The mean concentration of B-MEL in miners (44.3 ng/L) was significantly higher (p < 0.01) than in the controls (14.9 ng/L). The mean value of U-MEL sulphate (31.8 μg/L) in miners was significantly lower (p < 0.01) than in the control group (46.9 μg/L). Among the observed lipid peroxidative products, the mean concentration of U-MDA was statistically higher (p < 0.01) in miners (0.21 μmol/mmol creatinine) than in the controls (0.17 μmol/mmol creatinine).

In the group of miners with high mercury accumulation and the presence of some nonspecific symptoms and signs of micromercurialism, the results of our study partly support the assumption that long-term occupational exposure to Hg⁰ enhances the formation of free radicals even several years after termination of occupational exposure. Therefore, long-term occupational exposure to Hg⁰ could be one of the risk factors for increased lipid peroxidation and increased mortality due to ischaemic heart disease (ICH) found among the mercury miners of the Idrija Mine.     

The influence of urinary flow rate on mercury excretion in children

ProjectThere is limited literature concerning the effect of urinary flow rate on mercury excretion at low-level exposure. The aim of the present study is to examine the influence of urinary flow rate on mercury excretion in children. Also of interest is the influence of flow rate on creatinine excretion and creatinine-corrected mercury, which arisearises with spot urine samples.ProcedureA substudy of the New England Children's Amalgam Trial collected pairs of urine samples from children aged 10–16 years: a timed overnight collection and a spot daytime sample collected the following day. These samples were analyzed for mercury and creatinine concentration. Regression analysis was used to model the effect of urinary flow rate in the timed overnight samples. A paired t-test compared concentrations and creatinine-corrected mercury between overnight and daytime samples.ResultsCreatinine excretion rate (mg/h) increased significantly with urinary flow rate (mL/h), whereas creatinine concentration (g/L) decreased with flow rate. We found a non-significant increase in mercury excretion rate (ng/h) with flow rate, and mercury concentration decreased with flow rate. Mercury and creatinine concentrations were significantly higher in the overnight compared to daytime samples. For creatinine-corrected mercury, no significant impact of urinary flow rate was found.ConclusionsAlthough the creatinine excretion rate, and probably the mercury excretion rate, increased with urinary flow rate, the mercury/creatinine ratio seemed relatively unaffected by urinary flow rate.     

Induction of metallothionein in rat tissues following subchronic exposure to mercury shown by radioimmunoassay

Although the analysis of metallothionein (MT) by radioimmunoassay (RIA) is not a common technique, its use is preferred over other methods since it offers the advantages of sensitivity and specificity. In this paper we present data on the basal levels of MT in rat tissues and physiological fluids of female Sprague-Dawley rats. The mean basal MT concentrations of the following organs and fluids were determined by RIA to be: liver (9.8 μg/g), kidney (68 μ/g), brain (0.8 μg/g), spleen (1.0 μg/g), heart (5.4 μg/g), plasma (11 ng/ml), and urine (200–300 μg/g creatinine). Following subcutaneous exposure to inorganic mercury (0.2 μmol/kg/d, 5 d a week for up to 4 wk), the metal accumulated primarily in the kidney. There was also a simultaneous accumulation of zinc in the liver and of zinc and copper in the kidney. Induction of MT did take place in liver, kidney, brain, and spleen. No increases in the MT contents of blood and urine were noted. The excess zinc and copper in the kidney of exposed animals were found to be associated predominantly with MT. No overt signs of mercury toxicity were noted in these animals and the incidence of proteinurea was nil. The data are discussed with reference to methods of MT determination in animal tissues and in relation to mercury metabolism and toxicity.     

Displacement of zinc and copper from copper-induced metallothionein by cadmium and by mercury: in vivo and ex vivo studies

The in vitro affinity of metals for metallothionein (MT) is Zn less than Cd less than Cu less than Hg. In a previous study Cd(II) and Hg(II) displaced Zn(II) from rat hepatic Zn7-MT in vivo and ex vivo (Day et al., 1984, Chem. Biol. Interact. 50, 159-174). The ability of Cd(II) or Hg(II) to displace Zn(II) and/or Cu(II) from metallothionein in copper-preinduced rat liver (Zn, Cu-MT) was assessed. Cd(II) and Hg(II) can displace zinc from (Zn, Cu)-MT both in vivo and ex vivo. The in vitro displacement of copper from MT by Hg(II) was not confirmed in vivo and ex vivo. Cd(II) treatment did not alter copper levels in (Zn, Cu)-MT, as expected. Hg(II) treatment, however, did not decrease copper levels in MT, but rather increased them. The sum of the copper increase and mercury incorporation into MT matched the zinc decrease under in vivo conditions and actually exceeded the zinc decrease under ex vivo conditions. Short-term exposure of rat liver to exogenous metals can result in incorporation of these metals into MT by displacement of zinc from pre-existing MT. Displacement of copper from pre-existing MT by mercury, as predicted by in vitro experiments, was not confirmed under the conditions of our in vivo and ex vivo experiments. This result is explainable based on the differing affinities and/or preferences of the two metal clusters in MT.     

Comparison of hair, nails and urine for biological monitoring of low level inorganic mercury exposure in dental workers.

Creatinine-corrected urine mercury measurements in spot urine samples are routinely used in monitoring workers exposed to inorganic mercury. However, mercury measurement in other non-invasive biological material has been used in some epidemiological studies. Dentists and dental nurses remain a group of workers with potential exposure to inorganic mercury through their handling of mercury-containing amalgam, although changes in work practices have reduced the current, likely exposure to mercury. Therefore, dental workers remain an occupational cohort in whom the value of using different biological media to identify exposure to low level inorganic mercury can be investigated. Samples of head hair, pubic hair, fingernails, toenails and urine were analysed for mercury content from a cohort of UK dentists (n=167) and a socioeconomically similar reference population (n=68) in whom any mercury exposure was primarily through diet. The mercury content in all biological material was significantly higher in the dental workers than in the control population (p<0.0001). The geometric mean and 90th percentile mercury concentrations in the urine samples from dentists were 1.7 and 7.3 micromol mol(-1) creatinine, respectively, with only one sample having a value at around the UK's Health and Safety Executive biological monitoring health guidance level of 20 micromol mol(-1) creatinine. Receiver operator characteristic analyses suggested that the ability of the biological material to discriminate between dentists and referents were fingernails>urine approximately equal to toenails>pubic hair approximately equal to head hair. Further investigation is warranted as to why fingernails appear to be such a good discriminator, possibly reflecting some contribution of direct finger contact with amalgam or contaminated surfaces rather than systemic incorporation of mercury into growing nails. Good correlation between head hair and pubic hair mercury levels in all subjects was obtained (r=0.832), which was significantly improved when hair samples weighing <10 mg were excluded (r=0.868). Therefore, under these exposure conditions and using the described pre-analytical washing steps, there is little influence from atmospheric contamination on the level of mercury content of head hair. The choice of non-invasive biological materials for mercury analysis depends on a number of considerations. These include the toxicokinetics of urinary mercury excretion, the growth rates of hair and nail, the nature and time-frame of exposure, and the fact that urine mercury may not reflect the body burden level from dietary methyl mercury. However, the data from this study suggests that urine mercury remains the most practical and sensitive means of monitoring low level occupational exposure to inorganic mercury.     

In vivo and ex vivo displacement of zinc from metallothionein by cadmium and by mercury

Divalent cadmium and mercury ions are capable in vitro of displacement of zinc from metallothionein. This process has now been studied in vivo and ex vivo, using the isolated perfused rat liver system, in order to determine if this process can occur in the intact cell. Rats with normal and elevated (via preinduction with zinc) levels of hepatic zinc thionein were studied. Cd(II) completely displaces zinc from normal levels of metallothionein and on a one-to-one basis from elevated levels of metallothionein, both in vivo and ex vivo. Hg(II) displaces zinc from metallothionein (normal or elevated) rather poorly, as compared with Cd(II), in vivo, probably due to the kidneys preference for absorbing this metal. Ex vivo Hg(II) displaces zinc from metallothionein (normal or elevated) on a one-to-one basis, with considerably more mercury being incorporated into the protein than in vivo. The results of double-label ex vivo experiments using metal and [35S]cysteine (+/- cycloheximide) were consistent with the above experiments, indicating that de novo thionein synthesis was not required for short term incorporation of cadmium and mercury into metallothionein. These data are supportive of the hypothesis that cadmium and mercury incorporation into rat hepatic metallothionein during the first few hours after exposure to these metals can occur primarily by displacement of zinc from preexisting zinc thionein by a process which does not require new protein synthesis.     

Increased urinary excretion of zinc and copper by mercuric chloride injection in rats

The effects of HgCl₂ on urinary excretion of Zn, Cu and metallothionein at different time intervals were observed in male Wistar rats. The rats were given a daily intraperitoneal injection of²⁰³HgCl₂ (0.5 or 1.0 mg Hg kg^–1) for 2 days.²⁰³Hg, Zn, Cu and metallothionein in urine, kidney and liver were analyzed. Significant increases in urinary Zn and Cu concentrations were found in HgCl₂-dosed groups. Elevated urinary Zn and Cu concentrations were accompanied by an increased metallothionein excretion in urine at different time periods. Zn concentration in urine remained elevated during the entire observation period of 7 days. There were also increased concentrations of Cu and Zn in the renal cortex in one of the two exposed groups. The results indicate that urinary Cu and Zn are related to the manifestation of renal toxicity and/or the synthesis of metallothionein in kidney induced by mercury.     

Elevated mercury bound to serum proteins in methylmercury poisoned rats after selenium treatment

Methylmercury is a toxic pollutant and is generated by microbial methylation of elemental or inorganic mercury in the environment. Previous study found decreased hepatic MDA levels and urinary mercury levels in methylmercury poisoned rats after sodium selenite treatment. This study further found increased mercury levels in serum samples from methylmercury poisoned rats after selenium treatment. By using size exclusion chromatography coupled to inductively coupled plasma mass spectrometry, three Hg- binding protein fractions and two Se-binding protein fractions were identified with the molecular weight of approximately 21, 40, and 75 kDa and of 40 and 75 kDa, respectively. Elevated mercury level in the 75 kDa protein fraction was found binding with both Hg and Se, which may explain the decreased urinary Hg excretion in MeHg poisoned rats after Se treatment. MALDI-TOF-MS analysis of the serum found that the 75 kDa protein fractions were albumin binding with both Hg and Se and the 21 kDa fraction was Hg- binding metallothionein.     

汞中毒患者尿中性粒细胞明胶酶脂质相关运载蛋白的含量及其意义

目的：检测汞中毒患者尿中性粒细胞明胶酶脂质相关运载蛋白（U－NGAL）的含量,探讨其在汞中毒早期肾损伤中的意义。方法：以24例我科收住院患者为汞中毒组、无汞接触史的15例健康成人为对照组,分别进行临床体检并测定尿－N－乙酰－D－葡萄糖苷酶（U－NAG）、24h尿蛋白定量（UPQ）、尿β2微球蛋白（U－β2－MG）、尿α1微球蛋白（U－α1－MG）、尿汞（U－Hg）、血汞（B－Hg）、血肌酐（Scr）、血尿素氮（BUN）,排除既往肾脏病史,ELISA法测定U－NGAL含量,并分析上述结果。结果：汞中毒组B－Hg、U－Hg、U－NAG、UPQ、U－β2－MG、U－α1－MG、U－NGAL与对照组相比均有统计学差异（P〈0．05）,传统指标Ser、BUN与对照组相比无统计学差异;U－α1－MG、U－β2－MG、U－NAG、UPQ、U－NGAL与B－Hg均有相关性,且相关系数逐渐递增。结论：长期汞接触可造成肾功能损害,U－α1－MG、U－β2－MG、U－NAG、UPQ、U－NGAL可作为汞中毒肾早期损害的敏感指标,且灵敏性依次递增;U－NGAL可能比U－NAG早出现。     

Dental amalgam mercury exposure in rats

The aim of this study was to measure the distribution of mercury, in tissues of rats exposed to amalgam over a two months period. Possible interaction of mercury with copper and zinc in organs was also evaluated. Rats were either exposed to mercury from 4 dental amalgams, or fed the diet containing powdered amalgam during two months. Mercury was measured in the kidney, liver and brain, copper in kidney and brain and zinc in kidney. The results showed significantly higher concentrations of mercury in the kidneys and the brains of rats in both exposed groups compared to control. Even after two months of exposure to mercury brain mercury concentration in rats with amalgam fillings was 8 times higher than in the control and 2 times higher than in rats exposed to amalgam supplemented diet. The highest mercury concentration in the latter group was found in the kidneys and it was 5 times higher than in the control group. We found no significant differences between mercury levels in exposed and control rat's liver. Exposure to mercury from dental amalgams did not alter the concentrations of copper and zinc in the tissues. Histopathological analyses of rats tissues did not show any pathological changes. These results support previously proposed nose-brain transport of mercury released from dental amalgam fillings.     

Reaction of 3-ethoxy-2-oxobutyraldehyde bis(thiosemicarbazonato) Cu(II) with Ehrlich cells. Binding of copper to metallothionein and its relationship to zinc metabolism and cell proliferation

The copper complex of 3-ethoxy-2-oxobutyraldehyde bis(thiosemicarbazone) or CuKTS is reduced and dissociated upon reaction with Ehrlich cells. Titration of the cells with the complex leads to the specific binding of copper to metallothionein with 1 to 1 displacement of its complement of zinc. Under conditions of complete titration of metallothionein, 1.25-2.5 nmol CuKTS/10(7) cells, cellular DNA synthesis is rapidly inhibited but no long term effects on cell proliferation are observed. The kinetics of redistribution of Cu and Zn in Ehrlich cells in culture and in animals were studied after pulse reaction of CuKTS with cells. After exposure of cells to the noncytotoxic concentration of 2.5 nmol of CuKTS/10(7) cells, nonmetallothionein bound copper is lost rapidly from the cells, after which copper in metallothionein decays. New zinc metallothionein is made as soon as exposed cells are placed in culture. New synthesis stops when the level of zinc in metallothionein reaches control levels. A second pulse treatment of cells with CuKTS to displace zinc from metallothionein again stimulates new synthesis of the protein to restore its normal concentration. The kinetics of metal metabolism in Ehrlich cells exposed to 5.5 nmol of CuKTS/10(7) cells, which inhibits cell proliferation, are qualitatively similar except there is a pronounced lag before new zinc metallothionein is synthesized. The Ehrlich ascites tumor in mice responds to CuKTS similarly to cells in culture. It is also shown that cultured Ehrlich cells do not make extra zinc metallothionein in the presence of high levels of ZnCl2, and fail to accumulate copper in the presence of large concentrations of CuCl2.     

Whole-body retention,and urinary and fecal excretion of mercury after subchronic oral exposure to mercuric chloride in rats

The effects of long-term daily intake of mercury on its urinary and fecal excretion, whole-body retention, and blood concentration in male rats were observed. The animals were exposed to mercuric chloride labeled with ²⁰³Hg via drinking water for 8 weeks (5, 50 and 500 m Hg). ²⁰³Hg in urine, feces and blood was quantified. The blood mercury concentration did not keep a linear relationship with the increasing dose. The percentage of the total amount of mercury intake which is excreted by the fecal route in rats exposed to 500 m Hg was significantly lower than in those exposed to 5 and 50 m. The daily dose percentage of mercury excreted in urine increased with dose size. The results show that the absorption fraction of mercury through the gastrointestinal tract (30–40%) was higher than values previously reported.     

A comparison of urinary mercury between children with autism spectrum disorders and control children

Background

Urinary mercury concentrations are used in research exploring mercury exposure. Some theorists have proposed that autism is caused by mercury toxicity. We set out to test whether mercury concentrations in the urine of children with autism were significantly increased or decreased compared to controls or siblings.

Methods

Blinded cohort analyses were carried out on the urine of 56 children with autism spectrum disorders (ASD) compared to their siblings (n = 42) and a control sample of children without ASD in mainstream (n = 121) and special schools (n = 34).

Results

There were no statistically significant differences in creatinine levels, in uncorrected urinary mercury levels or in levels of mercury corrected for creatinine, whether or not the analysis is controlled for age, gender and amalgam fillings.

Conclusions

This study lends no support for the hypothesis of differences in urinary mercury excretion in children with autism compared to other groups. Some of the results, however, do suggest further research in the area may be warranted to replicate this in a larger group and with clear measurement of potential confounding factors.     

Human epidermal growth factor-on molecular forms present in urine and blood.

A sensitive enzyme-linked immunosorbent assay (ELISA) for quantitation of human epidermal growth factor (EGF) was employed to study EGF in urine and blood. The EGF/creatinine ratio in urine was significantly higher for women (range and (median); 0.20-0.83 (0.50) nmol EGF/mmol creatinine) than for men (0.17-0.63 (0.30) nmol EGF/mmol creatinine). We were not able to demonstrate EGF in plasma (median plasma EGF < 0.01 nmol/l) whereas serum contained a range and (median) of 0.02-0.31 (0.12) nmol EGF/l. The amount of EGF in serum showed a weak correlation to the platelet count (r = 0.327). EGF was partly purified by affinity chromatography from urine (urine EGF) and from activated platelets in platelet rich plasma (blood EGF). Both blood and urine contained a high molecular weight form of EGF (HMW EGF) as well as 6 kDa EGF. HMW EGF from blood was similar to HMW EGF from urine concerning behaviour upon gel filtration, pI and apparent affinity constant for binding to the EGF receptor. However, HMW EGF constituted approx. 40% of blood EGF but only 10% of urinary EGF. The 6 kDa EGF from both blood and urine contained two isopeptides with pI around 4.40 and 4.15 but in various proportions. The apparent affinity constant for binding to the EGF receptor for blood 6 kDa EGF was 1.8 x 10(10) l/mol compared to 1.0 x 10(10) l/mol for urinary 6 kDa EGF and 0.8 x 10(10) l/mol for HMW EGF from both blood and urine. The present study suggests that the processing of the EGF precursor differs in the blood and in the kidneys and that 6 kDa EGF from blood and urine binds to the EGF receptor with a higher apparent affinity constant than does HMW EGF.     

Urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine and 5-(hydroxymethyl) uracil in smokers

Cigarette smoke is known to generate free radicals by various mechanisms. In this study involving 30 non-smokers and 30 smokers, we show that urinary excretion of 5-(hydroxymethyl) uracil (HMUra) was not different in the two groups (6.54±2.07 vs. 6.70±1.68 nmol/mmol creatinine). In contrast, 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dGuo) excretion increased by 16% (1.16±0.35 vs. 1.35±0.50 nmol/mmol creatinine, p=0.039). Results concerning 8-oxo-dGuo are in agreement with those of previous studies. We observed significant multiple correlations between HMUra and creatinine (r_p=0.44), BMI (r_p=-0.27) and nicotine derivatives (r_p=0.26). Multiple correlation analysis showed relations between 8-oxo-dGuo on the one hand, and: creatinine (r_p=0.36), nicotine derivatives (r_p=0.29), BMI (r_p=-0.24) on the other.     

Urinary zinc excretion and zinc status of patients with Β-thalassemia major

In this study, zinc status and urinary zinc excretion with and without desferrioxamine (DFO) infusion and the relationship between urinary zinc excretion and renal tubular dysfunction in thalassemia major (TM) patients were investigated. Forty TM patients were given four DFO infusions on alternate days over a 1-wk period prior to the transfusion. On each day that DFO was given, a 24-h urine collection initiated. DFO was omitted for 1-wk before the following transfusion and during the period four 24-h urine collections were performed. Twenty healthy children provided 24-h urine collection as controls. Blood samples were taken on each of two consecutive transfusion days of the patients and from the controls. Urinary zinc excretion was measured and plasma and red blood cell (RBC) zinc analysis were performed by inductively coupled plasma-atomic emission spectrophotometry. UrinaryN-acetyl-Β-D-glucosaminidase (NAG) activity and creatinine were determined in morning urine specimens. The mean plasma zinc concentration was significantly lower in the patients not given DFO compared to the values of the patients given DFO and the control group. The mean RBC zinc concentration (Μmol/g Hb) in the patients (with and without DFO) and the control group were similar. Urinary zinc excretion was significantly higher in the patients receiving DFO compared to the control group, whereas urinary zinc excretion in the patients not given DFO was not different from the controls. Urinary NAG indices (U/g Cr) were significantly higher in the patients compared to controls. Urinary zinc excretion was correlated with the urinary NAG indices.     

Evaluation of the nocturnal levels of urinary biogenic amines in men exposed overnight to 50-Hz magnetic field

The aim of this study was to determine whether exposure to magnetic fields might affect human health and to look for possible effects of acute exposure (9 hours) to 50-Hz magnetic fields (10 microT) on the urinary concentration of biogenic amines. Thirty-two young men (20-30 years old) were divided into two groups (sham-exposed and exposed group) of 12 to 16 subjects each. All subjects participated in two 24-hour experiments to evaluate the effects of both continuous and intermittent exposure to magnetic fields. The subjects were exposed to the magnetic field from 2300 to 0800, while lying down. Total urine (from 2300 to 0800) was collected at 0800. The results (expressed as a ratio of biogenic amine excretion to creatinine excretion (nmol/mmol)) did not differ significantly between sham-exposed and exposed men for any of the parameters measured: adrenaline, noradrenaline, dopamine, dihydroxyphenylalanine, 3,4-dihydroxyphenylacetic acid, homovanillic acid and 5-hydroxyindoleacetic acid. These results suggest that nocturnal exposure to either continuous or intermittent 50-Hz magnetic fields of 10 microT does not affect, at least under our experimental conditions, the nocturnal excretion of biogenic amines in healthy young men.