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Biomedical subjects

L Magos

Publications and source records attributed to L Magos.

At least 19 recordsLinked to original sources
PubMed1998

Three cases of methylmercury intoxication which eluded correct diagnosis.

Three casual workers engaged in the production of mercuric acetate were admitted to hospital within 22 calendar days of each other, respectively 30, 48 and 5 days after their last working day. The workers served the same reactor in which elemental mercury was oxidized by peroxide and mercuric acetate was formed by the reaction of mercuric oxide with acetic acid. The diagnosis of mercury vapour intoxication of the first two patients was made 21 and 16 days after their admission when the third patient was admitted and hospitals were informed about their exposure. This diagnosis was made without considering: (a) that the observed signs were characteristic of methylmercury intoxication and are rarely present in mercury vapour intoxication; (b) the degree of deterioration after removal from exposure implicated methylmercury; (c) that blood mercury concentrations extrapolated to the last day at work were in the range, which had been associated with severe intoxication in the Iraq methylmercury epidemic; (d) at the time of the first blood mercury estimations the blood urinary mercury concentration ratios were 11.2, 5.4 and 2.4 while this ratio is below 0.5 in mercury vapour intoxication or in workers exposed to mercury vapour.

Adult↗
PubMed1994

Lead poisoning from retained lead projectiles. A critical review of case reports.

Case reports demonstrate that embedded lead projectiles (bullets, pellets) have the potential to cause lead poisoning. They also show that the relationship between blood lead concentration and lead poisoning is the same as in lead poisonings of occupational origin and that latent periods between lodgement and the onset of lead poisoning varies from less than a half year to several decades. Nevertheless neither the quantitative relationships between projectiles and blood concentrations nor the number at risk and the number affected are known. The aim of this review is to show the limitations of case studies through the analysis of negative and positive case reports, diagnostic and monitoring methods, differences between bullets and pellets, and factors affecting the disintegration of projectiles and the distribution of released lead.

Female↗
PubMed1991

Epidemiological and experimental aspects of metal carcinogenesis: physicochemical properties, kinetics, and the active species.

The carcinogenic properties of selected metals and their compounds are reviewed to provide a useful reference for existing knowledge on relationships between physical and chemical forms, kinetics and carcinogenic potential and between epidemiology, bioassays, and short-term tests. Extensive consideration is given to arsenic, beryllium, cadmium, chromium, lead, and nickel. Other metals such as antimony, cobalt, copper, iron, manganese, selenium, and zinc are discussed briefly.

Animals↗
PubMed1989

The effects of dose of elemental mercury and first-pass circulation time on exhalation and organ distribution of inorganic mercury in rats.

The lung plays a major role in the removal of dissolved elemental mercury (Hg0) from the bloodstream. During the first passage through the lung after an intravenous dose of Hg0 dissolved in aqueous buffer, from 10 to 17% was exhaled depending on the dose (0.11 or 1.1 micrograms Hg/rat) and the injection site (jugular versus tail vein). Furthermore, evidence is presented that subsequent exhalation over the next 50 s, before the rats were killed and the mercury determined in the lung at that time, was largely Hg0-extracted during the first pass. The total mercury extracted during the 60 s period was in the range of 40-49% of the dose. The oxidation of Hg0 to Hg2+ in red cells is important in limiting the availability of Hg0 to certain tissues. Thus, after a short residence time in blood (0.6 s after jugular vein injection), 12.9-17% is exhaled in the first pass as compared to 10.4-12.2% with a longer residence time (1.8 s after tail vein injection). Furthermore, there was a general tendency, even at 60 s after dosing, for certain tissues - lung, brain, and heart - to have higher values after dosing from the jugular vein. It was estimated that the half-time for oxidation was 3.3 s. Our results confirm previous observations that the form of inorganic mercury greatly influences the short-term deposition in certain tissues. Thus as compared to Hg2+, administration of Hg0 increases lung levels 5-10-fold; brain, 4-fold; and heart, 3-fold. Blood levels are lower after Hg0, particularly after the higher dose. Such findings are consistent with a model wherein Hg0 is in part oxidized by red blood cells, the remainder rapidly diffusing in tissues where it is also oxidized to Hg2+.

Animals↗
PubMed1989

A versatile mercury vapour generating system suitable for long-term inhalation experiments.

A mercury vapour generating system is described that is based on the reduction of HgCl2 by SnCl2 in the input airstream of the inhalation chamber. The solutions of the two chemicals are pumped by peristaltic pumps from reservoirs through a miniature mixing chamber into the upper part of a sloping glass tube (reduction chamber) through which air is sucked into the inhalation assembly. The liquid flows down the slope and through a port into a Quickfit flask. Reservoirs can be filled and the collecting flask emptied without interruption of exposure. The desired vapour concentration is achieved by varying the rate of mercury injection and the rate of airflow. Concentration in the inhalation chamber can be measured by passing air through a mercury vapour monitor or by radioactivity when 203HgCl2 is used and a known volume of air is passed through a hopcalite absorber. Operation instructions and an experimental example with mice are given.

Administration, Inhalation↗
PubMed1988

The effect of sodium chromate pretreatment on mercuric chloride-induced nephrotoxicity.

Sodium chromate (20 mg/kg, s.c.), which in male rats inflicted necrotic damage mainly in the P1 region (proximal part of the proximal convoluted tubules), protected against proximal tubular necrosis induced by 0.5 or 3.0 mg Hg2+/kg in the P2 (distal part of the proximal convoluted tubules) and P3 (pars recta part of the proximal tubules) regions. Histochemical staining for mercury indicated that chromate increased mercury deposition in those cells of the P1 region which were unaffected by chromate (had intact brush border) but did not decrease mercury deposition in the most severely affected P3 region. Chromate pretreatment actually increased mercury deposition in the kidneys of animals killed 24 h after the injection of 0.5 mg Hg2+. The protective effect was mutual. Cellular proliferation and fibrosis observed 4-5 days after chromate were prevented by injecting 0.5 mg Hg2+/kg 3 days after chromate treatment.

Animals↗
PubMed1987

The potentiation of the non-behavioural effects of amphetamine by carbon disulphide.

In agreement with the inhibition of dopamine-beta-hydroxylase by exposure to CS2, the extension of exposure time from 4 to 16 h increased dopamine concentrations in the hypothalmus and adrenals, and decreased noradrenaline concentration in the hypothalmus. The extension of exposure time also increased the toxicity of amphetamine. In conscious animals the stereotypic activity produced by 6.0 mg/kg and even that of 3.0 mg/kg amphetamine sulphate was suppressed by severe hyperthermia resulting in exhaustion, prostration and eventually death. A 16 h exposure to CS2 did not increase the lethal or hyperthermic effects of amphetamine in rats anaesthetized with 60 mg/kg sodium pentobarbitone. In fact the CS2 exposed rats became more hypothermic than non-exposed rats.

Adrenal Glands↗
PubMed1987

Comparison of the protection given by selenite, selenomethionine and biological selenium against the renotoxicity of mercury.

The protective effect of selenite, seleno-dl-methionine and biological selenium against the renotoxicity of mercury was tested in rats. As the source of biological selenium, the liver soluble fraction of rats given 60 mumoles/kg selenite 3 days before sacrifice was used. The aim of the experiments was to test whether protective efficiency follows the reported order of ability to form HgSe. Mercury was given subcutaneously in doses of 2.5, 5.0 and 7.5 mumoles/kg HgCl2 and selenium was given in equimolar doses at the same time as Hg2+. Liver soluble fraction, biological selenium or liver soluble fraction supplemented with selenite or seleno-dl-methionine were given orally, while in experiments without liver soluble fraction the two selenium compounds were given subcutaneously. Biological selenium was tested only at the two lower dose levels. Both biological selenium and seleno-dl-methionine decreased the urinary excretion of mercury in the first 48 h, but less so than selenite and only selenite decreased the renal content of mercury at the end of this period. Urinary alkaline phosphatase activity and plasma urea nitrogen at the 2.5 and 5.0 mumoles/kg dose levels decreased in the order of no selenium greater than biological selenium greater than seleno-dl-methionine greater than selenite. As the reported HgSe formation increases in the same order, the experiments support the role of HgSe formation in the protective effect. The degree of necrotic damage in the P2 and P3 regions of the proximal tubular cells increased in the same order as the biochemical indicators at the 5.0 and 7.5 mumoles/kg dose levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The effects of treatment with selenite before and after the administration of [75Se]selenite on the exhalation of [75Se]dimethylselenide.

The exhalation of dimethylselenium, as indicated by the respiratory loss of 75Se from injected Na75SeO3, depends not only on the dose, but also on previous exposure. Three days pretreatment with 1.2 mumol/100 g unlabelled selenite increased exhalation of 75Se from 0.1 or 1.2 mumol/100 g Na2 75SeO3 and decreased the retention of 75Se in blood and liver from the higher dose. Similarly the injection of 1.2 mumol/100 g unlabelled selenite 24 h after the last of 3 daily doses of 1.2 mumol/100 g labelled selenite increased the exhalation of 75Se in the following 24 h period. Thus, pre-exposure to selenium increased the exhalation of 75Se by making a higher proportion of the newly injected dose accessible for methylation. The exhaled dimethylselenide, however, is not derived solely from the injected dose, since in pretreated animals, it is possible to demonstrate exchange between injected and deposited selenium.

Animals↗
PubMed1986

The stimulation and inhibition of the exhalation of volatile selenium.

Administration of methylmercury (1.5-24 mumol kg-1; s.c.) to female rats simultaneously with Na2 75SO3 (0.25 or 24 mumol kg-1; s.c.) causes a dose-dependent increase in the exhalation of dimethylselenide. At the low selenite dose level, exhalation of 75Se over a 24 hr period is about fourfold greater after treatment with 24 mumol kg-1 methylmercury than that (approximately 0.75% of the dose) in the controls, but excretion by other routes (urine, faeces) and the liver and kidney contents of 75Se are not affected significantly. At the higher selenite dose level (24 mumol kg-1) exhalation of 75Se is correlated with the log dose of methylmercury. The faecal and urinary excretion remains essentially unaffected, and in rats treated with 24 mumol kg-1 methylmercury the 75Se contents of the liver, kidneys and blood are reduced by 78%, 86% and 18% respectively. The effects of the alkylmercurial are not specific since, at this selenite dose level, ethylmercury increases the exhalation and decreases the liver and kidney contents of 75Se approximately to the same extent as an equimolar dose of methylmercury. In methylmercury-treated and control animals dosed with 24 mumol kg-1 Na 75SeO3 the exhalation of 75Se is inhibited to the same extent by periodate-oxidized adenosine (PAD; 15 mumol kg-1, i.p.) in the first 6 hr. Later inhibition is less pronounced in methylmercury-treated rats. Under these conditions PAD has little effect on the renal content, but increases the hepatic content of 75Se. It seems, therefore, that the methylation of selenite occurs mainly in the liver and in both control and methylmercury-treated animals, S-adenosylmethionine is the major methyl donor. It is possible that methylmercury does not affect directly the methylation enzyme system but, by competition for protein sulphydryl groups, increases the availability of the intermediary selenide anion.

Animals↗
PubMed1985

The dependence of biliary methylmercury secretion on liver GSH and ligandin.

The biliary secretion of methylmercury was investigated in male rats which were given i.p. 400 mumoles/kg azathioprine or 96 mumoles/kg benziodarone 2 hr after the i.v. injection of 5 mumoles/kg MeHgCl. A group of rats were given 400 mg/kg trans-stilbene oxide (TSO) for 4 days before treatment with 10 mumoles/kg MeHgCl. A common link between these three compounds is their interference with ligandin. Azathioprine is a competitive inhibitor of glutathione S-transferase, benziodarone is covalently bound to ligandin and TSO is an inducer of liver ligandin. Although only azathioprine depletes liver GSH stores, both azathioprine and benziodarone inhibited the biliary secretion of methylmercury. As there is published proof that the reaction of MeHg+ with GSH does not require enzymatic help, the inhibitory effect of azathioprine and benziodarone confirms the role of ligandin in the transport of methylmercury or its GSH complex. However, the biliary secretion of methylmercury was increased only slightly by TSO pretreatment, but when 2 hr after the injection of MeHgCl animals received 2 mmoles/kg GSH, secretion increased twice as much in TWO pretreated than in control rats. This indicates the dual dependance of biliary methylmercury secretion on liver GSH and ligandin.

Animals↗
PubMed1985

The comparative toxicology of ethyl- and methylmercury.

Neurotoxicity and renotoxicity were compared in rats given by gastric gavage five daily doses of 8.0 mg Hg/kg methyl- or ethylmercuric chloride or 9.6 mg Hg/kg ethylmercuric chloride. Three or 10 days after the last treatment day rats treated with either 8.0 or 9.6 mg Hg/kg ethylmercury had higher total or organic mercury concentrations in blood and lower concentrations in kidneys and brain than methylmercury-treated rats. In each of these tissues the inorganic mercury concentration was higher after ethyl- than after methylmercury. Weight loss relative to the expected body weight and renal damage was higher in ethylmercury-treated rats than in rats given equimolar doses of methylmercury. These effects became more severe when the dose of ethylmercury was increased by 20%. Thus in renotoxicity the renal concentration of inorganic mercury seems to be more important than the concentration of organic or total mercury. In methylmercury-treated rats damage and inorganic mercury deposits were restricted to the P2 region of the proximal tubules, while in ethylmercury-treated rats the distribution of mercury and damage was more widespread. There was little difference in the neurotoxicities of methylmercury and ethylmercury when effects on the dorsal root ganglia or coordination disorders were compared. Based on both criteria, an equimolar dose of ethylmercury was less neurotoxic than methylmercury, but a 20% increase in the dose of ethylmercury was enough to raise the sum of coordination disorder scores slightly and ganglion damage significantly above those in methylmercury-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗