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Biomedical subjects

L Magos

Publications and source records attributed to L Magos.

At least 37 records · Page 2Linked to original sources
PubMed1985

Methylmercury stimulates the exhalation of volatile selenium and potentiates the toxicity of selenite.

The aim of the present experiments was to investigate whether a single dose of 24 mumol/kg methylmercuric chloride (MeHgCl) in rats can influence the effect of an equimolar dose of sodium selenite (Na2SeO3) on body weight or the exhalation of dimethylselenide, a volatile metabolic product of selenium. Due to the difference in their single-dose toxicities, only selenite depressed body weight gain, when given alone. The experiments indicated that methylmercury, irrespective of whether it was given 1-2 h before, or at the same time as sodium selenite, potentiated the effect of the latter on body weight. Methylmercury also increased the exhalation of volatile selenium, but this effect decreased when the administration of selenite was delayed.

Animals↗
PubMed1985

Carbon disulphide exposure affects the response of rat adrenal medulla to hypothermia and hypoglycaemia.

The effects of hypothermia and hypoglycaemia on adrenal catecholamines and dopamine-beta-hydroxylase were compared in control and carbon disulphide (CS2) exposed rats 24 h after the last of ten daily 4 h inhalation exposures to CS2, 2 mg 1(-1) air. Animals were either kept in a cold room (0 degrees C) for 210 min with or without immobilization or were injected with insulin 100 u kg-1. Before these treatments CS2 exposed rats had more dopamine and less adrenaline in their adrenals than controls, and CS2 exposure also elevated the adrenal synthesis of catecholamines. Cold with immobilization or insulin treatment depressed the adrenal adrenaline content and increased the plasma concentrations of noradrenaline and adrenaline. There were no consistent differences between control and CS2 exposed rats. The adrenal dopamine content increased during cold exposure with immobilization or after insulin treatment both in CS2 exposed and control rats. The increase was smaller in CS2 exposed rats but the final dopamine values were nearly identical in the two groups. Exposure to cold (without immobilization) increased the adrenal dopamine content and the rate of catecholamine synthesis in control, but not in CS2 exposed rats. The increase in controls was less than the difference between the pre-cold exposure values of control and CS2 exposed rats. It is concluded that the elevation of adrenal dopamine content and catecholamine synthesis in CS2 exposed rats satisfy part of the demand placed on the adrenal medulla by hypothermia and hypoglycaemia. Consequently the changes induced by the latter treatments were smaller in CS2 exposed than in non-exposed rats. Moreover, when CS2 exposed rats were subjected to cold stress without immobilization their catecholamine synthesis was higher than the level measured in control rats after cold exposure.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Stimulation of dopamine-beta-hydroxylase in rat adrenals by repeated exposures to carbon disulphide.

The conversion of dopamine to noradrenaline, measured shortly after exposure to carbon disulphide, is reduced in the adrenals of rats. However, alongside this effect, carbon disulphide produces a gradual increase in the adrenal content of dopamine-beta-hydroxylase indicated by the increase of in vitro estimated enzyme activity and by the increased in vivo conversion of dopamine to noradrenaline observed 24 hr after the ninth exposure. Thus, after repeated exposures, the reduced rate of noradrenaline synthesis detectable immediately after the exposure alternates with the increased rate of synthesis.

Adrenal Glands↗
PubMed1984

In vivo inhibition of dopamine-beta-hydroxylase in rat adrenals during exposure to carbon disulphide.

Male rats were exposed for a maximum of 4 h to carbon disulphide at atmospheric levels of 1.0-4.0 mg/l and the turnover rates of adrenal dopamine was determined by injecting alpha-methyl-p-tyrosine and measuring the rate at which dopamine disappears. Although the level of exposure was significantly higher than the 30.0 micrograms/l permissible limit, or the average occupational exposure, similar or even higher peak exposure values were reported from the viscose rayon industry. After inhibition of tyrosine hydroxylase by alpha-methyl-p-tyrosine, adrenal dopamine contents declined at a slower rate in rats exposed to carbon disulphide than in controls. The reduced rate of dopamine metabolism during exposure to carbon disulphide indicates inhibition of dopamine-beta-hydroxylase in vivo. The size of this effect, which could be detected as soon as 30 min after starting the exposure to carbon disulphide, was dose dependent. The rate of dopamine turnover was still reduced 2 h after the end of a single exposure. However at that time, because of the larger dopamine pool present in the adrenals, the amount of dopamine converted per unit of time was again at pre-exposure levels.

Adrenal Glands↗
PubMed1984

The effect of interaction between subsequent doses of MeHgCl or HgCl2 on the biliary excretion of mercury from each individual dose.

The biliary excretion and organ distribution of mercury was investigated in male rats which received mercuric chloride (HgCl2) (0.65 mg/kg Hg2+) or methylmercury chloride (MeHgCl) (2 mg/kg Hg) i.p. and 48 h later the same compound i.v. Mercury was labelled with 203Hg either in the first or second injection. In controls saline was substituted for unlabelled mercury. In one experiment rats pretreated with HgCl2 were given Me203HgCl 48 h later. The biliary excretion and organ distribution of 203Hg were not influenced by the injection of cold MeHgCl given before or after Me203HgCl or by HgCl2 given 48 h after 203HgCl2. HgCl2 given 48 h before the injection of 203HgCl2 or Me203HgCl significantly decreased biliary excretion of 203Hg despite increased 203Hg levels in blood and liver.

Animals↗
PubMed1984

Differences in the effects of selenite and biological selenium on the chemical form and distribution of mercury after the simultaneous administration of HgCl2 and selenium to rats.

The interaction was compared between inorganic (HgCl2) mercury and selenite (Na2SeO3) vs. the interaction between inorganic mercury and biological selenium (a freeze-dried preparation of liver from rats treated with selenite). Organ concentrations of selenium were always significantly lower after biological selenium than after selenite. Biological selenium affected the organ distribution of inorganic mercury differently than selenite. Furthermore, the speciation of mercury was affected by this form of selenium. A mercury-selenide compound (presumably HgSe) accounted for a greater proportion of total mercury in tissues after selenite than after a dose of biological selenium. Administration of selenomethionine had a similar effect on the speciation of mercury to that seen after biological selenium. As the forms of selenium in selenomethionine or selenium deposited in the liver are most likely nearer than selenite to selenium present in food, our results suggest that, as far as the reaction of mercury with selenide is concerned, experiments with selenite overestimate the protective effect of dietary selenium against inorganic mercury and possibly against methylmercury.

Animals↗
PubMed1984

Effect of prolonged saline loading on HgCl2-induced renal tubular damage.

Male Porton-Wistar rats, 32 weeks old, were given i.p. one of the following doses of HgCl2; 0.5, 1.0 or 1.5 mg Hg/kg. In the preceding 4-week period and throughout the experiment the animals had free access to either tap water or 1.0% saline. The urinary excretion of alkaline phosphatase measured in urine samples, collected during the first 24 h after treatment with mercury, indicated that chronic saline loading significantly attenuated tubular damage caused by 0.5 mg or 1.0 mg Hg/kg, but not by 1.5 mg Hg/kg. Tubular necrosis 12 and 24 h after mercury was also less severe and extensive in saline than in tap water-drinking rats. This difference was still noticeable 4 days after mercury treatment in rats dosed with 0.5 mg Hg/kg, but death in the two higher dose groups prevented further pair-to-pair histological comparison. At the selected dose levels chronic saline loading did not decrease renal mercury content at 12 or 24 h and therefore protection was not associated with decrease in renal mercury uptake. The experiment indicates that chronic saline drinking, which at higher doses attenuates HgCl2-induced acute renal failure but not tubular necrosis, is able to moderate the severity of tubular necrosis when the dose of HgCl2 is as low as 0.5 mg Hg/kg. This protective effect diminishes as the dose is increased.

Acute Kidney Injury↗
PubMed1982

Isotoxic oral and inhalation exposure of carbon tetrachloride in Porton-Wistar and Fischer rats.

Male Fischer or Porton-Wistar rats were exposed for 4 h to different atmospheric concentrations of CCl4 or were given increasing oral doses, of CCl4 in order to estimate isotoxic exposures or doses. Animals were killed 20 h after treatment, their serum glutamic-pyruvic transaminase activities were measured and their livers were processed for histological examination. It has been found that the equitoxic oral dose in Wistars is 1.5 times that in Fischer rats and more than 3 times after inhalation. Therefore, the conversion factors from inhalation exposure to oral dose were much higher for Fischer than for Porton-Wistar rats. After oral dosing, the extent of centrilobular damage in Fischer rats was approximately twice that in Porton-Wistar rats. After inhalation exposure, the extent of damage was the same in the two strains, but at least at the two lower exposure levels hydropic degeneration definitely contributed to the size of the damaged areas more in Porton-Wistar than in Fischer rats.

Administration, Oral↗
PubMed1982

The comparative renotoxicology of phenylmercury and mercuric chloride.

The acute renotoxicity of HgCl2 and phenylmercuric acetate (PhHgAc) was compared at two intraperitoneal dose levels: 0.5 and 1.0 mg Hg/kg. There was no difference in the type of proximal tubular damage caused by the two mercurials, but 1.0 mg Hg/kg as PhHgAc produced approximately the same degree of damage as 0.5 mg Hg/kg as HgCl2. At the selected dose levels only HgCl2, but not PhHgAc increased the urinary excretion of alkaline phosphatase. At 12 and 24 h after PhHgAc the content of mercury was higher in blood and lower in the kidneys and urine than after the administration of equimolar doses of HgCl2. As the difference in the rectal mercury contents of HgCl2 and PhHgAc treated groups declined with time, difference in renotoxicity seems to relate only to renal mercury taken up within 24 h of administration. It is suggested that the slower renal extraction of mercury - as in regenerating kidneys (Tandon and Magos 1980) - was responsible for the lower degree of renotoxicity in phenylmercury treated rats.

Alkaline Phosphatase↗
PubMed1981

Ethanol reveals novel mercury detoxification step in tissues.

Volatile mercury was produced de novo by mouse tissue homogenates that contained mercuric ions. Ethanol stimulated the release of tissue mercury into the vapor phase, and the mechanism appears to be an inhibition of reoxidation of volatile mercury. Components responsible for mercury volatilization are heat-labile. The highest volatilizing activity in the liver is associated with the soluble fraction obtained after centrifugation at 105,000g.

Animals↗
PubMed1981

The inhibitory effect of serum from diethyldithiocarbamate treated rats on bovine adrenal dopamine-beta-hydroxylase activity.

The activity of serum dopamine-beta-hydroxylase does not depend solely on the presence of exogenous inhibitors: its activity also depends on the rate of release into plasma and is influenced by sympathetic activity or pathological conditions. This fluctuation may disguise the effect of an exogenous inhibitor on the enzyme. It has been shown in the present work that boiling of serum obtained from sodium diethyldithiocarbamate treated rats did not eliminate the dopamine-beta-hydroxylase inhibitory effect on a bovine adrenal dopamine-beta-hydroxylase preparation. Thus it is possible to measure the dopamine-beta-hydroxylase inhibitory effect of an exogenous inhibitor of this type without interference from the enzyme present in serum. Serum taken from rats treated with sodium diethyldithiocarbamate depressed in a time and dose dependent way the activity of bovine adrenal dopamine-beta-hydroxylase preparation.

Adrenal Glands↗
PubMed1981

Comparative study of the sensitivity of male and female rats to methylmercury.

Male and female rats were dosed daily by gastric gavage four or five times with 8.0 mg/kg Hg as methylmercury. Treatment lowered the body weight in relation to the body weight of untreated rats to the same extent in male and female rats but when body weight was related to the initial body weight, the effect of methylmercury was more pronounced in females than in males. The important of differences in growth or loss of body weight is that in spite of the similar whole body clearance mercury concentrations were higher in females than in males. After identical doses the brains of females always contained more mercury than those of males and in both sexes the brain concentration of mercury showed a disproportionate elevation when the number of doses was increased from four to five. However, weight change alone does not explain the sex related difference in the brain concentration of mercury as this was evident even 72 h after a single dose. In agreement with the brain concentration of mercury, female rats developed more intensive co-ordination disorders and after five doses they had more extensive damage in the granular layer of the cerebellum than males.

Animals↗
PubMed1981

Tests of efficacy of antidotes for removal of methylmercury in human poisoning during the Iraq outbreak.

Three complexing agents and a thiolated resin were tested for their ability to reduce the T 1/2 of methylmercury in blood during an outbreak of human poisoning. The slope of the line relating the natural logarithm of the blood concentration to time during treatment was calculated by a parametric (linear regression) and a nonparametric (two-point) method. The mean slope for each treatment group was calculated and the T 1/2 was calculated from the mean slope. Both the linear regression and two-point methods yield similar mean values. The "two-point" T 1/2 will be quoted here. The mean T 1/2 in six patients receiving no specific treatment was 65 days and in 10 patients receiving placebo was 61 days, and these values did not differ from those reported in the literature. All four treatments significantly reduced the mean T 1/2 values below the mean for the combined placebo and no treatment groups. Sodium 2,3-dimercaptopropane-1-sulfonate was the most effective agent, reducing the mean T 1/2 in 10 patients to 10 days. The thiolated resin given to eight patients produced a mean T 1/2 of 20 days. The penicillamines also produced a significant reduction in T 1/2 values; the mean T 1/2 for D-penicillamine in 12 patients was 26 days and N-acetyl-DL-penicillamine in 17 patients yielded a mean T 1/2 of 24 days. This is the first report of the effects of sodium 2,3-dimercaptopropane-1-sulfonate and resin in human subjects exposed to methylmercury. No adverse effects were observed in any of the treatment groups. A clinical trial was not possible but it is concluded that agents that reduce blood levels and accelerate excretion are probably clinically useful if given before irreversible damage has occurred.

Adolescent↗
PubMed1981

Interaction of ethanol and inorganic mercury: generation of mercury vapor in vivo.

Mercury exhalation increased after parenteral administration of ethanol to mice injected with a single dose of mercuric chloride (0.5 mg of Hg/Kg). Increased output of the metal was ethanol dose-dependent (blood EC50 = 215 mg/dl) and maximal rates (0.2% of the body burden per 30 min) were about 10-fold higher than controls. The chemical form of exhaled mercury was determined to be the elemental vapor (Hg degrees) indicating an ethanol-sensitive reduction pathway for ionic mercury (Hg++) in the body. Ethanol appeared to selectively affect mercury exhalation inasmuch as no large differences in whole-body mercury retention times or in the distribution of the metal in organs could be detected even after repeated daily doses of ethanol. The results show that at least a portion of the ionic mercury in the body can be mobilized via reduction and Hg++ in tissues is more labile than generally recognized.

Animals↗
PubMed1980

Comparative study of the sensitivity of virgin and pregnant rats to methylmercury.

Pregnant and virgin female rats were dosed by gastric lavage 10 times or 5 times with 5 mg/kg mercury as methylmercury. Treatment of pregnant animals started on day 3 of gestation and ended on day 14 of gestation with two days break between the 5th and the 6th doses. In Group B, treatment lasted from day 10 to day 14 of gestation. Pregnant and virgin rats responded identically to methylmercury in terms of body weight changes, coordination disorders, and cerebellar histological changes. Furthermore, the brain, liver and kidney concentrations and the rates of methylmercury elimination in the post-treatment period were identical. Thus the results indicate no difference in sensitivity of pregnant versus non-pregnant animals.

Animals↗
PubMed1980

The effect of lactation on methylmercury intoxication.

Four days after parturition 17 weeks old rats of Porton Wistar strain were given 8 mg/kg mercury as methylmercury chloride for 5 days. Virgin females or mothers separated from their offspring immediately after delivery received the same treatment and served as controls. Compared with these controls, lactation delayed the onset of weight loss, shortened the time between the end of treatment and the onset of weight gain, accelerated the elimination of mercury from the whole body and prevented the development of severe co-ordination disorders. However, lactation had no detectable effect on the elimination of mercury from the brain. Moreover control and lactating females had the same degree of histological abnormalities both in the granular layer of the cerebellum and in the dorsal root ganglion cells.

Animals↗
PubMed1980

The interaction of cadium-induced rat renal metallothionein with bivalent mercury in vitro.

Addition of Hg2+ in vitro to metallothionein (Cd : Cu : Zn = 6.5 : 4 : 1) from the kidneys of Cd2+ exposed rats appears to result initially in the replacement of Zn2+, then Cd2+ and finally copper. The ionic stoichiometries between Hg2+-binding and the release of Cd2+ (or Zn2+) and copper are 3 : 2 and 1 : 1 respectively. After treatment with amounts of Hg2+ sufficient to displace completely either the bound Zn2+ and Cd2+, or all of the original cations, the metallothionein has little or no negative charge at pH 8.0 and is not resolved into the two isometallothioneins, which characterize the (Cd, Cu, Zn)-thionein, by ion exchange chromatography at this pH. Cation substitution occurs in both isometallothioneins and there is no evidence that Hg2+ interacts preferentially with one of them. Treatment of the metallothionein with increasing amounts of Hg2+, equivalent to approx. 25% and 50% of the bound cations gives rise to a range of molecular species of progressively decreasing negative charge. The consistent stiochiometry between Hg2+ uptake and Cd2+ or Zn2+ release at all concentrations of Hg2+ indicates that free thiol groups are not formed during the substitution reaction.

Animals↗