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Biomedical subjects

L Magos

Publications and source records attributed to L Magos.

At least 55 records · Page 3Linked to original sources

The in vivo effects of maleate on the cation-distribution in rat kidney metallothionein sub-fractions after induction by cadmium and/or mercury.

The metallothionein fractions, isolated by gel filtration from the kidneys of rats that have been dosed with Cd2+, Hg2+ or Cd2+ followed by Hg2+, yield very different elution profiles on ion-exchange chromatography. The metallothionein from Cd2+-treated animals is resolved into the isomethallothioneins I and II and a minor, less negatively-charged species (B), which contains Cd2+ and copper, but little Zn2+. The corresponding fraction from the kidneys of rats doses with Hg2+ yields five components, all of which contain Hg2+, Zn2+ and Cu, but in different ratios. Three of these compounds correspond in their elution characteristics from DE-cellulose with the above-mentioned isometallothioneins I and II and fraction B. The last of these, which also is rich in Cu, is the major Hg2+-binding component. The distribution of Hg2+ and of other cations between these five sub-fractions, but not the number of sub-fractions, is altered by Cd2+-pretreatment of the animals. Treatment of Cd2+-dosed rats with sodium maleate has no significant effect on the distribution of cations (Cd2+, Zn2+ and copper) amongst the renal metallothionein subfractions. The same treatment, applied to animals dosed with either Hg2+ only, or Cd2+ followed by Hg2+, causes the elimination of 70--75% of the Hg2+ from the metallothionein fraction. Loss occurs from all subfractions, but is greatest in subfraction B, which also loses copper. Whilst it is possible that Hg2+ may induce metallothionein and other metalloproteins in the kidney, Hg2+ appears to bind to both isometallothioneins I and II, when these are induced by Cd2+-pretreatment. The loss of Hg2+, but not of Cd2+, from these metalloproteins after treatment with sodium maleate may be related to differences in the relative binding affinities of the two cations for thionein and other cellular proteins.

Animals↗

The effects of bromosulphophthalein, indocyanine green and bilirubin on the biliary excretion of methylmercury.

The effects of three ligands for ligandin on the biliary excretion of methylmercury were investigated in male rats injected intravenously with 1.0 mg/kg Hg as Me203 HgCl. Bromosulphophthalein and indocyanine green inhibited the biliary excretion of methylmercury, while bilirubin had no such effect. None of the compounds tested which inhibited the biliary excretion of methylmercury decreased bile flow or changed the hepatic concentration of mercury of non-protein thiols. The possibility of the involvement of ligandin in the biliary excretion of methylmercury is discussed.

Animals↗

Complex formation between selenium and methylmercury.

Methylmercury, after incubation at 3k7 degrees C and pH 7.0 with selenite in the presence of rat erythrocytes, can be extracted into benzene as an unstable 2 : 1 complex with selenium. The same complex, possibly bis-methylmercury selenide, is formed when methylmercury is treated with hydrogen selenide at pH 7.0 in the absence of erythrocytes.

Animals↗

Maleate induced change in the kidney binding of mercury in rats pretreated with cadmium.

The kidney uptake of Hg2+ was increased by Cd2+-pretreatment when Hg2+ was given intraperitoneally but not subcutaneously. Subsequent s.c. administration of maleate increased Hg2+ release from the kidneys only if Hg2+ was given subcutaneously. Neither the effect of Cd2+, nor that of maleate, on the distribution of Hg2+ among the renal soluble protein fractions was affected by the route of Hg2+ administration. The protective effect of Cd2+-pretreatment against the nephrotoxic effect of Hg2+ was also independent of the route of Hg2+ administration. Maleate given in nephrotoxic doses removed Hg2+ and copper, but not Cd2+ from the renal metallothionein fraction. Mercury in the urine, however, was not complexed by proteins with the molecular weight of thionein, but was bound to high molecular weight proteins and diffusible molecules. These findings are discussed in relation to the role of metallothionein in the interaction between Cd2+ and Hg2+.

Animals↗

The hepatotoxicity of 3-amino-1,2,4-triazole and carbon disulphide in phenobarbitone-treated starved rats.

In phenobarbitone-treated starved male rats 1 g/kg 3-amino-1,2,4-triazole produced moderate liver necorsis and increased the serum glutamic-pyruvic transaminase activity. If half an hour after the administration of aminotriazole animals were exposed for 4 h to 2.0 mg/l CS2, the necrotic damage in the liver was larger and the serum glutamic-pyruvic transaminase activity higher than in rats not exposed to CS2. Carbon-disulphide in phenobarbitone-treated starved male rats caused only a very slight increase in the serum transminase activity in spite of the widespread hydropic degeneration in the liver. These experiments indicated that increase in serum transaminase activity is the consequence of necrosis and not hydropic degeneration; aminotriazole is hepatotoxic in rats when microsomal enzymes are induced and the hepatotoxicity of aminotriazole and carbon disulphide is potentiated by the administration of the other compound.

Alanine Transaminase↗

Ethanol-increased exhalation of mercury in mice.

CBA/J mice injected three days beforehand with 203HgCl2 were given ethanol or water by gavage and placed in a chamber designed to collect exhaled mercury. Ethanol treatment led to an eight-fold increase of counts accumulated on a filter over a four-hour period, compared with water-treated mice. The mercury-collection apparatus tested for extracorporeal contribution of volatilised mercury indicated that the counts originated from the air exhaled by the mice.

Animals↗

Theoretical and practical considerations on the problem of metal--metal interaction.

The interaction between two metals, which can be either synergistic or antagonistic, implies that the behavior of one is changed by the presence of the other. Possible mechanisms of these interactions, which include chemical association, competition for carriers, metabolic changes, induction of binding proteins, membrane alterations are discussed.

Animals↗

The effect of selenium on the brain uptake of methylmercury.

Twenty-four h after the subcutaneous administration of 0.5 mumoles selenite labelled with 75Se to rats of 200 g body weight, the retention of selenium at the injection site was significantly increased by the presence of equimolar amounts of methylmercury in the injection solution. The retention of Me203HgCl was not affected by the presence of selenite. The most significant shift caused by interaction was a decrease in the blood content and an increase in the brain content of 203Hg. The brain content of 75Se was also increased to a lesser extent. The shift in the distribution--which was the same whether the two metals were injected at the same site or separately--continuously decreased from 6-48 h. The same interaction pattern was observed when methylmercury and selenite were administered by gastric gavage and differences in distribution increased when the dose was increased from 1.25 mumoles/kg to 2.5 mumoles/kg. The increase in the brain content of mercury caused by selenite was not restricted to simultaneous administration and occurred when selenite was given 2-7 days after methylmercury.

Animals↗

Cardiac sensitization induced by phenobarbitone and prolonged by CS2.

The arrhythmogenic effect of 8 microgram/kg noradrenaline given i.v. was increased in male rats pretreated 1-2 days earlier with phenobarbitone and starved from the time of the first phenobarbitone injection (80 mg/kg followed by 50 mg/kg 6 h later). Daily exposure to 4.0 mg/l CS2 (first exposure 24 h after the first phenobarbitone injection) for 4 h prevented the decline in susceptibility on the 3rd and 4th days after phenobarbitone, when the reaction of unexposed rats to noradrenaline returned to normal.

Animals↗