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At least 19 recordsLinked to original sources
PubMed2002

Carcinogenicity, mutagenicity and teratogenicity of manganese compounds.

Manganese, an essential trace element, is one of the most used metals in the industry. Recently, several new manganese compounds have been introduced as fungicide, as antiknock agent in petrol and as contrasting agent in nuclear magnetic resonance tomography. Manganese displays a somewhat unique behaviour with regard to its toxicity. It is relatively non-toxic to the adult organism except to the brain where it causes Parkinson-like symptoms when inhaled even at moderate amounts over longer periods of time. Relatively high doses of manganese affect DNA replication and repair in bacteria and causes mutations in microorganism and mammalian cells although the Ames test does not appear to be particularly responsive to manganese. In mammalian cells, manganese causes DNA damage and chromosome aberrations. Information on organic manganese derivatives is still insufficient. Large amounts of manganese affect fertility in mammals and are toxic to the embryo and foetus. The fungicide MANEB and the contrasting agent MnDPDP also can be embryotoxic, but the latter only at doses much higher than those clinically employed. Information on the anti-knock agent MMT is inadequate. On the other hand, manganese deficiency can also affect fertility and be teratogenic. Information on cancer due to manganese is scanty but the results available do not indicate that inorganic manganese is carcinogenic. More information is desirable with regard to the organic manganese derivatives. It may surprise that an agent that causes mutations is not also carcinogenic. The experience with manganese shows that conclusions with regard to carcinogenicity of an agent based on the observation of mutations are subject to uncertainties. Altogether, it appears that, because of the very high doses at which positive effects have been found, manganese would not represent a significant carcinogenic risk to the population and workers. Care must, however, be exercised with respect to central-nervous symptoms after chronic exposure and with respect to effects on the embryo. Pregnant women should not be exposed to manganese at the work place.

Abnormalities, Drug-Induced↗
PubMed1992

Effects of manganese forms on biogenic amines in the brain and behavioral alterations in the mouse: long-term oral administration of several manganese compounds.

This work has identified the relative toxicity of four forms of manganese, using biogenic amine levels, tissue retention, weight gain, and activity scores as criteria. Male mice were chronically treated with four forms of manganese administered orally, mixed with the diet, for 12 months. The food intake for the control mice and the mice exposed to manganese was similar, but the manganese treatment reduced normal weight gain in the mice. The Mn levels were higher in some parts of brain after feeding insoluble salts than after the soluble salts. The concentration of manganese was significantly increased in the liver and spleen of the manganese carbonate-exposed group, compared with the concentration in the control group. Manganese dioxide feeding lowered dopamine and increased homovanilic acid. Since manganese dioxide is a powerful oxidizing agent in organic chemistry, it possibly enhanced the oxidative metabolite of dopamine. Accumulation of manganese in the brain correlated with reduced hypothalamic dopamine levels in the manganese acetate-exposed group; and the amount of manganese accumulated correlated with the intensity of suppression of motor activity. These findings indicate that manganese dioxide is more toxic than divalent manganese. Of the divalent manganese compounds, manganese acetate seemed to have the greatest toxic effect.

Animals↗
PubMed1983

Effects of manganese compounds on carcinogenicity of nickel subsulfide in rats.

The effects of manganese compounds upon the carcinogenicity of alpha Ni3S2 were tested in male Fischer rats. In Experiment I, rats were given i.m. injections of alpha Ni3S2 (2.5 mg) and Mn dust (2.0 mg), singly or in combination. By 100 weeks, sarcomas occurred at the injection site in 0 of 24 rats in the vehicle control group, in 0 of 24 rats that received Mn dust alone, and in 23 of 24 rats that received alpha Ni3S2 alone. Combined administration of alpha Ni3S2 plus Mn dust as a single i.m. injection resulted in sarcomas in 14 of 23 rats (p less than 0.05 versus alpha Ni3S2 alone). In rats that received injections of alpha Ni3S2 in one thigh and Mn dust in the opposite thigh, the sarcoma incidence at the site of alpha Ni3S2 injection was 24 of 24 rats. In Experiment II, rats were given i.m. injections of alpha Ni3S2 (1.2 mg) and Mn compounds (MnS, Mn2O3, MnO2 or MN2(CO)10, in dosages equivalent to 1.0 mg of Mn), singly or in combination. No sarcomas occurred at the injection site in rats that received the vehicle or any of the manganese compounds alone. Sarcomas occurred in 13 of 27 rats that received alpha Ni3S2 alone; this sarcoma incidence was not reduced by admixture of any of the Mn compounds. The median tumor latent period and the median survival period were significantly longer (p less than 0.05) in rats that received MnS plus alpha Ni3S2, compared with rats that received alpha Ni3S2 alone, suggesting that MnS may have weak anticarcinogenic effect. These experiments demonstrate that inhibition of alpha Ni3S2-carcinogenesis by Mn dust is a local rather than a systemic effect, and that, with the possible exception of MnS, the other manganese compounds that were tested are ineffective as inhibitors of alpha Ni3S2-carcinogenesis.

Animals↗
PubMed1975

Dermal irritancy of metal compounds. Studies with palladium, platinum, lead, and manganese compounds.

Dermal irritancy of 14 materials, including several compounds of palladium, platinum and lead, and methylcyclopentadienyl manganese tricarbonyl, plus deionized water (negative control) and glacial acetic acid (positive control), was tested on male albino rabbits weighing 2 to 3 kg. Procedures and evaluation criteria were adopted from those in use by the National Institute for Occupational Safety and Health. Five materials were evaluated as unsafe for intact or abraded skin contact as judged by severity of responses: glacial acetic acid (C3H5PDCl)2, (NH4)2PdCl4, (NH4)2PdCl6, and PtCl4; one as safe for intact, but not for abraded, skin: K2PdCl6; and two as safe for intact skin but not for abraded skin unless protected: K2PdCl4 and PdCl2. The remainder were evaluated as safe for intact or abraded skin contact (irritancy grade less than 1 on a scale of 4): H2O, Pd(NH3)2Cl2, PdO, PtO2, PtCl2, PbCl2, PbO, MMT.

Acetates↗
PubMed2003

Binuclear manganese compounds of potential biological significance. Part 2. Mechanistic study of hydrogen peroxide disproportionation by dimanganese complexes: the two oxygen atoms of the peroxide end up in a dioxo intermediate.

The dimanganese(II,II) complexes 1a [Mn(2)(L)(OAc)(2)(CH(3)OH)](ClO(4)) and 1b [Mn(2)(L)(OBz)(2)(H(2)O)](ClO(4)), where HL is the unsymmetrical phenol ligand 2-(bis-(2-pyridylmethyl)aminomethyl)-6-((2-pyridylmethyl)(benzyl)aminomethyl)-4-methylphenol, react with hydrogen peroxide in acetonitrile solution. The disproportionation reaction was monitored by electrospray ionization mass spectrometry (ESI-MS) and EPR and UV-visible spectroscopies. Extensive EPR studies have shown that a species (2) exhibiting a 16-line spectrum at g approximately 2 persists during catalysis. ESI-MS experiments conducted similarly during catalysis associate 2a with a peak at 729 (791 for 2b) corresponding to the formula [Mn(III)Mn(IV)(L)(O)(2)(OAc)](+) ([Mn(III)Mn(IV)(L)(O)(2)(OBz)](+) for 2b). At the end of the reaction, it is partly replaced by a species (3) possessing a broad unfeatured signal at g approximately 2. ESI-MS associates 3a with a peak at 713 (775 for 3b) corresponding to the formula [Mn(II)Mn(III)(L)(O)(OAc)](+) ([Mn(II)Mn(III)(L)(O)(OBz)](+) for 3b). In the presence of H(2)(18)O, these two peaks move to 733 and to 715 indicating the presence of two and one oxo ligands, respectively. When H(2)(18)O(2) is used, 2a and 3a are labeled showing that the oxo ligands come from H(2)O(2). Interestingly, when an equimolar mixture of H(2)O(2) and H(2)(18)O(2) is used, only unlabeled and doubly labeled 2a/b are formed, showing that its two oxo ligands come from the same H(2)O(2) molecule. All these experiments lead to attribute the formula [Mn(III)Mn(IV)(L)(O)(2)(OAc)](+) to 2a and to 3a the formula [Mn(II)Mn(III)(L)(O)(OAc)](+). Freeze-quench/EPR experiments revealed that 2a appears at 500 ms and that another species with a 6-line spectrum is formed transiently at ca. 100 ms. 2a was prepared by reaction of 1a with tert-butyl hydroperoxide as shown by EPR and UV-visible spectroscopies and ESI-MS experiments. Its structure was studied by X-ray absorption experiments which revealed the presence of two or three O atoms at 1.87 A and three or two N/O atoms at 2.14 A. In addition one N atom was found at a longer distance (2.3 A) and one Mn at 2.63 A. 2a can be one-electron oxidized at E(1/2) = 0.91 V(NHE) (DeltaE(1/2) = 0.08 V) leading to its Mn(IV)Mn(IV) analogue. The formation of 2a from 1a was monitored by UV-visible and X-ray absorption spectroscopies. Both concur to show that an intermediate Mn(II)Mn(III) species, resembling 4a [Mn(2)(L)(OAc)(2)(H(2)O)](ClO(4))(2), the one-electron-oxidized form of 1a, is formed initially and transforms into 2a. The structures of the active intermediates 2 and 3 are discussed in light of their spectroscopic properties, and potential mechanisms are considered and discussed in the context of the biological reaction.

Crystallography, X-Ray↗