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At least 19 recordsLinked to original sources
PubMed2002

Brain manganese concentrations in rats following manganese tetroxide inhalation are unaffected by dietary manganese intake.

Manganese-deficient individuals have decreased manganese elimination. This observation has prompted suggestions that relative manganese deficiency may increase the risk for manganese neurotoxicity following inhalation exposure. The objective of this study was to determine whether dietary manganese intake influences the pharmacokinetics of inhaled manganese tetroxide (Mn3O4). Postnatal day (PND) 10 rats were placed on either a low (2 ppm), sufficient (10 ppm), or high-normal (100 ppm) manganese diet for 2 months. Beginning on PND 77 +/- 2, male littermates were exposed 6 h per day for 14 consecutive days to 0, 0.042, or 0.42 mg Mn3O4/m3. End-of-exposure tissue manganese concentrations and whole-body 54Mn elimination rates were determined. Tissue manganese concentrations were dependent on the dietary intake of manganese, thus confirming that altered hepatic manganese disposition or metabolism occurred. Male rats given 100 ppm manganese diet developed increased manganese concentrations in the femur, liver, and bile and had elevated whole-body 54Mn clearance rates when compared to animals given 2 ppm manganese diet. Male rats exposed to 0.42 mg Mn3O4/m3 had increased manganese concentrations in the olfactory bulb, lung, liver, and bile when compared to air-exposed male rats. A significant interaction between the concentration of inhaled Mn3O4 and dietary manganese level was observed only with the end-of-exposure liver manganese concentration. Our results indicate that animals maintained on either a manganese-deficient or high manganese diet do not appear to be at increased risk for elevated brain manganese concentrations following inhalation exposure to high levels of Mn3O4.

Administration, Inhalation↗
PubMed1989

Manganese in scalp hair: problems of exogenous manganese and implications for manganese monitoring in Groote Eylandt Aborigines.

The use of scalp hair to monitor manganese was studied as part of an investigation of manganese intoxication amongst a group of Aborigines living on manganese-rich soil on Groote Eylandt, in the Northern Territory of Australia. High scalp-hair manganese values were due largely to manganese from exogenous sources. Manganese (IV) dioxide in dust, trapped in hair, was reduced by the components of sweat, leading to the diffusion of manganese (II) into the hair shaft. At least 15 micrograms Mn g-1 hair could be incorporated into hair via this exogenous route. To overcome the problems of manganese contamination, the ability of a number of leaching agents to remove exogenous manganese selectively from hair was tested. Measurements of manganese along the length of hair strands were extrapolated back to zero length to estimate the amount of manganese in the hair as it emerged from the scalp. Using this extrapolation technique, Aborigines on Groote Eylandt had a mean scalp-hair manganese of 16 ppm. Aborigines in non-manganese areas had 2 ppm manganese in hair. Caucasians living in the same manganese-rich area had 2.5 ppm manganese in hair, compared to 0.5 ppm manganese in non-manganese areas. Measurements of manganese in hair and blood of Groote Eylandt Aborigines showed that the population had a high exposure to manganese, but did not distinguish between those individuals affected/unaffected by the neurological condition, Groote Eylandt Syndrome.

Australia↗
PubMed1994

Manganese status, gut endogenous losses of manganese, and antioxidant enzyme activity in rats fed varying levels of manganese and fat.

We hypothesized that manganese deficient animals fed high vs moderate levels of polyunsaturated fat would either manifest evidence of increased oxidative stress or would experience compensatory changes in antioxidant enzymes and/or shifts in manganese utilization that result in decreased endogenous gut manganese losses. Rats (females in Study 1, males in Study 2, n = 8/treatment) were fed diets that contained 5 or 20% corn oil by weight and either 0.01 or 1.5 mumol manganese/g diet. In study 2, 54Mn complexed to albumin was injected into the portal vein to assess gut endogenous losses of manganese. The manganese deficient rats: 1. Had 30-50% lower liver, tibia, kidney, spleen, and pancreas manganese concentrations than manganese adequate rats; 2. Conserved manganese through approximately 70-fold reductions in endogenous fecal losses of manganese; 3. Had lower heart manganese superoxide dismutase (MnSOD) activity; and 4. Experienced only two minor compensatory changes in the activity of copper-zinc superoxide dismutase (CuZnSOD) and catalase. Gut endogenous losses of manganese tended to account for a smaller proportion of absorbed manganese in rats fed high-fat diets; otherwise fat intake had few effects on tissue manganese concentrations.

Analysis of Variance↗
PubMed2001

Influence of particle solubility on the delivery of inhaled manganese to the rat brain: manganese sulfate and manganese tetroxide pharmacokinetics following repeated (14-day) exposure.

Dissolution rate can influence the pulmonary clearance of a metal and thus affect its delivery to the brain and other organs. The goal of this study was to determine the exposure-response relationship for the relatively soluble sulfate (MnSO(4)) and insoluble tetroxide (Mn(3)O(4)) forms of inhaled manganese in adult male CD rats. Rats were exposed 6 h/day for 7 days/week (14 exposures) to either MnSO(4) or Mn(3)O(4) at 0, 0.03, 0.3, or 3 mg Mn/m(3). End-of-exposure olfactory bulb, striatum, cerebellum, bile, lung, liver, femur, serum, and testes (n = 6 rats/concentration/chemical) manganese concentrations and whole-body (54)Mn elimination were then determined. Increased whole-body (54)Mn clearance rates were observed in animals from the high-dose (3 mg Mn/m(3)) MnSO(4) and Mn(3)O(4) exposure groups. Elevated manganese concentrations in the lung were observed following MnSO(4) and Mn(3)O(4) exposure to > or=0.3 mg Mn/m(3). Increased olfactory bulb and femur manganese concentrations were also observed following MnSO(4) exposure at > or=0.3 mg Mn/m(3). Elevated striatal, testes, liver, and bile manganese concentrations were observed following exposure to MnSO(4) at 3 mg Mn/m(3). Elevated olfactory bulb, striatal, femur, and bile manganese concentrations were observed following exposure to Mn(3)O(4) at 3 mg Mn/m(3). Animals exposed to MnSO(4) (3 mg Mn/m(3)) had lower lung and higher olfactory bulb and striatal manganese concentrations compared with levels achieved following similar Mn(3)O(4) exposures. Our results suggest that inhalation exposure to soluble forms of manganese results in higher brain manganese concentrations than those achieved following exposure to an insoluble form of manganese.

Animals↗
PubMed2002

Glutamate/aspartate transporter (GLAST), taurine transporter and metallothionein mRNA levels are differentially altered in astrocytes exposed to manganese chloride, manganese phosphate or manganese sulfate.

Manganese (Mn)-induced neurotoxicity can occur due to environmental exposure (air pollution, soil, water) and/or metabolic aberrations (decreased biliary excretion). High brain manganese levels lead to oxidative stress, as well as alterations in neurotransmitter metabolism with concurrent neurobehavioral deficits. Based on the few existing studies that have examined brain regional Mn concentration, it is likely that in pathological conditions, Mn concentration can reach between 100 and 500 microM. Environmental Mn exposure as a result of methylcyclopentadienyl manganese tricarbonyl (MMT) combustion is in the form of phosphate or sulfate (MnPO4, MnSO4, respectively). Pharmacokinetic studies have shown that the Mn salt will determine the rate of transport into the brain: MnCl2 > MnSO4 > MnPO4. The salt-specific neurotoxicity of these species is unknown. The primary goal of this study was to examine gene expression of glutamate/aspartate transporter (GLAST), taurine transporter (tau-T), and metallothionein-I (MT-I) in astrocytes exposed to manganese chloride (MnCl2), manganese sulfate (MnSO4), and manganese phosphate (MnPO4). We hypothesized that the effects of MnPO4 and MnSO4 exposure on GLASTexpression in astrocytes would be similar to those induced by MnCl2, since irrespective of salt species exposure, once internalized by astrocytes, the Mn ion would be identically complexed. At the same time, we hypothesized that the magnitude of the effect would be salt-dependent, since the chemical speciation would determine the rate of intracellular uptake of Mn. MnCl2 caused a significant overall decrease (P < 0.0001) in astrocytic GLAST mRNA levels with MnSO4 causing a moderate decrease. MnPO4 exposure did not alter GLAST mRNA in astrocytes. We also sought to examine astrocytic metallothionein and taurine transporter gene expression as markers of manganese exposure. Our findings suggest that manganese chloride significantly decreased (P < 0.0001) astrocytic metallothionein mRNA compared to both the sulfate and phosphate species. However, astrocytic taurine transporter mRNA was not affected by Mn exposure, irrespective of the salt species. These data are consistent with the hypothesis that astrocytic neurotoxicity due to Mn exposure is dependent upon its species, with solubility, and by inference, intracellular concentration, representing a major determinant of its neurotoxicity.

Amino Acid Transport System X-AG↗
PubMed1995

Relative biological availability of manganese from manganese proteinate, manganese sulfate, and manganese monoxide in broilers reared at elevated temperatures.

The relative biological availabilities of Mn from Mn proteinate, MnSO4, and MnO were compared under two different environmental conditions. Commercial broilers were reared in brooder batteries between Days 1 and 21 and fed diets containing 0, 1,000, 2,000, or 3,000 mg supplemental Mn/kg diet. On Day 22, birds were transferred to individual cages in two environmental chambers maintaining the same dietary Mn sources and supplemental levels. The temperature in one chamber cycled between 18 and 23.9 C (thermoneutral, TN), and in the other chamber cycled between 23.9 and 35 C (heat distress, HD). Birds in the HD environment were exposed to 8 h of 23.9 C, 4 h of 23.9 to 35 C, 4 h of 35 C, and 8 h of 35 to 23.9 C. Tibia Mn increased linearly (P < .05) with level of supplementation when measured on Days 22 and 47. Based on ratios of slopes from multiple linear regression analysis of bone Mn on Mn intake from various sources, the biological availabilities of Mn proteinate and MnO relative to MnSO4 (100%) were 120 and 91%, respectively, in 21-d-old chicks. In 49-d-old birds, corresponding relative biological availabilities of Mn from proteinate and oxide were 125 and 83%, respectively, in birds reared under TN, and 145 and 82%, respectively, for HD birds.

Animals↗
PubMed1986

Bioavailability of manganese sulfate and manganese monoxide in chicks as measured by tissue uptake of manganese from conventional dietary levels.

The biological availability of reagent grade manganese sulfate and manganese monoxide was determined in broiler chicks fed conventional dietary Mn levels. A basal corn-soybean meal diet (35 ppm Mn) was supplemented with 40, 80, or 120 ppm Mn from the two sources and fed ad libitum for 21 days. There were no differences in average daily feed intake, daily gain, or feed conversion among treatments. There was a linear (P less than .001) increase in bone, kidney, and liver Mn as dietary Mn increased. Manganese monoxide averaged 66% of the availability of manganese sulfate as determined by a combination of linear regression, multiple linear regression and tissue Mn increase. Bioavailability was similar to that obtained when sources were fed at high dietary levels in a previous study.

Animals↗
PubMed1968

Bacteriology of manganese nodules. II. Manganese oxidation by cell-free extract from a manganese nodule bacterium.

A cell-free extract from Arthrobacter 37, isolated from a manganese nodule from the Atlantic Ocean, exhibited enzymatic activity which accelerated manganese accretion to synthetic Mn-Fe oxide as well as to crushed manganese nodule. The reaction required oxygen and was inhibited by HgCl(2) and p-chloromercuribenzoate but not by Atebrine dihydrochloride. The rate of enzymatic action depended on the concentration of cell-free extract used. The enzymatic activity had a temperature optimum around 17.5 C and was destroyed by heating at 100 C. The amount of heat required for inactivation depended on the amount of nucleic acid in the preparation. In the cell-free extract, unlike the whole-cell preparation, peptone could not substitute for NaHCO(3) in the reaction mixture. An enzyme-containing protein fraction and a nucleic acid fraction could be separated from cell extract by gel filtration, when prepared in 3% NaCl but not in seawater. The nucleic acid fraction was not required for enzymatic activity.

Arthrobacter↗
PubMed1987

Influence of heme-surrounding amino acid residues on the manganese (V)-nitrido bond in manganese-substituted hemoproteins: resonance Raman evidence for porphyrin core expansion and reduction of the manganese(V)-nitrido stretching force constant.

Nitridomanganese(V) protoporphyrin IX was prepared by hypochlorite oxidation of the corresponding manganese(III) protoporphyrin IX derivative in the presence of ammonium ion and by photolysis of the corresponding azidomanganese(III) complex. Myoglobin and horseradish peroxidase containing this novel protoporphyrin derivative were prepared for the first time. These remarkably stable species were examined by electronic absorption, electron paramagnetic resonance, and resonance Raman spectroscopies. The MnV-N stretching modes of the nitridomanganese(V)-substituted myoglobin and horseradish peroxidase were observed at 1010 and 1003 cm-1, respectively, by resonance Raman spectroscopy, while the MnV-N stretching frequency for nitridomanganese(V) protoporphyrin IX in 0.1 N aqueous NaOH was found at 1046 cm-1. The equilibrium dissociation energies of MnV-N bonds in these complexes were estimated from vibrational overtone spacings by introducing the Morse potential energy function, were found to be around 4.5 eV, and seemed independent of the surroundings of the manganese porphyrin, although its force constant decreased from 7.3 to 6.7 mdyn/A upon incorporation into apoprotein. The porphyrin ring modes of these nitridomanganese(V) derivatives were influenced greatly upon incorporation into apoproteins, suggestive of the occurrence of porphyrin core expansion. Upon this core expansion the MnV center moves into the mean plane of porphyrin plane, but the access of nitrido (N) toward MnV is restricted due to a steric hindrance from porphyrin pyrrole nitrogens. The resulting stretched MnV-N bond might cause lowering of the MnV-N stretching frequency upon incorporation into apoprotein.

Binding Sites↗
PubMed2000

Pulmonary clearance of manganese phosphate, manganese sulfate, and manganese tetraoxide by CD rats following intratracheal instillation.

Manganese (Mn) is ubiquitous in ambient air due to both industrial and crustal sources. It is also a component of the octane-enhancing fuel additive methylcyclopentadienyl manganese tricarbonyl (MMT). The combustion of MMT by the automobile engine results in the formation of Mn particulates including phosphate, sulfate, and oxide forms. The objectives of this study were to determine the contribution of particle dissolution on pulmonary clearance rates of Mn sulfate (MnSO(4)), Mn phosphate, and Mn tetraoxide (Mn(3)O(4)) in CD rats following an intratracheal instillation exposure. In addition, brain (striatal) Mn concentrations were evaluated following exposure. Adult CD rats were intratracheally instilled with 0, 0.04, 0.08, or 0.16 microg Mn/g of either MnSO(4), Mn phosphate, or Mn(3)O(4). Rats were euthanized at 0, 1, 3, or 14 days after instillation. Lung and striatal Mn concentrations were measured by neutron activation analysis. Pulmonary clearance following single intratracheal instillation of MnSO(4), Mn phosphate, or Mn(3)O(4) was similar for each of the three compounds at each of the three doses used. All pulmonary clearance half-times were less than 0.5 day. At the concentrations used, striatal Mn levels were unaffected, and lung pathology was unremarkable. The dissolution rate constant of the Mn particles was determined in vitro using lung simulant fluids. The solubility of the Mn compounds was in general 20 to 40 times greater in Hatch artificial lung lining fluid than in Gamble lung simulant fluid. The dissolution rate constant of the water-soluble MnSO(4) particles in Hatch artificial lung fluid containing protein was 7.5 x 10(-4) g (Mn)/cm(2)/day, which was 54 times that of relatively water-insoluble Mn phosphate and 3600 times that of Mn(3)O(4). The dissolution rate constants for these compounds were sevenfold slower in Gamble lung fluid simulant. For both solutions, the time for half the material to go into solution differed only by factors of 1/83 to 1/17 to 1 for MnSO(4), Mn phosphate, and Mn(3)O(4), respectively, consistent with measured differences in size distribution, specific surface, and dissolution rate constant. These data suggest that dissolution mechanisms only played a role in the pulmonary clearance of MnSO(4), while nonabsorptive (e.g., mechanical transport) mechanisms predominate for the less soluble phosphate and oxide forms of Mn.

Air Pollutants↗
PubMed1991

Interaction of dietary calcium, manganese, and manganese source (Mn oxide or Mn methionine complex) on chick performance and manganese utilization.

Two trials were conducted to determine the utilization of manganese (Mn) as influenced by the level and source of Mn and the level of dietary calcium (Ca) in broiler chickens. Trial One was a 2 x 2 x 3 factorial arrangement of two Mn sources (Mn methionine or manganous oxide), two levels of dietary Ca (1.8 or 1.0), and three levels of supplemental Mn (30, 60, or 200 mg/kg) fed until 4 wk of age. Total phosphorus (available phosphorus) levels were 0.70% (0.48%) during all ages. High levels of dietary Ca caused a slower early rate of growth (0.53 vs. 0.64 kg) for chicks fed 1.8 vs 1.0% Ca, respectively. Chick weight was equivalent for all diets within the Ca-treatment group, except the dietary combination of high Ca and 200 mg/kg Mn as Mn methionine. Bone and liver Mn were significantly increased as the Mn level increased, but were not affected by the Mn source. Chicks fed 1.8% Ca had higher levels of bone Mn (9.28 ppm) than chicks fed 1.0% Ca (7.23 ppm). High levels of dietary Ca and 200 ppm Mn methionine dramatically depressed early growth, feed intake, and bone ash in this trial, raising the question of a diet x environment (heat-stress) effect. Trial Two was a 2 x 2 factorial arrangement of two levels of dietary Ca (1.8 or 1.0%) and two Mn sources (200 mg/kg Mn as Mn methionine or MnO) up to 3 wk of age in a controlled heat-stress environment. No growth depression in the chicks fed high levels of Ca and Mn methionine was observed. In the presence of high levels of dietary Ca, bone Mn was significantly higher when chicks were fed the MnO source. In summary, dietary Ca did not decrease Mn utilization in these trials, and availability of Mn in Mn methionine as a source compared to MnO depended on dietary Ca levels.

Animals↗
PubMed1985

Hepatic subcellular distribution of manganese in manganese and manganese-bilirubin induced cholestasis.

Administration of non-cholestatic doses of manganese (Mn2+) followed by injection of bilirubin (BR) results in a severe reduction in rat bile flow. Male Sprague-Dawley rats were given various doses of Mn2+ (2, 4.5, 8, and 18 mg/kg, i.v.) and killed 0.25, 1, 3, or 5 hr later. 54Mn2+ was used to evaluate Mn2+ content (micrograms/g protein) in different liver fractions: homogenate, mitochondria, microsomes, cytoplasm, nuclei-membrane fraction and liver cell plasma membrane fractions, one containing bile canalicular complexes (LCPM-BCM), the other containing sinusoidal membranes (LCPM-PM). In LCPM-BCM and LCPM-PM, two time-related patterns of Mn2+ content were observed. With non-cholestatic doses (2, 4.5, and 8 mg/kg), Mn2+ content decreased with time and rarely exceeded 50 micrograms/g protein. With 18 mg/kg (a cholestatic dose), Mn2+ content increased with time and reached values over 100 micrograms/g protein (3-5 hr), reflecting possible modification in membrane structure. BR caused a marked increase in Mn2+ content (at a dose of 4.5 mg Mn2+/kg) in LCPM-BCM (240%), approaching values seen with 18 mg Mn2+/kg, whereas in LCPM-PM it was less striking (50%). These and other results obtained with various treatments (cholestatic and non-cholestatic) suggest than Mn2+ concentration in bile canalicular membranes is a critical factor in both forms of cholestasis, and that BR can facilitate Mn2+ incorporation in the bile canalicular membrane.

Animals↗
PubMed1985

Effects of high dietary manganese as manganese oxide or manganese carbonate in sheep.

Twenty-four crossbred Florida native wether lambs, 28 kg initially, were assigned randomly to a basal diet (31 ppm Mn dry matter basis) supplemented with either 0, 500, 1,000, 2,000 or 4,000 ppm Mn from feed grade MnO or 2,000, 4,000 or 8,000 ppm Mn from reagent grade MnCO3. There were three sheep/treatment, with ad libitum access to feed and tap water. After 84 d, all animals were slaughtered and tissues removed for analysis. Dietary Mn at the highest levels from either source reduced (P less than .05) average daily feed intake and average daily gain. Hemoglobin and hematocrit were not affected by dietary Mn. Manganese concentration in kidney, spleen, heart, skeletal muscle, bone, serum (P less than .01) and liver (P less than .05) increased as dietary Mn increased. Kidney P was reduced (P less than .05) as dietary Mn increased; however, no other tissue minerals were affected. At comparable levels of supplementation, sheep fed feed-grade MnO exhibited numerically greater tissue Mn concentration than did those fed reagent-grade MnCO3 and regression analysis indicated higher rates of tissue uptake in MnO-supplemented sheep. Reduced feed intake and gain and apparent Mn homeostatic failure in liver were the only observed effects that may have been related to Mn toxicosis.

Animals↗
PubMed2003

Manganese distribution across the blood-brain barrier. I. Evidence for carrier-mediated influx of managanese citrate as well as manganese and manganese transferrin.

Manganese (Mn) is an essential element and a neurotoxicant. Regulation of Mn movement across the blood-brain barrier (BBB) contributes to whether the brain Mn concentration is functional or toxic. In plasma, Mn associates with water, small molecular weight ligands and proteins. Mn speciation may influence the kinetics of its movement through the BBB. In the present work, the brain influx rates of 54Mn2+, 54Mn citrate and 54Mn transferrin (54Mn Tf) were determined using the in situ brain perfusion technique. The influx rates were compared to their predicted diffusion rates, which were determined from their octanol/aqueous partitioning coefficients and molecular weights. The in situ brain perfusion fluid contained 54Mn2+, 54Mn citrate or 54Mn Tf and a vascular volume/extracellular space marker, 14C-sucrose, which did not appreciably cross the BBB during these short experiments (15-180 s). The influx transfer coefficient (Kin) was determined from four perfusion durations for each Mn species in nine brain regions and the lateral ventricular choroid plexus. The brain Kin was (5-13) x 10(-5), (3-51) x 10(-5), and (2-13) x 10(-5) ml/s/g for 54Mn2+, 54Mn citrate, and 54Mn Tf, respectively. Brain Kin values for any one of the three Mn species generally did not significantly differ among the nine brain regions and the choroid plexus. However, the brain Kin for Mn citrate was greater than Mn2+ and Mn Tf Kin values in a number of brain regions. When compared to calculated diffusion rates, brain Kin values suggest carrier-mediated brain influx of 54Mn2+, 54Mn citrate and 54Mn Tf. 55Mn citrate inhibited 54Mn citrate uptake, and 55Mn2+ inhibited 54Mn2+ uptake, supporting the conclusion of carrier-mediated brain Mn influx. The greater Kin values for Mn citrate than Mn2+ and its presence as a major non-protein-bound Mn species in blood plasma suggest Mn citrate may be a major Mn species entering the brain.

Animals↗
PubMed2001

Influence of dietary manganese on the pharmacokinetics of inhaled manganese sulfate in male CD rats.

Concerns exist as to whether individuals with relative manganese deficiency or excess may be at increased risk for manganese toxicity following inhalation exposure. The objective of this study was to determine whether manganese body burden influences the pharmacokinetics of inhaled manganese sulfate (MnSO(4)). Postnatal day (PND) 10 rats were placed on either a low (2 ppm), sufficient (10 ppm), or high (100 ppm) manganese diet. The feeding of the 2 ppm manganese diet was associated with a number of effects, including reduced body weight gain, decreased liver manganese concentrations, and reduced whole-body manganese clearance rates. Beginning on PND 77 +/- 2, male littermates were exposed 6 h/day for 14 consecutive days to 0, 0.092, or 0.92 mg MnSO(4)/m(3). End-of-exposure tissue manganese concentrations and whole-body (54)Mn elimination rates were determined. Male rats exposed to 0.092 mg MnSO(4)/m(3) had elevated lung manganese concentrations when compared to air-exposed male rats. Male rats exposed to 0.92 mg MnSO(4)/m(3) developed increased striatal, lung, and bile manganese concentrations when compared to air-exposed male rats. There were no significant interactions between the concentration of inhaled MnSO(4) and dietary manganese level on tissue manganese concentrations. Rats exposed to 0.92 mg MnSO(4)/m(3) also had increased (54)Mn clearance rates and shorter initial phase elimination half-lives when compared with air-exposed control rats. These results suggest that, marginally manganese-deficient animals exposed to high levels of inhaled manganese compensate by increasing biliary manganese excretion. Therefore, they do not appear to be at increased risk for elevated brain manganese concentrations.

Administration, Inhalation↗
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↗
PubMed1992

Varying levels of manganese and iron affect absorption and gut endogenous losses of manganese by rats.

The interactive effects of manganese and iron on true absorption and endogenous losses of manganese were investigated by feeding rats three levels of manganese (0.9, 48 or 188 micrograms Mn/g diet) and two levels of iron (19 or 276 micrograms Fe/g diet) for 7 wk. After 45 d, half of the rats were fed 54Mn and half were injected intraportally with 54Mn complexed to albumin. The relative distribution of 54Mn in tissues was generally similar for rats when 54Mn was administered in these two ways. Manganese-deficient animals retained more of the isotope, had both higher apparent and higher true absorption of manganese, had a greater proportion of 54Mn in their livers and had a lower proportion of 54Mn in their muscles compared with animals fed adequate or high levels of manganese. High iron intake inhibited manganese true absorption, reduced tissue manganese concentrations and inhibited heart manganese-dependent superoxide dismutase activity. However, the greatest effect of dietary iron was on mucosal cell manganese concentrations. Endogenous losses of manganese were approximately 8% of the amount of manganese actually absorbed regardless of intake. Thus, control of absorption in the gut seems to be the major way that manganese homeostasis is maintained. Furthermore, iron seems to be depressing manganese absorption by inhibiting manganese uptake into the mucosal cells.

Absorption↗