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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↗
PubMed1975

Effect of the dietary manganese level on tissue manganese, iron, copper and zinc concentrations in female rats and their fetuses.

In order to study the effect of dietary manganese on the content of manganese, iron, copper and zinc in maternal and fetal tissues, six diets with different levels of manganese (4, 24, 54, 154, 504 and 1004 mg Mn/kg dry diet) were fed to Sprague-Dawley female rats from the time of weaning. The animals were mated and the offspring collected by cesarean section at day 21 of pregnancy. Non-pregnant female rats served as respective reference groups. Concentrations of copper as well as manganese were higher in the livers of pregnant rats with the highest manganese intake, whereas in non-pregnant animals the dietary manganese level had no appreciable effect on manganese or copper concentrations in the liver. On the other hand, the iron content of the livers of both pregnant and non-pregnant female rats fell as the manganese level of the diet increased. The hemoglobin values of dams on the highest levels of dietary manganese were also slightly reduced. The manganese content was highest in the offspring of dams given the largest amounts of manganese. The manganese level in the maternal diet had the opposite effect on the fetal iron concentration, and the zinc content of fetuses of dams on the highest dietary manganese level was slightly elevated. No gross malformations or bone structure anomalies could be observed in the fetuses, and the manganese intake of the dams was not found to have influenced essentially the fetal weights and the dry matter and ash contents.

Animals↗
PubMed1996

Biliary manganese excretion in conscious rats is affected by acute and chronic manganese intake but not by dietary fat.

We hypothesized that biliary excretion of manganese would be sensitive to acute and chronic variations in manganese and fat intakes. In the acute study, we gavaged rats with solutions containing 54Mn with either 0, 0.2, 1 or 10 mg Mn as MnCl2. We collected bile from unanesthesized rats that were simultaneously reinfused with bile acids. Total manganese excretion (from 0.5 to 6.5 h after dosing) was proportional to the acute doses (approximately 3.4% of doses). In the chronic study, weanling rats were fed diets containing 5 or 20 g corn oil/g diet and 0.49 or 72 micrograms Mn/g diet for 8 wk and then deprived of food for 12 h before bile collection. Manganese-deficient animals excreted only 0.7% as much manganese in bile as manganese-replete animals, but this reduction was not sufficient to prevent 50-80% reduction of tissue manganese concentrations. Moreover, biliary manganese excretion (calculated for 24 h) by both manganese-deficient and manganese-replete rats (deprived of food for previous 12 h) accounted for only 1% of their manganese intake on the previous day. Dietary fat and manganese concentrations had few effects on excretion of total or individual bile acids. Ours is the first report of biliary excretion of orally administered manganese by conscious rats.

Animals↗
PubMed2006

Correlation of brain magnetic resonance imaging changes with pallidal manganese concentrations in rhesus monkeys following subchronic manganese inhalation.

High-dose manganese exposure is associated with parkinsonism. Because manganese is paramagnetic, its relative distribution within the brain can be examined using magnetic resonance imaging (MRI). Herein, we present the first comprehensive study to use MRI, pallidal index (PI), and T(1) relaxation rate (R1) in concert with chemical analysis to establish a direct association between MRI changes and pallidal manganese concentration in rhesus monkeys following subchronic inhalation of manganese sulfate (MnSO(4)). Monkeys exposed to MnSO(4) at > or = 0.06 mg Mn/m(3) developed increased manganese concentrations in the globus pallidus, putamen, olfactory epithelium, olfactory bulb, and cerebellum. Manganese concentrations within the olfactory system of the MnSO(4)-exposed monkeys demonstrated a decreasing rostral-caudal concentration gradient, a finding consistent with olfactory transport of inhaled manganese. Marked MRI signal hyperintensities were seen within the olfactory bulb and the globus pallidus; however, comparable changes could not be discerned in the intervening tissue. The R1 and PI were correlated with the pallidal manganese concentration. However, increases in white matter manganese concentrations in MnSO(4)-exposed monkeys confounded the PI measurement and may lead to underestimation of pallidal manganese accumulation. Our results indicate that the R1 can be used to estimate regional brain manganese concentrations and may be a reliable biomarker of occupational manganese exposure. To our knowledge, this study is the first to provide evidence of direct olfactory transport of an inhaled metal in a nonhuman primate. Pallidal delivery of manganese, however, likely arises primarily from systemic delivery and not directly from olfactory transport.

Animals↗
PubMed1980

Synthesis and determination of manganese carbonate and manganese-54 carbonate.

A method was developed by which radioactive manganese, manganese-54 carbonate (with a high specific activity), could be produced. This was accomplished by reacting manganese-54 chloride, manganese chloride tetrahydrate, and sodium bicarbonate. This reaction produced manganese-54 carbonate (specific activity .35 mCi/mg manganese mixed with stable manganese. The purity of the manganese carbonate (manganese-54 carbonate) was determined by the use of x-ray diffraction methods. One method compared "d" spacings (distance in angstroms between lattice planes of a crystal) with standard and index values for pure manganese carbonate. Another method compared x-ray diffractograms of the synthesized product with standard manganese carbonate. By both methods all material was the carbonate form of manganese (manganese-54 carbonate).

Carbonates↗
PubMed1983

Acute manganese toxicity and the absorption and biliary excretion of manganese in cattle.

The concentration of manganese in the duodenum of three steers was increased by infusing manganese chloride intraduodenally at approximately 100, 515 and 840 mumol per minute for 30 hours and the rate at which manganese was excreted in bile was measured. In one steer an infusion of manganese chloride at 529 mumol per minute was toxic and in two steers infusions at approximately 840 mumol per minute were also toxic, causing inappetence, a reduced bile flow and abdominal discomfort. The maximum rates at which manganese was excreted in bile during the first three hours of the infusions at 515 and 840 mumol per minute were between 2.1 and 3.6 per cent of the rate of infusion. During the last three hours of all nontoxic infusions the rate of excretion of manganese in bile was 0.82 +/- 0.08 per cent of its rate of infusion. Systemic plasma manganese concentrations did not increase during these infusions. In a fourth steer the longer term capacity of the liver to excrete manganese in bile when the manganese chloride was given intravenously was measured, the concentration of manganese in the portal vein being increased by infusions of manganese chloride solution into a mesenteric vein. The rate of infusion was increased at hourly intervals. The liver's capacity to remove all manganese during first pass was only exceeded at an infusion rate of 84 mumol per minute. Infusions could be made into the mesenteric vein at 24 and 35.8 mumol per minute for 53 and 26 hours respectively before signs of toxicity were observed. Following signs of toxicity the excretion of copper in bile was decreased for two days.

Animals↗
PubMed2000

Comparative toxicokinetics of manganese chloride and methylcyclopentadienyl manganese tricarbonyl (MMT) in Sprague-Dawley rats.

The toxicokinetics of manganese (Mn) was investigated in male and female rats either following a single intravenous (iv) or oral dose of MnCl2 (6.0 mg Mn/kg), or following a single oral dose of methylcyclopentadienyl manganese tricarbonyl (MMT) (20 mg MMT/kg or 5.6 mg Mn/kg). The plasma concentrations of manganese were quantified by atomic absorption spectrophotometry (AAS). Upon iv administration of MnCl2, manganese rapidly disappeared from blood with a terminal elimination t1/2 of 1.83 h and CL8 of 0.43 L/h/kg. The plasma concentration-time profiles of manganese could be described by C = 41.9e(-424t) + 2.1e(-0.44t). Following oral administration of MnCl2, manganese rapidly entered the systemic circulation (Tmax = 0.25 h). The absolute oral bioavailability was about 13%. Oral dose of MMT resulted in a delayed Tmax(7.6 h), elevated Cmax (0.93 microg/ml), and prolonged terminal t1/2 (55.1 h). The rats receiving MMT had an apparent clearance (CL/F = 0.09 L/h x kg) about 37-fold less than did those who were dosed with MnCl2. Accordingly, the area under the plasma concentration-time curves (AUC) of manganese in MMT-treated rats was about 37-fold greater than that in MnCl2-treated rats. A gender-dependent difference in toxicokinetic profiles of plasma manganese was also observed. Female rats displayed a greater AUC than that of male rats. Although the apparent volume of distribution of manganese was similar in both sexes, the apparent clearance in males was about twice that observed in females. The results indicated that after oral administration, the MMT-derived manganese displayed higher and more prolonged plasma concentration-time profiles than MnCl2-derived manganese. Thus, MMT-derived manganese appeared likely to accumulate in the body following repeated exposure.

Administration, Oral↗
PubMed2006

Tissue manganese concentrations in young male rhesus monkeys following subchronic manganese sulfate inhalation.

High-dose human exposure to manganese results in manganese accumulation in the basal ganglia and dopaminergic neuropathology. Occupational manganese neurotoxicity is most frequently linked with manganese oxide inhalation; however, exposure to other forms of manganese may lead to higher body burdens. The objective of this study was to determine tissue manganese concentrations in rhesus monkeys following subchronic (6 h/day, 5 days/week) manganese sulfate (MnSO(4)) inhalation. A group of monkeys were exposed to either air or MnSO(4) (0.06, 0.3, or 1.5 mg Mn/m(3)) for 65 exposure days before tissue analysis. Additional monkeys were exposed to MnSO(4) at 1.5 mg Mn/m(3) for 15 or 33 exposure days and evaluated immediately thereafter or for 65 exposure days followed by a 45- or 90-day delay before evaluation. Tissue manganese concentrations depended upon the aerosol concentration, exposure duration, and tissue. Monkeys exposed to MnSO(4) at > or = 0.06 mg Mn/m(3) for 65 exposure days or to MnSO(4) at 1.5 mg Mn/m(3) for > or = 15 exposure days developed increased manganese concentrations in the olfactory epithelium, olfactory bulb, olfactory cortex, globus pallidus, putamen, and cerebellum. The olfactory epithelium, olfactory bulb, globus pallidus, caudate, putamen, pituitary gland, and bile developed the greatest relative increase in manganese concentration following MnSO(4) exposure. Tissue manganese concentrations returned to levels observed in the air-exposed animals by 90 days after the end of the subchronic MnSO(4) exposure. These results provide an improved understanding of MnSO(4) exposure conditions that lead to increased concentrations of manganese within the nonhuman primate brain and other tissues.

Animals↗
PubMedDate not supplied

On-off study of manganese administration to adult patients undergoing home parenteral nutrition: new indices of in vivo manganese level.

BACKGROUND: Recently, there have been reports that magnetic resonance imaging (MRI) reveals high-intensity T1-weighted images (HI) in the basal ganglia (especially in the globus pallidus) of patients receiving total parenteral nutrition (TPN). This finding is presumably due to excess administration of manganese. We investigated the reversibility and reproducibility of these changes by means of an on-off manganese administration study. We also investigated the temporal relationships between the intensity of T1-weighted images (MRI intensity) and the whole-blood and plasma manganese concentrations to evaluate the potential for the MRI intensity to serve as an index of the in vivo manganese level. METHODS: Eleven adult patients undergoing home parenteral nutrition received TPN solutions containing manganese (0 or 20 micromol/d) according to an on-off design. The whole-blood and plasma manganese concentrations were determined at the same time the brain MRI was performed. RESULTS: Both the whole-blood manganese concentration and the MRI intensity in the globus pallidus changed in response to the administration and withdrawal of manganese. It took at least 5 months for HI to disappear when manganese was withdrawn, and this change was reversible and reproducible. The whole-blood manganese concentration showed strong correlations with both the MRI intensity and the T1 value (r = 0.7693, -0.7011). The MRI intensity and the T1 value showed a strong correlation (r = -0.9051). CONCLUSIONS: The whole-blood manganese concentration, the MRI intensity in the globus pallidus and the T1 value, an objective index of the MRI intensity, may be useful indices of the manganese level in the body.

Adult↗
PubMed1989

[The effect of the dosage and route of manganese administration on manganese concentration in rat brain].

We investigated the differences in manganese concentration and distribution in the brains of rats administered MnCl2 perorally, intravenously and intraperitoneally for one week. Forty two male Wistar rats were divided into eight groups, designated A to H. Groups A (n = 5) and B (n = 7) were maintained with synthetic diets, with 50 and 1000 mg manganese per kg diets, respectively. Groups C (n = 5), D (n = 5) and E (n = 5) were administered manganese intravenously with dosages of 0.088, 0.88 and 2.2 mg/kg.b.w./day, respectively. Groups F (n = 5), G (n = 5) and H (n = 5) were administered manganese intraperitoneally with dosages of 0.088, 0.88 and 2.2 mg/kg.b.w/day, respectively. Four brain regions (cerebrum, cerebellum, basal ganglia and the remainder) were analyzed by atomic absorption spectrophotometry for manganese. The manganese concentrations in basal ganglia were increased proportionally to the administration dosages in intravenous administration groups (C, D and E). At the highest dosage of manganese administration, manganese concentrations in cerebrum and basal ganglia were higher with intravenous administration of manganese than with intraperitoneal administration. In addition, manganese concentrations were hardly increased in peroral administration groups. Therefore, we suggested that basal ganglia are vulnerable to manganese exposure and that liver and intestine might play the important roles in the reduction of manganese accumulation in the central nervous system.

Animals↗
PubMed2004

Tissue manganese concentrations in lactating rats and their offspring following combined in utero and lactation exposure to inhaled manganese sulfate.

There is little information regarding the tissue distribution of manganese in neonates following inhalation. This study determined tissue manganese concentrations in lactating CD rats and their offspring following manganese sulfate (MnSO4) aerosol inhalation. Except for the period of parturition, dams and their offspring were exposed to air or MnSO4 (0.05, 0.5, or 1 mg Mn/m3) for 6 h/day, 7 days/week starting 28 days prior to breeding through postnatal day (PND) 18. Despite increased manganese concentrations in several maternal tissues, MnSO4 inhalation exposure did not affect body weight gain, terminal (PND 18) body weight, or organ weights in the dams. Exposure to MnSO4 at 1 mg Mn/m3 resulted in decreased pup body weights on PND 19 and decreased brain weights in some PND 14 to PND 45 pups. Exposure to MnSO4 at > or =0.05 mg Mn/m3 was associated with increased stomach content, blood, liver, and skull cap manganese concentrations in PND 1 pups, increased brain, lung, and femur manganese concentrations in PND 14 pups, and elevated olfactory bulb, cerebellum, and striatum manganese concentrations in PND 19 pups. When compared to controls, MnSO4 exposure to > or =0.5 mg Mn/m3 increased liver and blood manganese concentrations in PND 14 pups and increased liver, pancreas, and femur manganese concentrations in PND 19 pups. Manganese concentrations returned to control values in all offspring tissues by PND 45 +/- 1. Our data demonstrate that neonatal tissue manganese concentrations observed following MnSO4 inhalation are dependent on the MnSO4 exposure concentration and the age of the animal.

Administration, Inhalation↗
PubMed2004

Nasal toxicity of manganese sulfate and manganese phosphate in young male rats following subchronic (13-week) inhalation exposure.

Growing evidence suggests that nasal deposition and transport along the olfactory nerve represents a route by which inhaled manganese and certain other metals are delivered to the rodent brain. The toxicological significance of olfactory transport of manganese remains poorly defined. In rats, repeated intranasal instillation of manganese chloride results in injury to the olfactory epithelium and neurotoxicity as evidenced by increased glial fibrillary acidic protein (GFAP) concentrations in olfactory bulb astrocytes. The purpose of the present study was to further characterize the nasal toxicity of manganese sulfate (MnSO(4)) and manganese phosphate (as hureaulite) in young adult male rats following subchronic (90-day) exposure to air, MnSO(4) (0.01, 0.1, and 0.5 mg Mn/m(3)), or hureaulite (0.1 mg Mn/m(3)). Nasal pathology, brain GFAP levels, and brain manganese concentrations were assessed immediately following the end of the 90-day exposure and 45 days thereafter. Elevated end-of-exposure olfactory bulb, striatum, and cerebellum manganese concentrations were observed following MnSO(4) exposure to > or = 0.01, > or = 0.1, and 0.5 mg Mn/m(3), respectively. Exposure to MnSO(4) or hureaulite did not affect olfactory bulb, cerebellar, or striatal GFAP concentrations. Exposure to MnSO(4) (0.5 mg Mn/m(3)) was also associated with reversible inflammation within the nasal respiratory epithelium, while the olfactory epithelium was unaffected by manganese inhalation. These results confirm that high-dose manganese inhalation can result in nasal toxicity (irritation) and increased delivery of manganese to the brain; however, we could not confirm that manganese inhalation would result in altered brain GFAP concentrations.

Air Pollutants↗
PubMed1993

Subcellular and gel chromatographic distribution of manganese in the mouse brain: relation to the chemical form of chronically-ingested manganese.

The subcellular distribution of manganese and the binding characteristics of manganese to protein in the mouse brain were examined on G-75 Sephadex gel columns. Four manganese compounds were included at 2 g/kg in each food eaten by ddY mice for 12 months. The cerebral cortex manganese concentrations in the virtually insoluble manganese compounds were significantly higher than those in the control group. The brain striatal subcellular distribution and gel chromatographic profiles of manganese were similar among the divalent manganese compounds. On the contrary, the behaviour of MnO2 was little different from the divalent manganese compounds. There was more manganese associated with fast-migrating ligands in the striatal cytosol of the manganese-exposed group than in the control groups.

Acetates↗
PubMed2004

Old age and gender influence the pharmacokinetics of inhaled manganese sulfate and manganese phosphate in rats.

In this study, we examined whether gender or age influences the pharmacokinetics of manganese sulfate (MnSO(4)) or manganese phosphate (as the mineral form hureaulite). Young male and female rats and aged male rats (16 months old) were exposed 6 h day(-1) for 5 days week(-1) to air, MnSO(4) (at 0.01, 0.1, or 0.5 mg Mn m(-3)), or hureaulite (0.1 mg Mn m(-3)). Tissue manganese concentrations were determined in all groups at the end of the 90-day exposure and 45 days later. Tissue manganese concentrations were also determined in young male rats following 32 exposure days and 91 days after the 90-day exposure. Intravenous (54)Mn tracer studies were also performed in all groups immediately after the 90-day inhalation to assess whole-body manganese clearance rates. Gender and age did not affect manganese delivery to the striatum, a known target site for neurotoxicity in humans, but did influence manganese concentrations in other tissues. End-of-exposure olfactory bulb, lung, and blood manganese concentrations were higher in young male rats than in female or aged male rats and may reflect a portal-of-entry effect. Old male rats had higher testis but lower pancreas manganese concentrations when compared with young males. Young male and female rats exposed to MnSO(4) at 0.5 mg Mn m(-3) had increased (54)Mn clearance rates when compared with air-exposed controls, while senescent males did not develop higher (54)Mn clearance rates. Data from this study should prove useful in developing dosimetry models for manganese that consider age or gender as potential sensitivity factors.

Administration, Inhalation↗
PubMedDate not supplied

Tissue manganese concentrations and antioxidant enzyme activities in rats given total parenteral nutrition with and without supplemental manganese.

BACKGROUND: Manganese is an essential but potentially toxic mineral. Parenteral administration of manganese via total parenteral nutrition (TPN) bypasses homeostatic mechanisms (intestinal absorption and presystemic hepatic elimination). Our objective in this study was to determine the effect of supplemental manganese in TPN solutions on manganese status in a rat model. METHODS: Male Sprague-Dawley rats underwent jugular catheterization and were given 61.0 +/- 0.4 g/d TPN solution providing 0.5 +/- 0.2 nmol manganese/g (Mn-; n = 6) or 16 +/- 3 nmol manganese/g (Mn+; n = 7) for 7 days. Reference rats (RF; n = 8) were fed a purified diet containing 1.3 mmol manganese/g. RESULTS: Liver manganese decreased in both TPN groups, but tibia, spleen, and pancreas manganese concentrations were greater in Mn+ rats than in Mn- or RF rats. Although no treatment differences were seen in heart or liver manganese superoxide dismutase activity, heart copper-zinc superoxide dismutase activity was lower in the Mn+ rats than in Mn- or RF rats (p < .05). Glutathione peroxidase activity was depressed in livers of both Mn- and Mn+ rats relative to RF rats (p < .0001), which was not due to selenium deficiency. CONCLUSIONS: Supplemental parenteral manganese is taken up to a greater extent by peripheral tissues than the liver. In this first report of antioxidant enzyme activities in animals maintained with TPN, we found that TPN as well as supplemental manganese can influence antioxidant enzyme activities. We conclude that it is generally unnecessary and potentially toxic to supplement TPN solutions with manganese during short-term usage.

Animals↗
PubMed2005

Maternal-fetal distribution of manganese in the rat following inhalation exposure to manganese sulfate.

Studies examining the pharmacokinetics of manganese during pregnancy have largely focused on the oral route of exposure and have shown that the amount of manganese that crosses the rodent placenta is low. However, limited information exists regarding the distribution of manganese in fetal tissues following inhalation. The objective of this study was to determine manganese body burden in CD rats and fetuses following inhalation of a MnSO4 aerosol during pregnancy. Animals were evaluated following pre-breeding (2 weeks), mating (up to 14 days) and gestational (from gestation day (GD) 0 though 20) exposure to air or MnSO4 (0.05, 0.5, or 1 mg Mn/m(3)) for 6h/day, 7 days/week. The following maternal samples were collected for manganese analysis: whole blood, lung, pancreas, liver, brain, femur, and placenta. Fetal tissues were examined on GD 20 and included whole blood, lung, liver, brain, and skull cap. Maternal lung manganese concentrations were increased following exposure to MnSO4 at >or=0.05 mg Mn/m(3). Maternal brain and placenta manganese concentrations were increased following exposure of pregnant rats to MnSO4 at >or=0.5 mg Mn/m(3). Increased fetal liver manganese concentrations were observed following in utero exposure to MnSO4 at >or=0.5 mg Mn/m(3). Manganese concentrations within all other fetal tissues were not different from air-exposed controls. The results of this study demonstrate that the placenta partially sequesters inhaled manganese, thereby limiting exposure to the fetus.

Animals↗
PubMed1992

Longitudinal changes of manganese-dependent superoxide dismutase and other indexes of manganese and iron status in women.

The effect of dietary factors on manganese-dependent superoxide dismutase (MnSOD) activity in humans has not been studied. We longitudinally evaluated changes in MnSOD activity and other indices of manganese and iron status in 47 women during a 124-d supplementation study. Subjects received one of four treatments: placebo, 60 mg iron, 15 mg manganese, or both mineral supplements daily. Manganese supplementation resulted in significant increases in lymphocyte MnSOD activity and serum manganese concentrations from baseline values but no changes in urinary manganese excretion or in any indices of iron status. Oral contraceptive use and the stage of the menstrual cycle did not confound the use of lymphocyte MnSOD activity or serum manganese to monitor manganese status, but fat intake affected both indices. This work demonstrated that lymphocyte MnSOD activity can be used with serum manganese concentrations to monitor manganese exposure in humans.

Adult↗
PubMed1989

Quantifying manganese in lymphocytes to assess manganese nutritional status.

To clarify whether manganese nutritional status is better reflected by the manganese concentration in lymphocytes or in whole blood, we injected manganese solutions intravenously into manganese-deficient rats and determined manganese concentrations in lymphocytes, whole blood, and various tissues. The manganese concentrations in lymphocytes and tissues, but not in whole blood, were significantly less in manganese-deficient rats than in normal rats. These low values could be prevented by intravenous injection of manganese in a dose-dependent manner. These results suggest that, for assessment of manganese nutritional status, measurement of manganese in lymphocytes is better than that in whole blood.

Animals↗