Dietary Manganese Research Articles

An Estimation of the Manganese Requirement for Broilers from 1 to 21 Days of Age

A dose-response experiment was conducted to find the sensitive and consistent biomarker for the estimation of dietary manganese (Mn) requirement and establish the optimal Mn level for broilers fed a practical corn-soybean meal diet from 1 to 21days of age post-hatching. A total of 480 1-day-old Arbor Acres male chicks were randomly allotted to one of eight treatments with five replicates of 12 birds each and fed diets supplemented with 0, 20, 40, 60, 80, 100, 120, or 140mg Mn/kg from reagent grade Mn sulfate. Tissue Mn concentrations, manganese-containing superoxide dismutase (MnSOD) activity, and MnSOD mRNA concentration within heart tissue were analyzed at 7, 14, and 21days of age. Tissue Mn concentrations and heart MnSOD activity showed significant quadratic responses, and heart MnSOD mRNA concentration showed an asymptotic response to dietary supplemental Mn level, respectively. The estimate of dietary Mn for chicks from 1 to 21days of age was 122-128 for heart Mn concentration, 141-159 for pancreas Mn concentration, 127-138 for liver Mn concentration, and 135-156mg/kg for heart MnSOD activity, respectively. Heart MnSOD mRNA concentration was a consistent index for the estimation of the Mn requirement of broilers. Based on this index, the estimate of dietary Mn requirement for broilers from 1 to 21days of age post-hatching was about 130mg/kg, which was a little more than two times of the current NRC (1994) requirement.

Intellectual Impairment in School-Age Children Exposed to Manganese from Drinking Water

BackgroundManganese is an essential nutrient, but in excess it can be a potent neurotoxicant. Despite the common occurrence of manganese in groundwater, the risks associated with this source of exposure are largely unknown.ObjectivesOur first aim was to assess the relations between exposure to manganese from drinking water and children’s intelligence quotient (IQ). Second, we examined the relations between manganese exposures from water consumption and from the diet with children’s hair manganese concentration.MethodsThis cross-sectional study included 362 children 6–13 years of age living in communities supplied by groundwater. Manganese concentration was measured in home tap water (MnW) and children’s hair (MnH). We estimated manganese intake from water ingestion and the diet using a food frequency questionnaire and assessed IQ with the Wechsler Abbreviated Scale of Intelligence.ResultsThe median MnW in children’s home tap water was 34 μg/L (range, 1–2,700 μg/L). MnH increased with manganese intake from water consumption, but not with dietary manganese intake. Higher MnW and MnH were significantly associated with lower IQ scores. A 10-fold increase in MnW was associated with a decrease of 2.4 IQ points (95% confidence interval: −3.9 to −0.9; p < 0.01), adjusting for maternal intelligence, family income, and other potential confounders. There was a 6.2-point difference in IQ between children in the lowest and highest MnW quintiles. MnW was more strongly associated with Performance IQ than Verbal IQ.ConclusionsThe findings of this cross-sectional study suggest that exposure to manganese at levels common in groundwater is associated with intellectual impairment in children.

Consequences of dietary manganese and copper imbalance on neuronal apoptosis in a murine model of scrapie

Copper and manganese levels are altered in mice both lacking PrPc and prion-infected brains. The aim of this study was to analyse the effects of manganese and copper imbalance on neuronal apoptosis in a scrapie-infected Tga20 mouse model. Immunoreactivities for the apoptotic proteins Bax and active caspase-3 were evaluated in nine regions of the brain of scrapie-infected and control Tga20 mice treated with one of several diets: depleted cooper (-Cu), loaded manganese (+Mn), depleted copper/loaded manganese (-Cu+Mn) and regular diet. Immunohistochemical determination of NeuN was used to detect possible neuronal loss. Intracellular Bax detection was significantly decreased in animals fed with modified diets, particularly in those treated with copper-depleted diets. A decrease in active caspase-3 was primarily observed in animals fed with enhanced manganese diets. Our results show that the -Cu, -Cu+Mn and +Mn diets protected against apoptosis in scrapie-infected mice. However, NeuN immunolabelling quantification revealed that no diet was sufficient to arrest neuronal death. With regard to apoptosis induction, the response of Tga20 mice to prion infection was similar to that reported for other mice models. Our results demonstrate the neuroprotective effects of -Cu, -Cu+Mn and +Mn diets in a murine model of scrapie. However, neuronal death induced by infection with prions seems to be independent of apoptosis marker signalling. Moreover, copper-modified diets were neuroprotective against the possible toxicity of the prion transgene in Tga20 control and infected mice even though manganese supplementation could not counteract this toxicity.

Diabetics of Northeast India are at risk of dietary zinc and manganese deficiency: Possible improvement through consumption of some traditional edibles or edibles of limited popularity

Background: Restricted diets of Northeast India were found to be low in both zinc and manganese. Aim: To explore the possibilities of compensating for the low zinc and manganese content in restricted diet by supplementing with traditional edibles and edibles of limited popularity. Materials and Method: Concentration of these two elements in a number of edibles from Northeast India was assessed along with some traditional edibles and edibles of limited popularity. Results: Relatively high concentration of zinc and manganese were recorded in some traditional edibles and edibles of limited popularity, which when added to diabetic diet could elevate the concentration of zinc and manganese, and bring the level of these two elements close to the recommended level. Conclusion: It is suggested that, the deficiency of essential elements in the restricted diet of diabetics in Northeast India should be monitored and appropriate supplementation may be tried, preferably through some traditional edibles and edibles of limited popularity.

Preweaning manganese exposure causes hyperactivity, disinhibition, and spatial learning and memory deficits associated with altered dopamine receptor and transporter levels

Epidemiological studies in children have reported associations between elevated dietary manganese (Mn) exposure and neurobehavioral and neurocognitive deficits. To better understand the relationship between early Mn exposure and neurobehavioral deficits, we treated neonate rats with oral Mn doses of 0, 25, or 50 mg Mn/kg/day over postnatal day (PND) 1-21, and evaluated behavioral performance using open arena (PND 23), elevated plus maze (PND 23), and 8-arm radial maze (PND 33-46) paradigms. Brain dopamine D1 and D2-like receptors, and dopamine transporter (DAT) densities were determined on PND 24, and blood and brain Mn levels were measured to coincide with behavioral testing (PND 24, PND 36). Preweaning Mn exposure caused hyperactivity and behavioral disinhibition in the open arena, but no altered behavior in the elevated plus maze. Manganese-exposed males committed significantly more reference and marginally more working errors in the radial arm maze compared to controls. Fewer Mn exposed males achieved the radial maze learning criterion, and they required more session days to reach it compared to controls. Manganese-exposed animals also exhibited a greater frequency of stereotypic response strategy in searching for the baited arms in the maze. These behavioral and learning deficits were associated with altered expression of the dopamine D1 and D2 receptors and the DAT in prefrontal cortex, nucleus accumbens, and dorsal striatum. These data corroborate epidemiological studies in children, and suggest that exposure to Mn during neurodevelopment significantly alters dopaminergic synaptic environments in brain nuclei that mediate control of executive function behaviors, such as reactivity and cognitive flexibility.

Antioxidant intake from fruits, vegetables and other sources and risk of non‐Hodgkin's lymphoma: the Iowa Women's Health Study

Antioxidant nutrients found in fruits, vegetables and other foods are thought to inhibit carcinogenesis and to influence immune status. We evaluated the association of these factors with risk of non-Hodgkin's lymphoma (NHL) overall and for diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma specifically in a prospective cohort of 35,159 Iowa women aged 55-69 years when enrolled at baseline in 1986. Diet was ascertained using a validated semiquantitative food frequency questionnaire. Through 2005, 415 cases of NHL (including 184 DLBCL and 90 follicular) were identified. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox regression, adjusting for age and total energy. The strongest associations of antioxidants with risk of NHL (RR for highest versus lowest quartile; p for trend) were observed for dietary vitamin C (RR = 0.78; p = 0.044), alpha-carotene (RR = 0.71; p = 0.015), proanthocyanidins (RR = 0.70; p = 0.0024) and dietary manganese (RR = 0.62; p = 0.010). There were no associations with multivitamin use or supplemental intake of vitamins C, E, selenium, zinc, copper or manganese. From a food perspective, greater intake of total fruits and vegetables (RR = 0.69; p = 0.011), yellow/orange (RR = 0.72; p = 0.015) and cruciferous (RR = 0.82; p = 0.017) vegetables, broccoli (RR = 0.72; p = 0.018) and apple juice/cider (RR = 0.65; p = 0.026) were associated with lower NHL risk; there were no strong associations for other antioxidant-rich foods, including whole grains, chocolate, tea or nuts. Overall, these associations were mainly observed for follicular lymphoma and were weaker or not apparent for DLBCL. In conclusion, these results support a role for vegetables, and perhaps fruits and associated antioxidants from food sources, as protective factors against the development of NHL and follicular lymphoma in particular.

Proteins involved in iron metabolism in beef cattle are affected by copper deficiency in combination with high dietary manganese, but not by copper deficiency alone1

A 493-d study was conducted to determine the impact of a severe, long-term Cu deficiency on Fe metabolism in beef cattle. Twenty-one Angus calves were born to cows receiving one of the following treatments: 1) adequate Cu (+Cu), 2) Cu deficient (-Cu), and 3) Cu deficient plus high Mn (-Cu+Mn). Copper deficiency was induced through the addition of 2 mg of Mo/kg of DM. After weaning, calves remained on the same treatment as their dam through growing (basal diet analyzed 7 mg of Cu/kg of DM) and finishing (analyzed 4 mg of Cu/kg of DM) phases. Plasma Fe concentrations were positively correlated (P < 0.01; r = 0.49) with plasma Cu concentrations. Liver Fe concentrations were greater (P = 0.05) in -Cu vs. +Cu calves and further increased (P = 0.07) in -Cu+Mn vs. -Cu calves. There was a negative relationship (P < 0.01; r = -0.31) between liver Cu and Fe concentrations. This relationship is likely explained by less (P < 0.01) plasma ceruloplasmin activity in -Cu than +Cu calves. As determined by real-time reverse transcription-PCR, relative expression of hepatic hepcidin was significantly downregulated (>1.5 fold) in -Cu compared with +Cu calves (P = 0.03), and expression of hepatic ferroportin tended (P = 0.09) to be downregulated in -Cu vs. +Cu. In the duodenum, ferritin tended to be upregulated in -Cu. vs. +Cu calves (P < 0.06). No significant change (P > 0.2) due to Cu-deficiency was detected at the transcriptional level for either isoform of divalent metal transporter 1 (DMT1 mRNA with or without an iron responsive element; dmt1IRE and dmt1-nonIRE) in liver or intestine. Duodenal expression of hephaestin and ferroportin protein was not affected by dietary treatment (P > 0.20). However, duodenal expression of DMT1 protein was less (P = 0.04) in -Cu+Mn steers vs. -Cu steers. In summary, Cu deficiency alone did affect hepatic gene expression of hepcidin and ferroportin, but did not affect duodenal expression of proteins important in Fe metabolism. However, the addition of 500 mg of Mn/kg of DM to a diet low in Cu reduced duodenal expression of the Fe import protein DMT1.

Incorporating genetics and genomics in risk assessment for inhaled manganese: From data to policy

Manganese is an essential nutrient, and a healthy human with good liver and kidney function can easily excrete excess dietary manganese. Inhaled manganese is a greater concern, because it bypasses the body's normal homeostatic mechanisms and can accumulate in the brain. Prolonged exposure to high manganese concentrations (>1 mg/m 3) in air leads to a Parkinsonian syndrome known as “manganism.” Of greatest concern are recent studies which indicate that neurological and neurobehavioral deficits can occur when workers are exposed to much lower levels (<0.2 mg/m 3) of inhaled manganese in welding fumes. Consequently, researchers at NIOSH are conducting a risk assessment for inhaled manganese. Novel components of this risk assessment include an attempt to quantify the range of inter-individual differences using data generated by the Human Genome Project and experimental work to identify genetically based biomarkers of exposure, disease and susceptibility. The difficulties involved in moving from epidemiological and in vivo data to health-based quantitative risk assessment and ultimately enforceable government standards are discussed.

Evaluation of manganese balance status in Korean adults

Few data are available to establish recommendations for manganese in Korea. This study assessed the status of manganese balance among 51 free‐living Korean adults. We measured dietary manganese intake using 3‐day dietary records, and analyzed the manganese contents in 24 hr urine, feces and serum of the subjects. Average age, height, weight and body mass index were 24.7 years, 173.2 cm, 73.6 kg and 24.6 kg/m2 in males and 22.8 years, 160.8 cm, 55.5 kg and 21.6 kg/m2 in females. The daily manganese intakes of male and female subjects were 3.2 mg and 3.7 mg, respectively. Average serum manganese level was 10.49 ug/dl in male and 6.11 ug/dl in females, and there was no significant difference. Urinary manganese excretion in male (344.5 ug/day) was significantly higher than that in female (184.7 ug/day). However, fecal manganese excretion was not significantly different between male (2078.0 ug/day) and female (1950.6 ug/day). Also, retention, retention rate and apparent digestibility of manganese were 765.6 ug/day, 18.4% and 30.9% for male, and 596.6 ug/day, 19.4% and 26.0% for female, it turned out that there was no significant difference. By continuous evaluating balance status of manganese, it is anticipated that reference intakes of manganese will be established. &lt;'This work was supported by the Korea Research Foundation Grant funded by the Korean Government (KRF‐2006‐531‐C00069).'&gt;

The effects of prion protein expression on metal metabolism

The prion protein is a glycoprotein that binds metals such as copper and manganese. When converted to a proteinase resistant isoform it is associated with prion diseases such as Creutzfeldt–Jakob disease and bovine spongiform encephalopathy. Although, the co-ordination and metal affinity of the prion protein has been well studied, the association of the protein with cellular metal metabolism has been less well investigated. We used transgenic manipulation of prion protein expression and other recombinant techniques to alter expression of known copper binding proteins to investigate the role of the prion protein in copper metabolism. We found that changing the expression of the prion protein alters proteins associated with copper uptake, storage and export from the cell. In addition, alteration in the expression of superoxide dismutases increased prion protein expression dramatically. Reducing copper in the diet decreased expression of the prion protein in the brain while increased dietary manganese dramatically increased the protein's expression. Cellular prion infection also increased the expression of metal transporting proteins and increased cellular manganese concentrations. Overall our results show a close link between cellular resistance to oxidative stress and also copper metabolism. These findings are in line with previous data suggesting that the prion protein is an antioxidant and associated with copper uptake into cells. The disturbance to copper metabolism, as a result of altered prion protein expression clearly demonstrates the important role of the prion protein in copper metabolism. The implication is that prion protein expression has a homeostatic role in copper metabolism.

Growth performance and tissue mineral content of juvenile grouper (Epinephelus coioides) fed diets supplemented with various levels of manganese

This study was conducted to investigate the effect of dietary manganese (Mn) on growth, vertebrae and whole-body Mn content of juvenile grouper, and to examine the effect of dietary Mn on copper (Cu), iron (Fe), zinc (Zn), calcium (Ca), phosphorus (P) and magnesium (Mg) content of vertebrae and whole body. Seven casein-gelatin-based diets were supplemented with 0, 5, 10, 15, 20, 50 and 1000 mg kg−1 of Mn from MnSO4·H2O. Grouper with an initial weight of 12.9 ± 0.4 g were fed to satiation with one of the seven diets for 8 weeks. Growth was not significantly affected by dietary Mn supplements. Vertebrae Mn increased from 31.7 to 118.1 mg kg−1 dry weight with dietary Mn supplement increasing from 0 to 50 mg kg−1 (y = −0.0002x3 + 0.0162x2 + 1.3903x + 26.27, R2 = 0.9561, where y is the vertebrae Mn content and x is the dietary Mn content). Whole-body Mn increased from 2.5 to 7.8 mg kg−1 wet weight with dietary Mn supplement increasing from 0 to 50 mg kg−1 (y = 0.00001x3 − 0.00107x2 + 0.11054x + 2.24615, R2 = 0.9080, where y is the whole-body Mn content and x is the dietary Mn content). Dietary Mn had no significant effect on vertebrae Fe, Ca, P and Mg content, and whole-body Cu, Zn and Mg content. However, vertebrae Zn and whole body Ca, P were highest in fish fed diet supplemented with 15 mg kg−1 of Mn. Based on this, Mn supplement of 15 mg kg−1 might be the optimum when the basal diet contained 4 mg kg−1 of Mn. Fish fed diet supplemented with 1000 mg kg−1 of Mn did not show any gross abnormality or change in feeding behaviour, but Mn contents of vertebrae and whole body were as high as 695.1 mg kg−1 dry weight and 42.5 mg kg−1 wet weight, respectively. Also, whole body Fe decreased significantly when Mn supplement was up to 1000 mg kg−1.

Dietary manganese requirements of juvenile tilapia, Oreochromis niloticus × O. aureus

To quantify the dietary manganese (Mn) requirements of juvenile tilapia ( Oreochromis niloticus × O. aureus), manganese sulfate was added to the basal diet at 0, 3, 6, 10, 15, 20, 30 and 60 mg Mn/kg diet providing the actual dietary value of 2.89, 5.86, 8.57, 13.54, 18.51, 23.48, 33.37 and 63.43 mg Mn/kg diet, respectively. Each diet was fed to triplicate groups of tilapia (initial body weight 0.64 ± 0.02 g) in a recirculated fresh water rearing system for 8 weeks. The Mn concentration in rearing water was monitored during the feeding period and was 1.0 μg Mn/l. Weight gain, feed efficiency and survival of tilapia were not affected ( P > 0.05) by the dietary treatment. Hepatic, bone and muscle Mn concentrations were increased as the dietary Mn supplementation level increased. Hepatic Mn superoxide dismutase (Mn SOD) activity was higher ( P < 0.05) in fish fed diets with 5.86–33.37 mg Mn/kg diet than that in fish fed the Mn-unsupplemented control diet. Analysis by broken-line regression of hepatic Mn SOD activity and by linear regression of whole body Mn retention indicated that the adequate requirement of dietary Mn for juvenile tilapia is 7 mg Mn/kg diet.

Effects of dietary manganese on growth and tissue manganese concentrations of juvenile gibel carp,Carassius auratus gibelio

A 68-day growth trial was conducted in a flow-through system to determine the effect of dietary manganese levels on growth and tissue manganese concentration of juvenile gibel carp (Carassius auratus gibelio). Seven purified diets containing 7.21, 8.46, 9.50, 10.50, 13.03, 19.72 and 22.17 mg manganese (as manganic sulfate) per kilogram diet were fed to triplicate groups of fish (initial weight 3.21 +/- 0.01 g). The results showed that dietary manganese levels did not significantly affect feed intake of the fish. Specific growth rate, feed efficiency, total hepatic superoxide dismutase activity, carcass and skeletal manganese concentration increased significantly with increased dietary manganese(P < 0.05) while condition factor decreased significantly(P < 0.05). It was concluded that dietary requirement of manganese was 13.77 mg Mn per kilogram diet. Carcass and skeletal manganese concentration could also be used to evaluate the manganese requirement. Total hepatic superoxide dismulase activity was not a sensitive indicator for dietary requirement.

Pharmacokinetic Modeling of Manganese. I. Dose Dependencies of Uptake and Elimination

Homeostatic mechanisms controlling uptake, storage, and elimination of dietary manganese (Mn) afford protection against fluctuations in tissue manganese (Mn) levels. Homeostatic control of inhaled Mn is less well understood, but important in assessing likely risks of Mn inhalation. Two compartmental kinetic models were used to characterize the influence of Mn exposure level and route (oral, inhalation) on uptake, elimination, and transport of Mn. The models were fitted to or used to interpret data from five whole-body Mn elimination studies: one dietary Mn balance study, two biliary elimination studies, and one acute and one chronic. As dietary Mn concentrations increased from low sufficiency (1.5 ppm) to sufficiency (20 ppm), control of Mn uptake shifts from the intestine (principally) to more proportional control by both intestinal tissues and liver. Using a two-compartment distribution model, the increased elimination of 54Mn tracer doses in response to increases in dietary Mn (rats and mice) or inhaled Mn (rats) resulted from elevation in Mn elimination rate constants rather than changes in intercompartmental transfer rate constants between a central compartment and deep compartment. The pharmacokinetic (PK) analysis also indicated differential control of absorption in single gavage oral dose studies versus continuous high oral doses in the feed. The gavage study indicated increased elimination rate constants, and the chronic study showed reduced rate constants for absorption. These dose dependencies in uptake and elimination are necessary inputs for comprehensive PK models guiding human health risk assessments with Mn.

Exposure to low dietary copper or low copper coupled with high dietary manganese for one year does not alter brain prion protein characteristics in the mature cow1,2

It is now widely accepted that abnormal prion proteins are the likely causative agent in bovine spongiform encephalopathy. Cellular prion proteins (PrP(c)) bind Cu, which appears to be required to maintain functional characteristics of the protein. The replacement of Cu on PrP(c) with Mn has resulted in loss of function and increased protease resistance. Twelve mature cows were used to determine the effects of Cu deficiency, alone and coupled with high dietary Mn, on brain Cu and Mn concentrations and on PrP(c) functional characteristics. Copper-adequate cows were randomly assigned to treatments: 1) control (adequate in Cu and Mn), 2) Cu-deficient (-Cu), and 3) Cu-deficient plus high dietary Mn (-Cu+Mn). Cows assigned to treatments -Cu and -Cu+Mn received no supplemental Cu and were supplemented with Mo to further induce Cu deficiency. After 360 d, Cu-deficient cows (-Cu and -Cu+Mn) tended to have lesser concentrations of Cu (P = 0.09) in the obex region of the brain stem. Brain Mn tended (P = 0.09) to be greater in -Cu+Mn cattle compared with -Cu cattle. Western blots revealed that PrP(c) relative optical densities, proteinase K degradability, elution profiles, molecular weights, and glycoform distributions were not different among treatments. The concentration of PrP(c), as determined by ELISA, was similar across treatment groups. Brain tissue (obex) Mn superoxide dismutase activity was greatest (P = 0.04) in cattle receiving -Cu+Mn, whereas immunopurified PrP(c) had similar superoxide dismutase-like activities among treatments. Immunopurified PrP(c) had similar Cu concentrations across treatments, whereas Mn was undetectable. We concluded that Cu deficiency, coupled with excessive Mn intake, in the bovine may decrease brain Cu and increase brain Mn. Copper deficiency, alone or coupled with high dietary Mn, did not cause detectable alterations in PrP(c) functional characteristics.

Interactive Effects of Zinc, Copper and Manganese in Diets for Broilers

An experiment was conducted to determine the interactive effects of Zn, Cu and Mn addition to diets of 0 to 14-d old broilers on growth performance, bone breaking strength, bone ash percentage and tissue mineral concentrations. Two levels of Zn (0 or 75 ppm, as Zn sulfate), 2 levels of Mn (0 or 100 ppm, as Mn sulfate) and 2 levels of Cu (0 or 7 ppm, as Cu sulfate) were supplemented to corn-soybean meal diets in a 2×2×2 factorial arrangement. Each treatment had 6 replications with 5 chicks each and the initial and final BW were 46 and 382 g. Daily gain, daily feed intake, gain:feed, bone breaking strength and bone and pancreatic Zn concentrations were increased (p<0.05) in chicks fed diets with supplemental Zn. Bone, liver and pancreatic Mn levels were increased (p<0.01) in chicks fed diets with supplemental Mn. Bone breaking strength was increased when Zn was added to the diets with or without Cu addition, but the increase was greater in chicks fed the diets without Cu addition (Zn×Cu, p<0.05). Bone ash percentage was increased in chicks fed the diets with Zn, Mn, or Cu addition but the increase was not additive (Zn×Mn×Cu, p<0.03). Liver Cu level was increased (p<0.01) in chicks fed diets with Cu addition. Bone and liver Cu levels were decreased (p<0.05) in chicks fed diets with Zn addition. Bone and pancreas Fe levels were decreased (p<0.05) in chicks fed diets with added Zn. Bone Zn level was decreased (p<0.03) in chicks fed diets with added Cu. Liver and pancreatic Mn levels were increased (p<0.05) in chicks fed diets with added Zn. This study indicates that Zn addition is necessary for normal growth and bone strength of chicks and that Zn addition had negative effects on tissue Cu and Fe levels and a positive effect on tissue Mn levels.

Historical copper and manganese levels in cattle feeds in Bavaria, Germany

Purpose. It has been repeatedly speculated that a deficiency in copper (Cu) or an excessive provision with dietary manganese (Mn) could play a role in spongiform encephalopathies [bovine (BSE) and others]. Therefore, commercial cattle feeds were screened for their content of these minerals.Design. The historical development of the levels of Cu and Mn in Bavarian cattle feeds was evaluated and the levels compared with feeding recommendations.Materials and methods. We report declared Cu and Mn contents from proprietary cattle feeds sold in Bavaria between 1978 and 1998.Results. Mn contents in ruminant feeds were generally high, and there was a trend of increasing Mn levels in ruminant feeds between 1980 and 1990, which was in synchrony with an increase in internationally recommended Mn levels for ruminants. Recently, the recommendations have been modified again to lower levels.Conclusion. Although no causative connection to the occurrence of BSE can be made, the practice of high Mn supplementation of propri...

Influence of dietary inclusion level of manganese on pork quality during retail display

Boneless pork loins ( n = 112) were used to test the influence of dietary manganese (Mn) inclusion level on pork quality traits during retail display. Crossbred barrows and gilts were fed diets formulated with 0, 20, 40, 80, 160, or 320 ppm Mn from Availa ®Mn (AvMn; a Mn–amino acid complex) from 23.8 to 106.8 kg live weight. At approximately 48 h postmortem, boneless pork loins were fabricated into longissimus thoracis et lumborum (LM) chops, which were subsequently placed in open-topped, coffin-chest display cases (2.6 °C) under continuous warm-white, fluorescent lighting (1600 lx) for 7 days. Dietary Mn level had no effect on LM pH ( P = 0.47), purge volume ( P = 0.60) and loss ( P = 0.53), or moisture loss ( P = 0.95) during retail display. Chops from pigs fed 80 ppm Mn received higher ( P < 0.05) American and Japanese color scores than pigs fed 0 and 40 ppm Mn. Even though the LM from pigs fed 80, 160, and 320 ppm Mn tended to be darker (lower L ∗ values; P = 0.07) than chops from pigs fed 40 ppm Mn, a ∗ (redness) and b ∗ (yellowness) values, as well as hue angle and chroma, were not ( P ⩾ 0.19) affected by dietary Mn. On days 0 and 1, the reflectance ratio of 630 nm/580 nm was similar ( P > 0.05) among dietary Mn supplementation levels; yet, by day 4 of retail display, chops from pigs fed 80 ppm Mn had higher ( P < 0.05) reflectance ratios than chops from pigs fed 0, 20, 40, and 160 ppm, whereas LM chops from pigs fed 40 ppm Mn had lower ( P < 0.05) reflectance ratios than all other dietary treatments on day 7 (Mn supplementation level × display day; P = 0.04). Although TBARS were greater ( P < 0.001) on day 7 than 0 of retail display, TBARS values did not ( P = 0.43) differ among dietary Mn levels. Results indicate that supplementing swine diets with 80 ppm Mn may improve pork color during retail display without increasing the likelihood of lipid oxidation.

Dietary manganese affects the concentration, composition and sulfation pattern of heparan sulfate glycosaminoglycans in Sprague-Dawley rat aorta

We examined the effect of dietary Mn on the composition and structure of heparan sulfate (HS) glycosaminoglycans (GAGs) of rat aorta. Animals were randomly assigned to either a Mn deficient (MnD), adequate (MnA) or supplemented (MnS) diet (Mn<1, 10-15 and 45-50 ppm, respectively). After 15 weeks, aortic tissue GAGs were isolated with papain digestion, alkaline borohydride treatment and anion-exchange chromatography. Cellulose acetate electrophoresis and treatment of the fractions with specific lyases revealed the presence of three GAG populations, i.e. hyaluronan (HA), heparan sulfate (HS) and galactosaminoglycans (GalAGs). Disaccharide composition of the HS fractions was determined by HPCE following treatment with heparin lyases I, II and III. In MnS aortas we observed increased concentration of total GalAGs and decreased concentration of HS and HA, when compared to MnA aortas. Aortas from MnD and MnA rats appeared to have similar distribution of individual GAGs. Heparan sulfate chains of MnS aortas contained higher (41%) concentration of non-sulfated units compared to MnA ones. Variable amounts of trisulfated and disulfated units were found only in MnD and MnA groups but not in MnS. Our results demonstrate that HS biosynthesis in the rat aorta undergoes marked structural modifications that depend upon dietary Mn intake. The reduced expression and undersulfation of HSPGs with Mn supplementation might indicate a reduced ability of vascular cells to interact with biologically active molecules such as growth factors. Alterations in cell-membrane binding ability to a variety of extracellular ligands might affect signal-transduction pathways and arterial functional properties.

Copper deficiency alone or in the presence of high dietary manganese does not affect brain prion protein concentration or functional characteristics in the bovine

Copper deficiency alone or in the presence of high dietary manganese does not affect brain prion protein concentration or functional characteristics in the bovine