Effect Of Manganese Deficiency Research Articles

Effects of manganese deficiency on the microstructure of proximal tibia and OPG/RANKL gene expression in chicks.

Manganese (Mn) deficiency can result in perosis in chicks, but the mechanism of Mn deficiency on tibia development remains poorly understood. Ninety one-day-old Arbor Acres male broiler chickens administered with control diet (60 mg Mn/kg) and Mn-deficient diets (40 mg Mn/kg, 8.7 mg Mn/kg) to investigate the effects of Mn deficiency on morphology of tibia and related signal transduction pathways in broiler chickens. At the age of 42 days, the bone trabecula, damaged osteoblasts and OPG/RANKL mRNA expression levels were investigated by histological assessment, electron microscopic examination and real-time quantitative PCR analysis, respectively. Results of histological observations showed that decreased trabecular thickness, trabecular number and trabecular bone area (%) together with increased trabecular bone separation were involved in perosis induced by Mn deficiency. The most striking ultrastructural modifications involved disruption of nuclear membrane and mitochondria outer membrane, loss of mitochondrion cristae and alteration in endoplasmic reticulum in osteoblasts of the Mn-deficient groups. Likewise, Mn deficiency results in a significant (P < 0.05) decrease in the relative mRNA expression levels of OPG and RANKL with a significantly higher RANKL/OPG ratio (P < 0.05). In conclusion, Mn deficiency can affect the development of tibia in broiler chickens, leading to metaphyseal osteoporosis which may be due to decreased OPG/RANKL mRNA expression.

Effects of manganese deficiency on chondrocyte development in tibia growth plate of Arbor Acres chicks

The aim of this study was to investigate the effects of manganese (Mn) deficiency on chondrocyte development in tibia growth plate. Ninety 1-day-old Arbor Acres chicks were randomly divided into three groups and fed on control diet (60mg Mn/kg diet) and manganese deficient diets (40mg Mn/kg diet, manganese deficiency group I; 8.7mg Mn/kg diet, manganese deficiency group II), respectively. The width of the proliferative zone of growth plate was measured by the microscope graticule. Chondrocyte apoptosis was estimated by TUNEL staining. Gene expression of p21 and Bcl-2, and expression of related proteins were analyzed by quantitative real time reverse transcription polymerase chain reaction and immunohistochemistry, respectively. Compared with the control group, manganese deficiency significantly decreased the proliferative zone width and Bcl-2 mRNA expression level, while significantly increased the apoptotic rates and the expression level of p21 gene in chondrocytes. The results indicate that manganese deficiency had a negative effect on chondrocyte development, which was mediated by the inhibition of chondrocyte proliferation and promotion of chondrocyte apoptosis.

Effects of manganese deficiency on serum hormones and biochemical markers of bone metabolism in chicks

In order to investigate the effect of manganese (Mn) deficiency on bone metabolism in chicks, ninety 1-day-old male Arbor Acre chicks were randomly divided into 3 groups and each group were given a diet having a different concentration of Mn (60 mg kg(-1), control group; 40 mg kg(-1), Mn-deficient group I; 8.7 mg kg(-1), Mn-deficient group II). The serum was collected at 42 days old. Tests were performed to evaluate the changes in the levels of PTH, CT, ALP, TrACP, HOP TNF-alpha, OC, Mn and Ca in the serum of the chicks and the results showed that the levels of CT, ALP, TrACP, HOP, and Mn decreased markedly (P < 0.05), while PTH, Ca, and TNF-alpha increased markedly (P < 0.05) due to manganese deficiency in the diet, which indicates that Mn deficiency results in disorder of bone regulatory hormones and enzymes of bone metabolism in the serum.

Effects of Manganese Deficiency on Growth and Contents of Active Constituents of Glycyrrhiza uralensis Fisch.

To investigate effects of manganese (Mn) deficiency (0 μM L–1) on concentrations of chlorophyll, superoxide dismutase (SOD) activity, biomass, and accumulations of active constituents in Glycyrrhiza uralensis Fisch., seedlings of 1-year-old G. uralensis were grown in a nutrient solution for 60 days. In this experiment, three concentrations of Mn were set up: 0 (–Mn), 7 μM L–1, and 14 μM L–1 Mn. The results showed that –Mn decreased the concentration of chlorophyll a with no significant differences in concentrations of chlorophyll b, total chlorophyll a + b, carotenoids, and chlorophyll a/b ratio. On days 45 and 60, SOD activity significantly decreased. However, dry weight of roots under –Mn showed no significant difference during the whole experiment. The accumulations of glycyrrhizic acid and liquiritin were significantly inhibited by Mn deficiency at different times. Thus results indicated that Mn deficiency could affect growth and contents of its secondary metabolites of G. uralensis.

Effects of Manganese Deficiency and Added Cerium on Photochemical Efficiency of Maize Chloroplasts

The mechanism of the fact that manganese deprivation and cerium addition affect the photochemical efficiency of plants is unclear. In this study, we investigated the improvement by cerium of the damage of the photochemical function of maize chloroplasts under manganese-deprived stress. Chlorophyll fluorescence induction measurements showed that the ratio of variable to maximum fluorescence (Fv/Fm) underwent great decreases under manganese deficiency, which was attributed to the reduction of intrinsic quantum efficiency of the photosystem II units. The electron flow between the two photosystems, activities of Mg(2+)-ATPase and Ca(2+)-ATPase, and rate of photophosphorylation on the thylakoid membrane of maize chloroplasts were reduced significantly by exposure to manganese deprivation. Furthermore, the inhibition of cyclic photophosphorylation was more severe than non-cyclic photophosphorylation under manganese deficiency. However, added cerium could relieve the inhibition of the photochemical reaction caused by manganese deprivation in maize chloroplasts. It implied that manganese deprivation could disturb photochemical reaction of chloroplasts strongly, which could be improved by cerium addition.

Effects of Manganese Deficiency on Spectral Characteristics and Oxygen Evolution in Maize Chloroplasts

The effects of Mn(2+) deficiency on light absorption, transmission, and oxygen evolution of maize chloroplasts were investigated by spectral methods. Several effects of Mn(2+) deficiency were observed: (1) the skeleton of pigment protein complexes and oxygen-evolving center and the combination between pigment and protein were damaged; (2) the light absorption of chloroplasts was obviously decreased; (3) the energy transfer among amino acids within PS II protein-pigment complex and decreased energy transport from tyrosine residue to chlorophyll a and from chlorophyll b and carotenoid to chlorophyll a were inhibited; (4) the oxygen-evolving of chloroplast was significantly inhibited. However, Mn(2+) addition decreased the damage of light absorption, transmission, and oxygen evolution of maize chloroplasts caused by Mn(2+) deficiency.

Manganese and birth outcome

Manganese is an essential mineral nutrient needed for proper fetal development and other important aspects of metabolism. However, manganese excess can have a potent neurotoxicity effect, especially in infants. Little is known about the effects of manganese deficiency or excess on the developing human fetus. The findings of two recent studies indicate that lower maternal blood manganese is associated with fetal intrauterine growth retardation (IUGR) and lower birth weight. In light of the importance of IUGR and birth weight on neonatal morbidity and mortality, additional basic studies of maternal and fetal manganese physiology are needed, as well as more epidemiologic studies in different populations of the association of manganese exposure and birth outcome.

MANGANESE DEFICIENCY AFFECTS HDL 1 AND HDL 2 COMPOSITION IN RATS

The effects of manganese deficiency on high density lipoprotein subclass (HDL 1 and HDL 2) composition was assessed. Weanling male Sprague-Dawley rats were fed a manganese-deficient (0.48 mg/kg) or a manganese-adequate (90 mg/kg) diet. After 15 weeks, mean body weights, liver manganese, plasma cholesterol and protein, and HDL 2 cholesterol and protein were significantly lower in the deficient group of rats. Plasma and HDL 2 phospholipids and triglycerides and HDL 1 protein and lipids were not significantly affected by manganese deficiency. The percentage of apolipoprotein A-I in HDL 1 was significantly greater (P < 0.05) in manganese-deficient rats, while the HDL 2 apolipoprotein composition was the same in both groups. The apparent molecular weights of apolipoproteins were not affected by manganese deficiency in either HDL subclass. © 1997 Elsevier Science Inc.

Effects of manganese deficiency on soluble apoplastic peroxidase activities and lignin content in needles of Norway spruce (Picea abies).

Apoplastic peroxidase activities were investigated in manganese-deficient and manganese-sufficient needles of field-grown Norway spruce trees (Picea abies L.). In Mn-sufficient needles, two sets of peroxidases, one with an alkaline pI >/= 9 and another with an acidic pI </= 3, were identified using guaiacol or coniferylalcohol as substrates for activity staining after isoelectric focusing in a pH gradient from 3 to 9. The acidic peroxidases were capable of Mn-dependent NADH oxidation and H(2)O(2) formation. Syringaldazine peroxidase activity was not found in apoplastic extracts, but was present in whole-needle extracts. Manganese deficiency did not affect the activity or the isoelectric focusing pattern (pH 3 to 9) of the apoplastic peroxidases. Soluble peroxidase activities from whole-needle extracts were significantly higher in Mn-deficient than in Mn-sufficient needles with all substrates tested. Mn-deficient needles contained slightly less cell wall material than Mn-sufficient needles, but the lignin content was similar. Neither apoplastic peroxidase activity nor lignification was affected by Mn deficiency, suggesting that apoplastic peroxidases are regulated independently from symplastic peroxidases.

Effect of manganese deficiency on seed yield of soybean cultivars

Abstract Manganese (Mn) deficiency is a problem in soybeans grown on high pH soils, which to date can only be controlled by chemical fertilizers. In view of the success of genetic resistance in reducing yield losses associated with iron (Fe) deficiency chlorosis, a one year study was initiated to determine whether genetic resistance could be used to control Mn deficiency related yield losses. For this study, twenty soybean genotypes ranging from Group I maturity to Group III maturity were planted at five locations which had previously exhibited symptoms of Mn deficiency. Individual plots were rated for Mn‐deficiency symptoms on a 1–5 scale (1 = no yellowing to 5 = severe yellowing with some necrosis) at the Rl growth stage and plants in the center rows were harvested for yield. The mean Mn‐deficiency rating was 2.8 with a range from 1.8 for NKS 23–03 and P9181 to a 3.9 for A3205. The mean yield was 3059.3 kg/ha with a range from 3670.6 for A3205 to 2567.5 kg/ha for Chapman. The correlation between Mn‐defi...

Effects of manganese deficiency on the pattern of tillering and development of barley ( Hordeum vulgare c.v. Galleon)

The effects severe, moderate or slight manganese (Mn) deficiency on tillering and development of Galleon barley were examined in field and growth-cabinet experiments. Manganese deficiency delayed maturity in both field and growth-cabinet experiments. In the field, Mn-deficient plants were still tillering when the plants in plots receiving Mn fertilizer had ceased tillering and their stems were elongating. In growth-cabinet experiments, plants with moderate or severe Mn deficiency did not reach the stem-elongation stage of development, and continued to tiller until they died. The pattern of tillering was altered by Mn deficiency. Moderate deficiency decreased the rate of tiller emergence without affecting the rate of leaf emergence on the main culm. Therefore, at early tillering, deficient plants had fewer tillers. Manganese deficiency extended the period of tillering, and after control plants ceased tillering and their stems began elongating, deficient plants continued to tiller, eventually reaching the number of tillers of the control plants. Moderate and severe Mn deficiency prevented stem elongation and reproduction and plants continued to tiller. Eventually, moderate Mn-deficient plants had produced significantly more tillers than control plants or slightly deficient plants. Severe Mn deficiency resulted in death of plants before any increased tiller production. Manganese status affected apical development. When moderately Mn-deficient plants had one tiller, the main stem apex was at the double-ridge stage, compared with four tillers on the control plants which were at the late double-ridge or triple-mound stage. When the number of tillers of the Mn-deficient plants had increased to that of the control plants, the apex of the main stem was dead (shrivelled and dry) in the deficient plants, while that of the controls was at the awn primordium stage. There was no difference in grain-yield of slightly Mn-deficient and control plants, even though early tillering had been depressed and shoot biomass at maturity was lower in the former. Although moderately Mn-deficient plants produced greater number of tillers than control plants, these tillers did not produce any heads.

Effect of Manganese Deficiency on Insulin Binding, Glucose Transport and Metabolism in Rat Adipocytes

The effect of manganese deficiency on insulin binding, glucose transport and metabolism in isolated adipose cells from Sprague-Dawley rats was investigated. Offspring from Mn-sufficient female rats fed 45 micrograms Mn/g diet (control) and from Mn-deficient (Mn-) female rats fed 1 microgram Mn/g diet were used in these studies. Both basal and insulin-stimulated 3-O-methylglucose transport in isolated adipose cells was significantly lower in Mn- rats, averaging 40% and 50% of control values, respectively. Kinetic analysis of glucose transport demonstrated a lower maximal transport velocity (Vmax) for glucose in adipose cells from Mn- rats compared to controls. No differences in the Km for glucose uptake were observed between the two groups. Insulin-stimulated glucose oxidation to CO2 and conversion to triglycerides was lower in isolated adipose cells from Mn- rats compared to controls. Mn- animals had fewer insulin receptors per cell compared to controls, although no differences in insulin receptor affinity were observed between the two groups. These data suggest that Mn deficiency affects glucose transport and metabolism in the adipose cell. The apparent defect lies distal to the insulin receptor and probably reflects a decreased number of glucose transporters in adipose tissue of Mn- rats.

Net fluxes of mineral nutrients, water, and carbohydrate influenced by manganese in root and shoot ofCucumis sativusL.1

Abstract An experiment was conducted with cucumber (Cueumis sativus L., cv. Sumter) plants in the vegetative phase of growth to determine effects of manganese deficiency (0.2 μM Mn) and toxicity (182 μM Mn) on fluxes of several mineral nutrients, water, and carbohydrate in the root and shoot, beginning 43 d after germination. Plants were sampled every three days from 34 to 58 d after germination. First and second derivatives of regression equations were used to estimate fluxes and study source/sink phenomena of dry weight (DW), fresh weight (FW), H2O, Cu, Fe, Mn, Zn, N, P, and K in root and shoot tissues. With Mn sufficiency (1.8 μM Mn), both root and shoot acted as sinks for of each of the 10 dependent variables through 58 d. In contrast, Mn deficiency caused net loss of K and N from the root beginning at 53 and 56 d, respectively, and net loss of P and Fe from the shoot beginning at 57 and 58 d, respectively. With Mn toxicity, net loss of Cu, N, and K from the root began at 46, 46, and 51 d, respectivel...

Effects of Manganese Deficiency and Dietary Composition on Rat Pancreatic Enzyme Content

Recent studies show that manganese (Mn) deficiency increases pancreatic amylase content. Pancreatic adaptation to dietary composition also alters enzyme content. The present study investigated whether Mn deficiency alters pancreatic adaptation to diet. Weanling rats that were fed for 6 wk a high carbohydrate (HC) diet with <1 mg Mn/kg diet (Mn deficient) or 40 mg Mn/kg diet (control) were divided into three control and deficient dietary subgroups: 1) HC, 2) high protein (HP) or 3) high fat (HF). Rats were then fed these diets for 10 d. Body weights and food consumption were comparable among the groups. Pancreatic and hepatic Mn contents were significantly lower in Mn-deficient rats than in respective controls. Digestive enzymes adapted to diet in both control and Mn-deficient rats with the greatest amylase, lipase and trypsin activities in HC, HF and HP rats, respectively. Mn deficiency resulted in significantly greater amylase activity in HC and HP groups and lipase activity in only the HF group than in respective controls. These data suggest that Mn participates in the regulation of pancreatic amylase content and in the adaptive response of pancreatic lipase to dietary fat.

Effects of manganese deficiency on pyruvate carboxylase and phosphoenolpyruvate carboxykinase activity and carbohydrate homeostasis in adult rats

The activities of two liver gluconeogenic enzymes, pyruvate carboxylase (PC) and phosphoenolpyruvate carboxykinase (PEPCK), as well as liver glycogen and plasma glucose, insulin, and glucagon were measured in first- and second-generation, manganese-sufficient (control) and manganese-deficient (Mn-) adult rats. Pyruvate carboxylase activity of first generation male Mn- rats was higher than that of controls in both the fed and fasted states. In contrast, PC activity in second generation male Mn- rats was lower than control levels. In female rats, PC activity was lower than controls in both fed, first- and second-generation Mn- rats; in the fasted state, PC activity was either the same or higher than controls. Phosphoenolpyruvate carboxykinase activity was lower in male first generation Mn- rats than in controls, but there was no difference in PEPCK activity in second-generation animals. Phosphoenolpyruvate carboxylase activity was lower in both fed and fasted Mn- female rats than in controls. Plasma insulin levels were lower in the deficient rats than in controls, whereas plasma glucagon levels were similar. Manganese-deficient rats had higher concentrations of liver glycogen than their controls. These findings provide further evidence that manganese affects carbohydrate homeostasis; however, the response of the animal to manganese deficiency depends on the parameter studied and the timing of the deficiency.

Pyruvate Carboxylase and Phosphoenolpyruvate Carboxykinase Activity in Developing Rats: Effect of Manganese Deficiency

The activities of two liver gluconeogenic enzymes, pyruvate carboxylase (PC) and phosphoenolpyruvate carboxykinase (PEPCK) as well as plasma glucose were measured in manganese-sufficient and manganese-deficient rats from birth to 30 d of age. Initial (d 0) PC activity was similar in the two groups. PC activity increased 1.5-fold in control pups and 2.4-fold in manganese-deficient pups from d 0 to 3 postnatally. PEPCK activity increased 1.5-fold in control pups and 2.2-fold in manganese-deficient pups from d 0 to 3. By d 8, the activity of PEPCK in manganese-deficient pups was 60% of control levels. Compared to control pups, plasma glucose concentration was lower in manganese-deficient pups on d 1 and 2, coinciding with a period of high neonatal mortality. These findings suggest that glucose homeostasis in the newborn may be compromised by manganese deficiency and may support the concept that changes in cellular manganese concentration may be important in the regulation of carbohydrate metabolism.

Effect of manganese deficiency on plasma-membrane lipid composition and glucose uptake in Aspergillus niger

Plasma membranes were isolated by means of the concanavalin A technique from protoplasts of manganese deficient (< 10−8 M Mn2+) and sufficient (10−5 M Mn2+) grown mycelium. The membranes differed with respect to their quantitative contents of fatty acids, sterols and phospholipids. These changes did not influence the glucose transport system, as shown by kinetic investigations using intact mycelia.

The effect of manganese deficiency and cereal cyst nematode infection on the growth of barley

Two factorial pot experiments, each with four rates of soil-applied manganese (Mn), four levels of cereal cyst nematodes (CCN) and four replicates, were conducted under controlled environmental conditions to investigate the interaction of these factors on growth of barley. The experiments were harvested sequentially to count numbers of nematodes at two developmental stages. Development of the nematodes was independent of the Mn status of the host, indicating no effect of Mn on host resistance. In the absence of CCN, decreased Mn had a small effect on vegetative growth, not significantly decreasing dry weight of tops but tolerance at the higher densities of CCN was considerably reduced at low Mn supply, both vegetative growth and grain yield being depressed. Increasing CCN density exerted little effect on the growth of Mn sufficient hosts. Two field surveys supported conclusions from the pot experiments in that increasing nematode densities were correlated with decreasing plant size only at the site where plants were low in Mn. An implication for the field is that crops infected with the nematode and also low in Mn may yield less than expected because the two factors interact to reduce growth and retard development.

The effects of manganese deficiency during prenatal and postnatal development on mitochondrial structure and function in the rat

The influence of manganese deficiency on liver trace element concentration, MnSOD activity, and mitochondrial structure and function during postnatal development was determined in rats. In both normal and manganese-deficient animals, liver manganese concentration increased with time, but in deficient rats liver manganese was lower than in controls at all ages measured. At 9 mo of age, liver manganese concentration in the deficient rats was only 20% that of controls. The developmental pattern observed for MnSOD paralleled that of liver manganese concentration in normal and deficient rats; it was lower than in controls on days 20 and 60. However, at 9 mo of age, MnSOD levels were similar in the two groups. Although there were no differences at 9 mo of age in MnSOD activity between the groups, manganese-deficient rats showed mitochondrial abnormalities in liver. Despite mitochondrial abnormalities, however, oxygen uptake and P/O ratios were normal. We suggest that the mitochondrial damage apparent at 9 mo of age is, at least in part, the result of lower than normal MnSOD activity occurring earlier. The functional significance of the abnormalities remains to be established.

Effect of Manganese Deficiency on Insulin Secretion and Carbohydrate Homeostasis in Rats

The effects of manganese (Mn) deficiency on carbohydrate metabolism in the Sprague-Dawley rat were investigated. Oral glucose tolerance tests were performed on offspring from Mn-sufficient female rats fed 45 µg Mn per gram diet (C-C), offspring from Mn-deficient female rats fed 1 µg Mn per gram diet (D1-D1) and rats not exposed to Mn deficiency in utero but fed D1 diet from weaning to maturity (D1). Mn-deficient rats, D1 and D1-D1, had significantly lower concentrations of Mn in liver, kidney, heart and pancreas than controls. D1-D1 rats responded with a diabetic type of glucose tolerance curve when given oral glucose. Insulin levels of D1-D1 rats were not commensurate with their high glucose levels. Measurements made by using an isolated perfused-pancreas preparation indicate that insulin output due to release of stored hormone was 76% of control levels in D1-D1 rats. This suggests either lower insulin stores or impaired release of insulin in D1-D1 rats. Second phase insulin release was also significantly lower in D1-D1 rats than in controls. Pancreatic insulin content was 63% of control levels in D1-D1 rats, further supporting the idea of lower insulin stores in Mn-deficient rats. No differences in plasma glucose levels were observed between D1 rats and controls after an oral-glucose load. These findings indicate that dietary Mn deficiency can result in impaired insulin secretion producing impaired carbohydrate metabolism; however, the timing of the deficiency may be a critical factor in the expression of this abnormality.