scholarly journals Changes in bioavailability and tissue distribution of zinc caused by magnesium deficiency in rats

1994 ◽  
Vol 72 (2) ◽  
pp. 315-323 ◽  
Author(s):  
Elena Planells ◽  
Pilar Aranda ◽  
Ana Lerma ◽  
Juan Llopis
Keyword(s):  
Skeletal Muscle ◽  
Tissue Distribution ◽  
Intestinal Absorption ◽  
Whole Blood ◽  
Wistar Rats ◽  
Magnesium Deficiency ◽  
Dry Weight ◽  
Deficient Diet ◽  
Mg Deficiency ◽  
Zn Concentration

The effect of a Mg-deficient diet (200 mg Mg/kg feed) on the bioavailability of dietary Zn and the concentration of this cation in plasma, whole blood, skeletal muscle, kidney, heart and brain of Wistar rats was studied after 7, 35, 42, 49, 56, 63 and 70 d. Mg deficiency significantly decreased Zn in whole blood on day 42 of the experiment, but there was no significant change in plasma Zn throughout the 70 d study period. The Mg-deficient diet significantly increased intestinal absorption of Zn, Zn balance, and Zn concentration in femur and kidney, but decreased Zn concentration in the heart despite the increase in dry weight of this organ. No change was found in brain Zn concentration.

Magnesium deficiency protects against Babesia hylomysci and mice become resistant to rechallenge with the parasite regardless of diet fed

Parasitology ◽  
1994 ◽  
Vol 108 (3) ◽  
pp. 245-248 ◽  
Author(s):  
P. Maurois ◽  
P.H. Delcourt ◽  
E. Gueux ◽  
Y. Rayssiguier
Keyword(s):  
Protective Effect ◽  
Magnesium Deficiency ◽  
Control Diet ◽  
Oxidant Stress ◽  
Membrane Properties ◽  
Deficient Diet ◽  
Mg Deficiency ◽  
Deficient Mice

SUMMARYMice were fed diets containing 960 mg (control), 100 mg (moderately Mg deficient) and 30 mg (severely Mg deficient) of Mg/kg. After 20 days, mice were inoculated with Babesia hylomysci (from Dr Wery, Anvers, Belgium). Significant increases in RBC Mg levels were observed following infection. All the control and moderately deficient mice died from infection, whereas the severely Mg-deficient diet protected mice against infection, as shown by a decrease in parasitaemia and mortality. The decrease in RBC Mg, modifications in membrane properties and increased oxidant stress are possible explanations for the protective effect of severe Mg deficiency. When mice were maintained for 2 months after inoculation on a severely Mg-deficient diet and were then switched to a control diet, all survived and had low parasitaemias. After 1 month, these mice were rechallenged with B. hylomysci and 89% survived.

scholarly journals Effects of Nitrogen, Phosphorus, Potassium, Calcium, or Magnesium Deficiency on Growth and Photosynthesis of Eustoma

HortScience ◽  
2018 ◽  
Vol 53 (6) ◽  
pp. 795-798 ◽  
Author(s):  
Chang-Tsern Chen ◽  
Ching-Lung Lee ◽  
Der-Ming Yeh
Keyword(s):  
Magnesium Deficiency ◽  
Weight Ratio ◽  
Carbon Dioxide Concentration ◽  
Dry Weight ◽  
Photosynthetic Parameters ◽  
Eustoma Grandiflorum ◽  
Node Number ◽  
Mg Deficiency ◽  
Root Dry Weight ◽  
Shoot Dry Weight

Growth and photosynthetic parameters were measured in Eustoma grandiflorum (Raf.) Shinn. ‘Umihonoka’ grown hydroponically under nitrogen (N), phosphorus (P), potassium (K), calcium (Ca), or magnesium (Mg) deficiency in 1/2 strength of modified Johnson’s solution. Plant height, node number, and leaf area were all reduced under N, P, K, and Ca deficiencies but not under Mg deficiency as compared with plants grown in the complete nutrient solution. Shoot and root dry weight were reduced in the N-, P-, K-, and Ca-deficient treatments, whereas root but not shoot dry weight was lowered by Mg-deficient treatment. Shoot-to-root dry weight ratio decreased under N and P deficiencies, increased under K and Mg deficiency, but was not altered under Ca deficiency. Decreased net photosynthetic rate (Pn) of N-, P-, and K-deficient leaves was all related to lower stomatal conductance (gS), whereas N-deficient leaves also accompanied by a higher intercellular carbon dioxide concentration (Ci). The Mg-deficient treatment did not alter chlorophyll fluorescence Fv/Fm, maximal fluorescence (Fm), or minimal fluorescence (Fo). Decreased Fv/Fm of N-, P-, K-, and Ca-deficient leaves was all related to lower Fm, whereas N- and P-deficient leaves also accompanied by lower Fo. A key was developed for the identification of N, P, K, Ca, and Mg deficiency symptoms.

scholarly journals Magnesium and calcium deficiencies additively increase zinc concentrations and metallothionein expression in the rat liver

2012 ◽  
Vol 109 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Megumi Kotani ◽  
Ki Hyun Kim ◽  
Natsumi Ishizaki ◽  
Masayuki Funaba ◽  
Tohru Matsui
Keyword(s):  
Rat Liver ◽  
Control Diet ◽  
Mrna Level ◽  
Male Rats ◽  
Mrna Levels ◽  
Deficient Diet ◽  
Mg Deficiency ◽  
Ca Deficiency ◽  
Zn Concentration ◽  
Dietary Treatments

Mg deficiency increases the concentration of Zn in the liver. We investigated the effect of Mg deficiency on the expression of Zn-regulating factors such as Zn transporters and metallothionein (MT) in the rat liver. Because Ca deficiency alleviates some of the effects of Mg deficiency, we also investigated the interactions associated with Ca and Mg deficiencies. Growing male rats were given a control diet, a Mg-deficient diet, a Ca-deficient diet and a Mg- and Ca-deficient diet for 3 weeks. Mg and Ca deficiencies additively increased the mRNA levels of MT-1 and MT-2, the MT protein concentration and the concentration of Zn in the liver. The hepatic mRNA level of Zip14 increased with Mg deficiency but not with Ca deficiency. The dietary treatments did not affect the mRNA levels of other Zn transporters such as Zip1, Zip5, ZnT1, ZnT5 and ZnT6 in the liver. Ca deficiency was found to decrease the amount of femoral Zn and increase serum Zn concentration. This did not occur in the case of Mg deficiency. These results suggest that Mg deficiency enhances hepatic Zn uptake by the up-regulation of Zip14 expression and increases hepatic Zn concentration, leading to the enhancement of MT expression. Ca deficiency causes a transfer of Zn from the bone to the liver, which increases hepatic Zn concentration and, in turn, up-regulates the expression of MT. Because Mg and Ca deficiencies increase hepatic Zn concentration and increase MT expression by different mechanisms, their effects are additive.

scholarly journals The effect of iron supplements on pregnancy in rats given a low-zinc diet

1984 ◽  
Vol 52 (1) ◽  
pp. 79-86 ◽  
Author(s):  
Susan J. Fairweather-Talt ◽  
Viv Payne ◽  
Christine M. Willians
Keyword(s):  
Fetal Growth ◽  
Normal Level ◽  
Dna Content ◽  
Wistar Rats ◽  
Dry Weight ◽  
Iron Supplements ◽  
Zn Concentration ◽  
Female Wistar Rats ◽  
Wet Weight ◽  
The Mean

1. Female Wistar rats were given an adequate-zinc (60 μg/g) or low-Zn (7 μg/g) diet for a minimum of 2 weeks and then mated. They were then either continued on the same diets (+Zn –Fe or –Zn –Fe) or given similar diets supplemented with four times the normal level of iron (+Zn + Fe or –Zn + Fe). The day before parturition they were killed and the fetuses removed and analysed.2. There were no differences in numbers of fetuses or the number of resorption sites. In the absence of Fe supplementation, the mean fetal wet weight was significantly less (P < 0.05) in the low-Zn group but there was no effect of Zn in the two Fe-supplemented groups. The addition of Fe significantly decreased (P < 0.05) the mean fetal wet weight in the adequate-Zn groups but had no effect in the low-Zn groups. There were no differences in fetal dry weight, fat, protein or DNA content. Both Fe-supplemented groups produced fetuses of higher Fe concentration (P < 0.01), and mothers with higher bone Fe-concentration (P < 0.01) compared with the non-supplemented groups. The low-Zn groups produced fetuses of lower Zn concentration (P < 0,001) than the adequate-Zn groups but there was no effect on maternal bone Zn concentration.3. It was concluded that Fe-supplements did not adversely affect fetal growth from mothers given a low-Zn diet, but the addition of Zn to the unsupplemented diet increased fetal wet weight. These findings were not accompanied by any other differences in fetal composition or dry weight, and do not therefore lend support to the suggestion of an Fe-Zn interaction.

Protection of the fetus in experimental potassium depletion

1961 ◽  
Vol 200 (4) ◽  
pp. 824-826 ◽  
Author(s):  
Edwin L. Stewart ◽  
Louis G. Welt
Keyword(s):  
Skeletal Muscle ◽  
Dry Weight ◽  
Maternal Serum ◽  
Potassium Depletion ◽  
Deficient Diet ◽  
Pregnant Rats ◽  
Experimental Animals ◽  
Significant Difference ◽  
The Mean ◽  
And Control

Pregnant rats were provided with a potassium-deficient diet on the day of mating. One group was sacrificed at 12–13 days of gestation and another group at 21 days. A third group was depleted of potassium acutely by utilizing peritoneal dialysis with an isotonic NaHCO3 solution. In all groups maternal serum and muscle potassium were found to be significantly lower and maternal serum CO2 significantly higher in the experimental animals than in the controls. However no significant difference in total fetal potassium concentrations was found when experimental and control animals were compared. As late as 15–17 days of gestation the total fetal potassium concentrations were found to be nearly double those of maternal skeletal muscle, but on day 21 the total fetal and the maternal muscle values were roughly equivalent. The mean dry weight of the experimental 21-day fetuses was significantly lower than that of the control fetuses. The mechanism of fetal sparing in maternal potassium depletion cannot be determined from the present data.

scholarly journals The effect of dietary zinc depletion and repletion on rats: Zn concentration in various tissues and activity of pancreatic γ-glutamyl hydrolase (EC3.4.22.12) as indices of Zn status

1990 ◽  
Vol 64 (1) ◽  
pp. 201-209 ◽  
Author(s):  
Mary C. Canton ◽  
F. M. Cremin
Keyword(s):  
Zinc Deficiency ◽  
Wistar Rats ◽  
Control Group ◽  
Zn Deficiency ◽  
Deficient Diet ◽  
Adequate Diet ◽  
Zn Concentration ◽  
Zinc Depletion ◽  
Male Wistar Rats ◽  
Zn Status

Unlike severe zinc deficiency, marginal Zn deficiency is difficult to identify in rats because no reliable indicator of suboptimal Zn status is currently available. We have previously observed reduced pancreatic γ-glutamyl hydrolase (EC3.4.22.12) activity and impaired pteroylpolyglutamate absorption in Zn-deficient rats. In the present study the effect of Zn depletion and repletion on the Zn concentration of various tissues and on the activity of this enzyme was investigated. The objective was to determine the sensitivity of these variables to Zn depletion and to evaluate their usefulness as indices of Zn status. Male Wistar rats (about 180 g), maintained from weanling on a purified Zn-adequate diet, were randomly allocated into twelve groups. A pretreatment control group was killed immediately. The remaining eleven groups were fed on a Zn-deficient diet and a group killed daily for 7 d (Zn-depleted groups). The remaining four groups were re-fed the Zn-adequate diet and a group killed daily (Zn-repleted groups). On analysis, pancreas and spleen Zn levels responded most rapidly to reduced Zn intake, followed by tibia, liver, kidney and plasma. Zn concentration was maintained in testes. Reduced plasma folate levels were also observed. A significant reduction in pancreatic γ-glutamyl hydrolase activity before the depletion of many tissue Zn stores confirms the Zn sensitivity of the enzyme. It was concluded that future investigation into the inter-relationship between Zn and folate metabolism may be useful in identifying a sensitive, biochemical index of Zn status.

scholarly journals The Hemolytic Anemia of Magnesium Deficiency in Adult Rats

Blood ◽  
1973 ◽  
Vol 41 (3) ◽  
pp. 451-459 ◽  
Author(s):  
Sergio Piomelli ◽  
Valerie Jansen ◽  
Joseph Dancis
Keyword(s):  
Structural Defect ◽  
Energy Production ◽  
Magnesium Deficiency ◽  
Osmotic Fragility ◽  
Deficient Diet ◽  
Adult Rats ◽  
In Vitro Synthesis ◽  
Mg Deficiency ◽  
Extrinsic Defect

Abstract The administration of a Mg-deficient diet to adult rats for 4-5 wk causes anemia. The RBC are slightly smaller and flatter, and have a reduced hemoglobin component and a decreased osmotic fragility. 51Cr survival time is shortened when the affected cells are infused into normal adult rats. In vitro synthesis of heme and globin, as measured with 14C-glycine was the same as in control rats with "reticulocytosis-rich" anemia produced by bleeding or immunologically. The activity of a series of enzymes associated with energy production also failed to yield findings specific for Mg deficiency. It is suggested that the anemia of Mg deficiency is hemolytic and results from the combination of a reversible extrinsic defect and of an irreversible structural defect in the RBC.

scholarly journals Effects of magnesium deficiency on reproduction in the white rat

1973 ◽  
Vol 29 (2) ◽  
pp. 203-210 ◽  
Author(s):  
C. Andrieux-Domont ◽  
Le Van Hung
Keyword(s):  
Magnesium Deficiency ◽  
In Utero ◽  
Deficient Diet ◽  
Mg Deficiency ◽  
Pregnant Females ◽  
Young Rats ◽  
Males And Females ◽  
And Control

1. Groups of rats were maintained from weaning on magnesium-deficient (30 mg Mg/kg) and control (460 mg Mg/kg) diets.2. Mg deficiency for a period of more than 3 months resulted in sterility of both males and females.3. A Mg deficiency of less than 3 months caused abortions or resorptions in utero of foetuses in pregnant females before other physical signs appeared.4. Mg deficiency during lactation rendered the survival of young rats uncertain. The mother rat died of exhaustion if she did not devour her litter.5. The growth of surviving young rats born of Mg-deficient mothers was noticeably retarded when they were nursed by mothers receiving the Mg-deficient diet.

scholarly journals Magnesium Deficiency Alters Expression of Genes Critical for Muscle Magnesium Homeostasis and Physiology in Mice

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2169
Author(s):  
Dominique Bayle ◽  
Cécile Coudy-Gandilhon ◽  
Marine Gueugneau ◽  
Sara Castiglioni ◽  
Monica Zocchi ◽  
...  
Keyword(s):  
Gastrocnemius Muscle ◽  
Magnesium Deficiency ◽  
Mitochondrial Dynamics ◽  
Body Weight Gain ◽  
Whole Body ◽  
Muscle Physiology ◽  
Deficient Diet ◽  
Muscle Weight ◽  
Magnesium Homeostasis ◽  
Expression Of Genes

Chronic Mg2+ deficiency is the underlying cause of a broad range of health dysfunctions. As 25% of body Mg2+ is located in the skeletal muscle, Mg2+ transport and homeostasis systems (MgTHs) in the muscle are critical for whole-body Mg2+ homeostasis. In the present study, we assessed whether Mg2+ deficiency alters muscle fiber characteristics and major pathways regulating muscle physiology. C57BL/6J mice received either a control, mildly, or severely Mg2+-deficient diet (0.1%; 0.01%; and 0.003% Mg2+ wt/wt, respectively) for 14 days. Mg2+ deficiency slightly decreased body weight gain and muscle Mg2+ concentrations but was not associated with detectable variations in gastrocnemius muscle weight, fiber morphometry, and capillarization. Nonetheless, muscles exhibited decreased expression of several MgTHs (MagT1, CNNM2, CNNM4, and TRPM6). Moreover, TaqMan low-density array (TLDA) analyses further revealed that, before the emergence of major muscle dysfunctions, even a mild Mg2+ deficiency was sufficient to alter the expression of genes critical for muscle physiology, including energy metabolism, muscle regeneration, proteostasis, mitochondrial dynamics, and excitation–contraction coupling.

Tissue Deposition of Zinc from a Zinc Chelate and from Inorganic Zinc in Rats

1994 ◽  
Vol 1994 ◽  
pp. 171-171 ◽  
Author(s):  
Ronan Power ◽  
Kevin Cashman ◽  
Albert Flynn
Keyword(s):  
Amino Acids ◽  
Tissue Distribution ◽  
Wistar Rats ◽  
Gel Filtration ◽  
Normal Diet ◽  
Farm Animals ◽  
Trace Minerals ◽  
Inorganic Salts ◽  
Male Wistar Rats ◽  
Differential Tissue

Some reports have suggested differential tissue deposition of dietary trace minerals such as Zinc (Zn) when supplied to farm animals either chelated to amino acids or as inorganic salts. To test this hypothesis, an experiment was conducted to determine the ultimate tissue distribution of Zinc in rats fed either a radioactively-labeled 65Zn-chelate or 65ZnSO4. The 65Zn-chelate was prepared by heating a solution of 65ZnSO4 and an equimolar mixture of glycine and methionine for 5 minutes at 90°C. The resulting chelate was then separated from unincorporated 65ZnSO4 by gel filtration chromatography. Ten 25-d old male wistar rats (mean weight 34.5 g) were randomized by weight into two groups (n = 5/group), fasted for 18 hours and given 0.4 ml (8 μg Zn, 1 μCi65Zn) of one or other labelled solution by gavage. Four hours later, animals were returned to their normal diet for the duration of the experiment. The 65Zn activity of the animals was determined two hours after administration and daily thereafter for 7 days.

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