ZINC, COPPER AND MANGANESE DEFICIENCIES AND THE RUMINANT SKELETON: A REVIEW

1980 ◽  
Vol 60 (3) ◽  
pp. 579-590 ◽  
Author(s):  
M. HIDIROGLOU

This review deals with changes in the morphology and composition of the skeleton of ruminants caused by trace element deficiencies, specifically with respect to zinc, copper and manganese. When ruminants are fed a zinc-deficient diet, bone abnormalities occur. Zinc is also reported to be of value in the prevention or cure of footrot in cattle and sheep. Depletion of zinc reserves appears to lead to alterations in bone mineralization and reduction of bone zinc concentration. The bones of copper-deficient ruminants are fragile and easily broken. The most prominent symptom of this deficiency is a very marked stiffness of the legs. Copper-deficient animals show symptoms of rickets with beading of the ribs and enlargement of the ends of the long bones. Histologically, the affected bones show widening of the growth plate and the overall appearance of the lesion is that of osteoporosis. Crosslinking between collagen precursors is impaired in copper deficiency, which affects the structural integrity of collagen. There is no evidence of any correlation between the concentration of copper in bone and the severity of malformation. A relationship between low manganese intake by gestating ruminants and increased incidence of deformed calves or lambs has been demonstrated. The deformities observed included enlarged joints and twisted forelimbs. Histological examinations of the affected bones revealed retarded growth. Since manganese plays an active role in bone matrix formation, synthesis of mucopolysaccharide is reduced in the deficient bones. The synthesis of chondroitin sulfate, which is involved in maintaining the rigidity of connective tissue, is also affected during manganese deficiency, resulting in skeletal abnormalities.

2009 ◽  
Vol 12 (1) ◽  
pp. 118-123 ◽  
Author(s):  
Jung-Tak Kim ◽  
Sang-Heum Baek ◽  
Sang-Han Lee ◽  
Eui Kyun Park ◽  
Eun-Cheol Kim ◽  
...  

1999 ◽  
Vol 53 (5) ◽  
pp. 549-570 ◽  
Author(s):  
Kazuyuki Ohkubo ◽  
Wenyu Dai ◽  
Takahiro Nishioka ◽  
Noritaka Yahara ◽  
Kazumasa Tsukamoto

1995 ◽  
Vol 268 (6) ◽  
pp. R1423-R1428 ◽  
Author(s):  
H. Izumi ◽  
H. Mori ◽  
T. Uchiyama ◽  
S. Kuwazuru ◽  
Y. Ozima ◽  
...  

A marked decrease in zinc concentration was observed in plasma (P < 0.001), hindpaw skin (P < 0.01), and dorsal skin (P < 0.01) in zinc-deficient rats (rats fed a zinc-deficient diet for 3 wk), compared with the control rats fed the same zinc-deficient diet supplemented with ZnCO3 (50 mg/kg diet). The threshold intensity needed to elicit vasodilatation in the hindpaw skin of the zinc-deficient rats on electrical stimulation of the saphenous nerve in a peripheral direction was markedly lower (P < 0.01) than that in the control rats. No difference was observed between control (n = 5) and zinc-deficient rats (n = 5) in the magnitude of the plasma extravasation evoked by either histamine or substance P. There was no difference between control and zinc-deficient rats in terms of the dose-response curve for release of histamine by substance P. Prostaglandin E2 (PGE2) concentration in the hindpaw skin of the zinc-deficient rats was nearly fourfold higher (P < 0.01) than that of the control rats, whereas no difference in the leukotriene B4 level in the hindpaw skin was observed between control and zinc-deficient rats. From the present study, it seems likely that an increased level of PGE2 in the vicinity of the nociceptive C-fiber terminals in the hindpaw skin of zinc-deficient rats may sensitize the terminals of the nociceptive C-fibers of the saphenous afferent nerve in the hindpaw and thus facilitate the production of antidromic vasodilatation.


Development ◽  
1982 ◽  
Vol 70 (1) ◽  
pp. 171-187
Author(s):  
A. M. Duprat ◽  
L. Gualandris ◽  
P. Rouge

Lectins (SBA and PSA) were used to provoke crowding and structural modifications of the presumptive ectoderm cell surface in order to investigate the role of the membrane organization of the competent target cells in neural induction. Are specific characteristics of the cell surface essential for this phenomenon to occur? From amphibian gastrulae, it is possible to obtain neural induction in vitro by association of presumptive ectoderm (target cells) with chordamesoderm (inductor tissue): 4 h of contact is sufficient in Pleurodeles waltl for transmission of the inductive signal. Very quickly, the treatment of the normal ectoderm by lectins (SBA-FITC or PSA-FITC) provoked surface modifications. Lectin-treatment (50 µg ml1−, 30 min) of presumptive ectoderm did not result in any neural induction. Lectin-treatment (50 µg ml1−, 30 min) of presumptive ectoderm previous to its association with the natural inductor for 4 h, disturbed the phenomenon: no induction. Similar treatment followed by association with the inductor for 24 h: induction. Treatment of SBA or PSA with their respective hapten inhibitors prior to addition to ectodermal cells completely blocked the suppressive effects on induction. The structural integrity of the membrane of competent target cells is necessary for neural induction to occur. The cell membrane could thus play, directly or indirectly, an active role in the specificity of this process


2016 ◽  
Vol 10 (2) ◽  
pp. 12-19
Author(s):  
Sahar S. Karieb ◽  
Mohammed M. Jawad ◽  
Hanady S. Al-Shmgani ◽  
Zahraa H.M. Kadri

Multiple studies have been reported the stimulatory effect of the combinations of nutrients factors on bone formation. One such factor is vitamin K2 which can be associated with bone protective activities. The effect of vitamin K2 alone and in combination with genistein, coumestrol and daidzein on osteoblast differentiation and mineralization were tested. Significantly, vitamin K2 increased bone mineralization in combination with genistein (10-5M), coumestrol (10-7M) and daidzein (10-5M). However, there is no additive effect of this vitamin on alkaline phosphatase (ALP) levels in osteoblasts. By contrast, vitamin K2 enhanced the stimulatory effect of type I collagen and osteocalcin expression. Vitamin K2 alone increased RUNX and OSX expression while there is no synergistic effect with tested compound; this vitamin also did not modulate nuclear factor kappa B ligand (RANKL)/ osteoprotegerin (OPG) ratio expression. These results suggested that vitamin K2 can be more effective factor in the presence of phytoestrogens on the improvement of bone formation after menopause.


2020 ◽  
Vol 10 (4) ◽  
pp. 168
Author(s):  
Ainia Herminiati

Background: Dried yogurt enriched by Difructose Anhydride III when used as a functional food has been observed to increase calcium absorption, making it useful in osteoporosis prevention. The objective of this study was to analyze the effectiveness of Difructose Anhydride III in increasing the absorption of calcium in female rat models, strain Sprague Dawley, in the pre-menopausal age during which they’re calcium deficient.Methods: The effectiveness test of Difructose Anhydride III to increase absorption of calcium in pre-menopausal Sprague Dawley rats was performed in calcium-deficient conditions. A completely randomized experimental design was used with 4 treatments for 6 weeks and 4 replications: normal rats fed with purified diet (C), calcium-deficient rats fed with calcium-deficient diet (CD), calcium-deficient rats fed with calcium-deficient diet and DFA III (dahlia tubers) fortified in dry yogurt (CD+DFA III dahlia), and calcium-deficient rats fed with a calcium-deficient diet and DFA III (chicory roots) fortified in dry yogurt (CD+DFA III chicory). The parameters measured were serum calcium concentration, femur bone calcium concentration, femur bone matrix condition, and femur bone strength.Results: DFA III (dahlia tubers and chicory roots) fortified in dry yogurt contained 0.334% and 0.322% of calcium concentration. The provision of a calcium-deficient diet for 12 weeks was shown to reduce the serum calcium concentration of the deficient calcium rat to 7.72±1.08 mg dL-1 and the control rat to 11.60±0.85 mg dL-1. CD+DFA III chicory treatments also showed a high calcium concentration in the femur bone (34.94±3.21%), a relatively higher bone strength (9.34±3.61 kg cm-2), and a denser femur bone matrix condition than the control. The femur bone calcium level of rats treated with CD+DFA III dahlia and chicory tubers was 28.95±1.95% and 34.94±3.21%, respectively. These results were significantly different than the CD treatment (17.49±4.38%).Conclusion: The evidence from this study suggests that sufficient calcium intake could provide high calcium deposits in the bones. Diets containing 3.60% w/w DFA III fortified in dry yogurt have been shown to enhance calcium absorption in calcium-deficient rats. Additionally, the effectiveness of dried yogurt enriched by DFA III from chicory tubers was higher than that of the dried yogurt enriched by DFA III from dahlia tubers.Preclinical Trial Registration: Animal Ethics Committee at IPB University No. 12-2013Keywords: Bone femur; calcium deficiency; effectivity of Difructose Anhydride III


1972 ◽  
Vol 20 (4) ◽  
pp. 279-292 ◽  
Author(s):  
D. BAYLINK ◽  
J. WERGEDAL ◽  
E. THOMPSON

In both ground sections and demineralized frozen sections of the rat tibial cortex, osteoid but not mature bone matrix stained for proteinpolysaccharides with the Alcian Blue and toluidine blue techniques. The loss of proteinpolysaccharide staining occurred precisely at the mineralizing front, which was identified by in vivo lead or procion markers, not only in normal animals but also in animals in which osteoid width was either increasing or decreasing. In vitro, both proteases and saccharidases abolished proteinpolysaccharide staining of osteoid. Critical electrolyte concentration and other procedures indicated that the major acid polysaccharide component in osteoid is chondroitin sulfate. Consistent with these findings, electron microprobe analyses revealed that sulfur concentration was high in osteoid but dropped abruptly as calcium concentration increased at the mineralizing front. The precise synchronization between loss of proteinpolysaccharides and onset of mineralization under various experimental conditions provides strong indirect evidence that the loss of these macromolecules is somehow involved in initiation of mineralization in bone.


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