scholarly journals Fulvic acid supplementation and selenium deficiency disturb the structural integrity of mouse skeletal tissue. An animal model to study the molecular defects of Kashin-Beck disease

1993 ◽  
Vol 289 (3) ◽  
pp. 829-835 ◽  
Author(s):  
C Yang ◽  
C Niu ◽  
M Bodo ◽  
E Gabriel ◽  
H Notbohm ◽  
...  
Keyword(s):  
Animal Model ◽  
Fulvic Acid ◽  
Structural Integrity ◽  
Selenium Deficiency ◽  
Collagen I ◽  
Bone Collagen ◽  
Deficient Diet ◽  
Skeletal Tissue ◽  
Collagen Ii ◽  
Beck Disease

High concentrations of fulvic acid and selenium deficiency are the main causative factors of Kashin-Beck disease, an endemic, chronic and degenerative osteoarticular disorder found in China. In the search for an animal model of this disease, mice were exposed to these pathogenetic conditions for two generations and the collagen types from skin, bone and cartilage were analysed. The growth of the treated mice was slightly retarded, and the rate of reproduction was lower in animals maintained on a fulvic acid-supplemented and/or selenium-deficient diet. Irregular bone formation was seen by radiography and morphometry. Biochemical analysis indicated that lysine residues in collagen I from bone and in collagen II from cartilage were overmodified. The values of Hyl/(Hyl+Lys) in bone collagen alpha 1(I) chains from treated mice were about 0.434-0.484, i.e. substantially higher than that of the control (0.277). The values of this parameter for collagen II were 0.482 for control and 0.546-0.566 for treated mice. The melting temperature of collagen I from bones of treated mice was 1 degrees C lower than that of control collagen, indicating decreased thermal stability. The breakage point of the tibiae of treated mice occurred at a lower preload force than for controls, suggesting that the overmodified and thermally less stable collagen molecules are causally related to a lower mechanical strength of bones.

Fulvic acid disturbs processing of procollagen II in articular cartilage of embryonic chicken and may also cause Kashin-Beck disease

1991 ◽  
Vol 202 (3) ◽  
pp. 1141-1146 ◽  
Author(s):  
Chunlin YANG ◽  
Michael BODO ◽  
Holger NOTBOHM ◽  
An PENG ◽  
Peter K. MULLER
Keyword(s):  
Articular Cartilage ◽  
Fulvic Acid ◽  
Embryonic Chicken ◽  
Beck Disease

scholarly journals Metabolic impact of partial hepatectomy in the non-alcoholic steatohepatitis animal model of methionine-choline deficient diet

2020 ◽  
Vol 178 ◽  
pp. 112958
Author(s):  
Eugenia Carril ◽  
María Pilar Valdecantos ◽  
Borja Lanzón ◽  
Santiago Angulo ◽  
Ángela M. Valverde ◽  
...  
Keyword(s):  
Animal Model ◽  
Partial Hepatectomy ◽  
Deficient Diet ◽  
Alcoholic Steatohepatitis

Establishment and comparison of different intrauterine adhesion modelling procedures in rats

2019 ◽  
Vol 31 (8) ◽  
pp. 1360 ◽  
Author(s):  
Li Sun ◽  
Siwen Zhang ◽  
Qiyuan Chang ◽  
Jichun Tan
Keyword(s):  
Animal Model ◽  
Interleukin 6 ◽  
Mechanical Injury ◽  
The Other ◽  
Collagen I ◽  
Rat Uterus ◽  
Cytokeratin 18 ◽  
Vimentin Expression ◽  
Intrauterine Adhesion ◽  
Modelling Procedure

Intrauterine adhesion (IUA) is caused by endometrial damage and leads to the formation of scar fibrosis and repair disorders. We compared four different rat IUA modelling procedures in order to establish a stable animal model suitable for investigating IUA. Twenty female Sprague­–Dawley rats were randomly divided into four groups. IUA was induced on one side of each rat uterus by ethanol instillation, heat stripping, mechanical injury or mechanical injury with infection (dual-injury); the other side of the uterus was left intact as a control. After 8 days the rats were sacrificed, their uteri were examined for histomorphology and expression of endometrial markers was checked using immunohistochemistry. All four IUA modelling procedures resulted in visual pathophysiological changes in the rat uterus, including stenosis, congestion and loss of elasticity. Endometrial thinning, shrinkage of glands and formation of fibrotic hyperplasia were also observed. All four procedures resulted in the downregulation of cytokeratin 18 and vimentin expression compared with control tissues, as well as the upregulation of collagen I expression. After mechanical injury and dual-injury the expression of interleukin 6 was significantly increased. Overall, our results suggest that ethanol instillation is the most stable IUA modelling procedure. Mechanical injury reliably yielded inflammatory indicators.

Glycosylation of Human Bone Collagen I in Relation to Lysylhydroxylation and Fibril Diameter

1997 ◽  
Vol 122 (1) ◽  
pp. 109-115 ◽  
Author(s):  
B. Batge ◽  
C. Winter ◽  
H. Notbohm ◽  
Y. Acil ◽  
J. Brinckmann ◽  
...  
Keyword(s):  
Human Bone ◽  
Collagen I ◽  
Bone Collagen ◽  
Fibril Diameter

scholarly journals Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence

1987 ◽  
Vol 242 (2) ◽  
pp. 383-386 ◽  
Author(s):  
C G Fraga ◽  
R F Arias ◽  
S F Llesuy ◽  
O R Koch ◽  
A Boveris
Keyword(s):  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Selenium Deficiency ◽  
Serum Levels ◽  
Hepatic Necrosis ◽  
Deficient Diet ◽  
Control Value ◽  
Weanling Rats

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.

scholarly journals Effect of selenium deficiency on hydroperoxide-stimulated release of glutathione from isolated perfused liver of rainbow trout (Salmo gairdneri)

1986 ◽  
Vol 56 (2) ◽  
pp. 421-428 ◽  
Author(s):  
J. G. Bell ◽  
J. W. Adron ◽  
C. B. Cowey
Keyword(s):  
Hydrogen Peroxide ◽  
Rainbow Trout ◽  
Weight Gain ◽  
Peroxidase Activity ◽  
Selenium Deficiency ◽  
Salmo Gairdneri ◽  
Perfused Liver ◽  
Deficient Diet ◽  
Significant Difference ◽  
Glutathione Disulphide

1. Duplicate groups of rainbow trout (Salmo gairdneri) were each given partially purified diets which were either adequate or depleted in selenium for 40 weeks.2. Although there was no significant difference in weight gain, liver Se concentration was significantly lower in fish given the deficient diet.3. Glutathione (GSH) peroxidase (EC 1. 11. 1. 9) activity was significantly reduced in liver of Se-deficient fish but a differential assay did not indicate the presence of a non-Se-dependent GSH peroxidase activity, although liver GSH S-transferase (EC 2. 5. 1. 18) was significantly increased.4. Perfusion of livers from trout given Se-adequate diets with t-butyl hydroperoxide (BuOOH) or hydrogen peroxide caused an increase in the rate of release of glutathione disulphide (GSSG) into the perfusate.5. Perfusion of livers from Se-deficient trout with BuOOH or H2O2 did not result in any change in rate of release of GSSG into the perfusate.6. These findings confirm the absence of any compensatory non-Se-dependent peroxidase activity in Se-depleted trout.

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

1980 ◽  
Vol 60 (3) ◽  
pp. 579-590 ◽  
Author(s):  
M. HIDIROGLOU
Keyword(s):  
Structural Integrity ◽  
Zinc Concentration ◽  
Bone Mineralization ◽  
Bone Matrix ◽  
Active Role ◽  
Deficient Diet ◽  
Prominent Symptom ◽  
Zinc Deficient Diet ◽  
Bone Abnormalities ◽  
Cattle And Sheep

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.

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