Radiographic Studies on Skeletal Parts of Zinc Deficient Pullets.

Zeigler, T. R.; Scott, M. L.; McEvoy, Richard K.; Greenlaw, Robert H.; Huegin, Felix; Strain, William H.

doi:10.3181/00379727-109-27165

Cited by 10 publications

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“…Skeletal abnormalities chondrogenesis and an associated elevation were a conspicuous feature of zinc-defi-in the amount of cartilage matrix (4,9). ciency in growing birds (4)(5)(6). In pullets, the Westmoreland (10) suggested that these ablong bones were shortened and thickened normalities may adversely influence bone in proportion to the degree of zinc-defi-calcification, ciency (6).…”

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Epiphyseal Plate Development in the Zinc-Deficient Rat

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Lykken

et al. 1982

The Journal of Nutrition

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The effect of zinc deficiency on shearing strength, histological changes and proline utilization of the epiphyseal plate of the tibia of the weanling male rat was studied. A diet was fed based on sprayed egg white and containing less than 2 mg of zinc per kilogram. Over 27 day, the force required to displace the epiphysis of the zinc-deficient (ZD) rats was always less than that required for pair-fed (PF) controls. After 18 days, approximately 15% more force was required to displace the epiphysis of the PF rats than was required in the ZD rats. The thickness of the outside compact bone next to the epiphyseal plate region as determined by scanning electron microscopy was thicker in the ZD rats than in the PF controls of comparable age. The epiphyseal plates narrowed as the rats aged, and were clearly discernible in PF controls but not in ZD rats. The incorporation of L-[U-14C]proline into the epiphysis was significantly less in rats deprived of zinc for 16-22 days than in PF controls.

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Epiphyseal Plate Development in the Zinc-Deficient Rat

Suwarnasarn

Wallwork

Lykken

et al. 1982

The Journal of Nutrition

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“…In the chick experiments of this study, there were no occurrences of severe zinc deficiencies in chicks as de scribed by Klussendorf andPensack (1958), 0'Dell et al (1958), and Zeigler et al (1962). Chick diets supplemented with zinc or EDTA did produce sizeable increases in chick gains and reduced feed required per gram of gain.…”

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confidence: 64%

Availability of complexed zinc to pigs and chicks

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“…Syncytia and fully differentiated osteoclasts were stimulated by Zn and bone remodelling occurred. Lack of remodelling would account for the thickened bones associated with Zn deficiency (O'Dell et al 1958;Zeigler et al 1962). Increased alkaline phosphatase levels were found in bone, although not in cartilage.…”

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confidence: 99%

“…If Zn-treated chondrocytes have prematurely aged by increased cell differentiation this would be indicated conclusively if chondrocytes no longer synthesized keratan sulphate characteristic of embryonic cartilage (Shulman & Meyer, 1968). Zn stimulated bone resorption, deficiency of which may cause the thickened bones of Zn deficiency (Zeigler et al 1962) and excess of which can cause bone rarefaction and collapse as found in Zn toxicosis (Grimmett et al 1937).…”

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The histological effects of copper and zinc on chick embryo skeletal tissues in organ culture

Rest

1976

Br J Nutr

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1. The effects of copper and zinc on organ cultures of chick embryo cartilage and bone maintained in low-trace-metal, chemically defined media for up to 8 d were studied macro-scopically, histologically and histochemically. Length and wet-weight measurement of explants were assessed statistically.2. No effects were found with Cu concentrations of 0·5–1·5μg/ml medium. Between concentrations of 5 and 40μg Cu/ml medium, lengths and wet-weights of cartilage cultures decreased significantly (P< 0·001) compared with controls. The decrease was directly proportional to increasing Cu concentration, and that of the length was greater with increasing period of culture (P< 0·001).3. With 5–20μg Cu/ml medium cartilage and bone became yellow in colour, and chondrocytes were swollen, rounded and basophilic. They were detached from their lacunae and the quantity of matrix was reduced. Loss of alkaline phosphatase (EC3.1.3.1) activity and disappearance of glycogen accompanied the degeneration. Osteogenesis ceased, cells failed to divide and mature, lost their enzymes and died. Cu did not accumulate in the bone matrix.4. The direct toxic effects of Cu for cartilage and bone may underlie some of the skeletal changes in hepatolenticular degeneration (Wilson’s disease).5. As Zn concentrations were increased from 2·5 to 7·5μg/ml medium, lengths and wet-weights of cartilaginous cultures were significantly increased (P< 0·001). As Zn concentrations were further increased (from 10 to 40μg/ml medium), lengths and wet-weights were significantly decreased (P< 0·001).6. Zn stimulated chondrocyte division and vacuolation of cytoplasm. With higher Zn concentrations toxic changes of granular basophilia, lacunar detachment and necrosis were seen. Differentiation and functioning of osteoblasts, osteoclasts and chondroclasts were stimulated by Zn.7. Zn was found in bone matrix, osteoblasts, osteocytes and hypertrophied chondrocytes.

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Radiographic Studies on Skeletal Parts of Zinc Deficient Pullets.

Abstract: Earlier investigations on the metabolism of pyridoxine in animals have involved the study of degradation products by chemical methods and microbiological assay procedures (1-5).

Cited by 10 publications

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Epiphyseal Plate Development in the Zinc-Deficient Rat

Epiphyseal Plate Development in the Zinc-Deficient Rat

Availability of complexed zinc to pigs and chicks

The histological effects of copper and zinc on chick embryo skeletal tissues in organ culture

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