Activity of Gallium on Prevention of Fatal Cage-Layer Osteoporosis

Chen, Xiuxia; Wang, Chao

doi:10.1007/s12011-009-8403-0

Cited by 5 publications

(3 citation statements)

References 13 publications

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“…Gallium readily adsorbs to hydroxyapatite, and it is rapidly incorporated into osteogenic foci [20] and within cells in metabolically active tissues [21]. Chen X reported that dietary gallium supplementation was an effective way to improve cage layer osteoporosis [15]. The present study was carried out to investigate the possible biochemical mechanism of gallium in preventing osteoporosis.…”

Section: Resultsmentioning

confidence: 99%

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Biochemical Mechanism of Gallium on Prevention of Fatal Cage-Layer Osteoporosis

Jiang

Liu³

2009

Biol Trace Elem Res

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The possible biochemical mechanism of gallium was studied in this paper. One-day-old hens were fed to up to 68 weeks on a control diet and diets containing gallium. Serum calcium and phosphorus, serum alkaline phosphatase, tartrate resistant acid phosphatase (TRAP), serum osteocalcin, homocysteine, C-terminal crosslinked telopeptides of collagen type I, and bone mineral content were measured, respectively. The beneficial effects of gallium supplementation on improvement of cage layer osteoporosis were attributable mainly to decrease TRAP activity, C-terminal crosslinked telopeptides of collagen type I level, plasma calcium and phosphate concentrations, and increase the mineral content in the bones and osteocalcin level in plasma.

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Section: Resultsmentioning

confidence: 99%

“…Preliminary evidence suggests that dietary gallium supplementation was an effective way to enhance the egg production and reduce mortality percentage. The beneficial effects of gallium supplementation over the lifetime of the hens were attributable mainly to improve cage layer osteoporosis [15].…”

mentioning

confidence: 99%

Biochemical Mechanism of Gallium on Prevention of Fatal Cage-Layer Osteoporosis

Jiang

Liu³

2009

Biol Trace Elem Res

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“…Gallium is a group IIIA metal and was first identified in 1875 by Paul-Émile Lecoq de Boisbaudran in France ( 2 ). Gallium has been demonstrated to be efficacious in the treatment of a number of diverse disorders that are characterized by accelerated bone loss, including cancer-associated hypercalcemia, bone metastases, Paget's disease, myeloma and fatal cage-layer osteoporosis ( 2 – 9 ). However, the adverse effects associated with gallium limits its use therapeutically for the treatment of osteoporosis ( 10 ).…”

Section: Introductionmentioning

confidence: 99%

Effect of gallium nitrate on the expression of osteoprotegerin and receptor activator of nuclear factor-κB ligand in osteoblasts in vivo and in vitro

Wang

Xue

et al. 2015

Molecular Medicine Reports

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Osteoporosis is characterized by the progressive loss of bone mass and the micro-architectural deterioration of bone tissue, leading to bone fragility and an increased risk of fracture. Gallium has demonstrated efficacy in the treatment of several diverse disorders that are characterized by accelerated bone loss. Osteoblasts orchestrate bone degradation by expressing the receptor activator of NF-κB ligand (RANKL), however they additionally protect the skeleton by secreting osteoprotegerin (OPG). Therefore, the relative concentration of RANKL and OPG in bone is a key determinant of bone mass and strength. The current study demonstrated that gallium nitrate (GaN) is able to counteract bone loss in an experimental model of established osteoporosis. Ovariectomized (OVX) rats exhibited significantly increased bone mineral density following GaN treatment for 4 and 8 weeks by 19.3 and 37.3%, respectively (P<0.05). The bone volume of the OVX + GaN group was increased by 40.9% (P<0.05) compared with the OVX group. In addition, the current study demonstrated that GaN stimulates the synthesis of OPG however has no effect on the expression of RANKL in osteoblasts, as demonstrated by RT-qPCR, western blotting and ELISA, resulting in an increase in the OPG/RANKL ratio and a reduction in osteoclast differentiation in vivo and in vitro.

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Yeast-Incorporated Gallium Attenuates Glucocorticoid-Induced Bone Loss in Rats by Inhibition of Bone Resorption

Ren

Yang

Xue

et al. 2013

Biol Trace Elem Res

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Glucocorticoids (GC) are potent anti-inflammatory agents and widely used for the treatment of many immune-mediated and inflammatory diseases, whereas GC-induced osteoporosis (GIOP) is the most common cause of secondary osteoporosis and significantly increases the patients' morbidity and mortality. GIOP is characterized as diminished osteogenesis and accelerated bone resorption. Yeast-incorporated gallium (YG) as an organic compound not only reduces elements-associated toxicity, but also maintains its therapeutic effect on improving bone loss or promoting fracture healing in ovariectomized female rats. The aim of this study was to examine whether YG could prevent GC-induced bone loss. Five-month-old male Sprague-Dawley rats were randomly divided into three groups (n = 6): two groups were administered dexamethasone (0.1 mg/kg/day) or vehicle (PBS) subcutaneously for 5 weeks; one other group was received dexamethasone subcutaneously and YG (120 μg/kg/day) orally. Trabecular bone microarchitectural parameters, bone mineral density (BMD), bone strength, body weight, and serum biochemical markers of bone resorption and formation were examined. Compared to the GC alone group, treatment with YG not only prevented microarchitectural deterioration of trabecular bone volume relative to tissue volume, trabecular number, and trabecular separation, but also significantly improved BMD, mechanical strength, and body weight in GC-treated rats. Moreover, YG decreased tartrate-resistant acid phosphatase 5b level but failed to change alkaline phosphatase level in GC-treated rats. This is the first study to show that YG prominently attenuates bone loss and microarchitectural deterioration and inhibits the increased bone resorption in GIOP. It implies that YG might be an alternative therapy for prevention of GC-induced bone loss in humans.

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Activity of Gallium on Prevention of Fatal Cage-Layer Osteoporosis

Cited by 5 publications

References 13 publications

Biochemical Mechanism of Gallium on Prevention of Fatal Cage-Layer Osteoporosis

Biochemical Mechanism of Gallium on Prevention of Fatal Cage-Layer Osteoporosis

Effect of gallium nitrate on the expression of osteoprotegerin and receptor activator of nuclear factor-κB ligand in osteoblasts in vivo and in vitro

Yeast-Incorporated Gallium Attenuates Glucocorticoid-Induced Bone Loss in Rats by Inhibition of Bone Resorption

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