Effect of cadmium on osteoclast differentiation during bone injury in female mice

He, Shuangjiang; Zhuo, Lang; Liu, Gang; Zhao, Hongyan; Song, Ruilong; Liu, Zongping

doi:10.1002/tox.22884

Cited by 46 publications

(35 citation statements)

References 36 publications

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“…In this process, Cd was more cytotoxic [ 20 ]. In addition, compared to male animals, females were more susceptible to Cd in bone [ 21 , 22 ]. One possible explanation is that Cd exposure can reduce the level of estrogen 2, which inhibits the osteoclast activity and reduce bone absorption [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Blood lead and cadmium levels are negatively associated with bone mineral density in young female adults

Lü

Lan

et al. 2021

Arch Public Health

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Background The organ toxicities of lead and cadmium have been extensively studied; however, studies of their toxic effects on bone remain limited, especially in young adults. The objective of this study was to examine the associations of blood lead levels (BLL) and blood cadmium levels (BCL) with bone mineral density (BMD) among young adults. Methods We performed a cross-sectional study using the National Health and Nutrition Examination Survey 2011–2018 database. Because of the skewed distribution, BLL and BCL were Ln-transformed for analysis. Weighted multivariate regressions were performed to evaluate the associations between LnBLL and LnBCL and lumbar BMD. Subgroup analyses were further performed. Results A total of 3234 participants aged 20–35 years were included in this study. No significant association between LnBLL and lumbar BMD was found (β = − 5.6, 95%CI: − 13.5–2.3). However, in the subgroup analysis stratified by sex, this association became negative in women (β = − 18.2, 95%CI: − 29.9– − 6.4). Moreover, this negative association was more prominent in female blacks (β = − 35.5, 95%CI: − 63.4– − 7.6). On the other hand, a negative association between LnBCL and lumbar BMD was found (β = − 7.4, 95%CI: − 14.0– − 0.8). In the subgroup analysis stratified by sex, this negative association only existed in women (β = − 18.7, 95%CI: − 28.0– − 9.5). Moreover, this negative association was more prominent in female whites (β = − 31.1, 95%CI: − 46.2– − 16.1). Conclusions Our finding showed that both BLL and BCL were independently and negatively associated with lumbar BMD among young females, but not among young males.

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Section: Discussionmentioning

confidence: 99%

Blood lead and cadmium levels are negatively associated with bone mineral density in young female adults

Lü

Lan

et al. 2021

Arch Public Health

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“…Cadmium is a serious environmental heavy metal pollutant, which has a half-life of 10-30 years, is widely deposited in the stomachs, intestines, livers, pancreases, testes, ovaries, bone marrow, lungs, muscles and fats of humans and animals, and induces apoptosis and autophagy (37,38). Studies on Cd toxicity in bone tissue have shown that Cd turns mesenchymal stem cells from osteogenic differentiation to adipogenic differentiation, and promotes the generation of osteoclasts with bone resorption, thereby affecting bone homeostasis and reducing long bone density and calcium content (39)(40)(41). Kalisińska et al showed that the content of Cd in cartilage tissue is higher than in bones and interferes with the absorption of copper, zinc, iron, manganese, and other trace elements in cartilage, thus causing osteoarthritis and osteoporosis (42,43).…”

Section: Discussionmentioning

confidence: 99%

Cadmium Toxicity on Chondrocytes and the Palliative Effects of 1α, 25-Dihydroxy Vitamin D3 in White Leghorns Chicken's Embryo

Wang

et al. 2021

Front. Vet. Sci.

Self Cite

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Cadmium (Cd) can causes osteoporosis and joint swelling. However, the mechanism of Cd toxicity in chondrocytes and how to alleviate Cd poisoning to chondrocytes are still unclear. Herein, we evaluated the toxicity of Cd to chicken chondrocytes, and whether vitamin D can relieve the toxicity of Cd to chondrocytes. Primary chondrocytes were collected from knee-joint cartilage of 15-day-old chicken embryos. They were treated with (0, 1, 2, and 4) μM Cd alone, 10−8 M 1α,25-(OH)2D3 alone, or 2 μM Cd combined with 10−8 M 1α,25-(OH)2D3. We found that Cd significantly inhibited Sox9 and ACAN mRNA expression, which are markers for chondrocyte differentiation, downregulated the mitochondrial membrane potential, upregulated the Bax/B-cell lymphoma 2 ratio. Furthermore, Cd significantly promoted matrix metalloproteinase (MMP)-9 expression, thus accelerating the degradation of extracellular matrix. And Cd also inhibited the expression of main macromolecular protein of extracellular matrix, Collagen type IIα1 (COL2A1) and acid mucopolysaccharide. However, 1α,25-(OH)2D3 pretreatment significantly alleviated the toxicity effects of Cd on the differentiation, apoptosis and extracellular matrix gene expression in primary chondrocytes. Conclusively, Cd exposure could inhibited chicken embryo chondrocytes differentiation, extracellular matrix gene expression, and induced chondrocyte apoptosis. However, these toxic effects of Cd are alleviated by the pretreatment of chondrocytes with 1α,25-(OH)2D3.

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“…Reduced ratio of OPG and RANKL via altered expression of IL-1, IL-17 and TGF- [72] Inhibited expression of RUNX2, OSX, OPN, OCN and COL1A2 by suppressing the Wnt/ -catenin pathway [ 72,74] Induction of osteoblast apoptosis Cytoskeleton disruption owing to actin depolymerization [75] DNA fragmentation probably by inducing ROS [76] Oxidative stress via activation of p38 MAPK pathway and inhibition of Erk1/2 pathway [77] Enhanced osteoclast differentiation Increased ratio of RANKL/OPG and TRAP activity [ 67,78] Increased levels of IL-6 and IL-8 in osteoblasts via TLR4 activation [78] Inhibited formation and enhanced degradation of extracellular bone matrix Induction of MMP1, MMP3, MMP9 and MMP13, and decreased synthesis of collagen 1, GAGs and PGs via inflammatory response (IL-1 and IL-6) and ROS production [ 78,81] Disturbed Ca and P homeostasis and inhibited mineralization…”

Section: Inhibited Osteoblast Differentiationmentioning

confidence: 99%

Adverse Impact of Heavy Metals on Bone Cells and Bone Metabolism Dependently and Independently through Anemia

Zhang

Sun²,

Zhang

et al. 2020

Advanced Science

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Mounting evidence is revealing that heavy metals can incur disordered bone homeostasis, leading to the development of degenerative bone diseases, including osteoporosis, osteoarthritis, degenerative disk disease, and osteomalacia. Meanwhile, heavy metal-induced anemia has been found to be intertwined with degenerative bone diseases. However, the relationship and interplay among these adverse outcomes remain elusive. Thus, it is of importance to shed light on the modes of action (MOAs) and adverse outcome pathways (AOPs) responsible for degenerative bone diseases and anemia under exposure to heavy metals. In the current Review, the epidemiological and experimental findings are recapitulated to interrogate the contributions of heavy metals to degenerative bone disease development which may be attributable dependently and independently to anemia. A few likely mechanisms are postulated for anemia-independent degenerative bone diseases, including dysregulated osteogenesis and osteoblastogenesis, imbalanced bone formation and resorption, and disturbed homeostasis of essential trace elements. By contrast, remodeled bone microarchitecture, inhibited erythropoietin production, and disordered iron homeostasis are speculated to account for anemia-associated degenerative bone disorders upon heavy metal exposure. Together, this Review aims to elaborate available literature to fill in the knowledge gaps in understanding the detrimental effects of heavy metals on bone cells and bone homeostasis through different perspectives.

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Effect of cadmium on osteoclast differentiation during bone injury in female mice

Cited by 46 publications

References 36 publications

Blood lead and cadmium levels are negatively associated with bone mineral density in young female adults

Blood lead and cadmium levels are negatively associated with bone mineral density in young female adults

Cadmium Toxicity on Chondrocytes and the Palliative Effects of 1α, 25-Dihydroxy Vitamin D3 in White Leghorns Chicken's Embryo

Adverse Impact of Heavy Metals on Bone Cells and Bone Metabolism Dependently and Independently through Anemia

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