Cadmium as a risk factor for osteoporosis in COPD

Singhania, Sumeet; Singh, Sunilkumar; Parikh, Pujan

doi:10.5588/ijtld.16.0736

Cited by 6 publications

(4 citation statements)

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“…Moreover, Cd exposure causes bone metabolism diseases, including bone softening, bone loss, and osteoporosis . Studies have shown that a reduction in bone density is closely related to the conditions of Cd pollution in the environment …”

Section: Introductionmentioning

confidence: 99%

“…shown that a reduction in bone density is closely related to the conditions of Cd pollution in the environment. 9,10 As an important metabolic process, "bone remodeling" activity is necessary for maintaining normal bone development, and its imbalance may seriously affect bone morphology and function. 11,12 Previous studies have reported that Cd affects bone metabolism through both indirect and direct methods.…”

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confidence: 99%

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

Zhuo

Liu

et al. 2019

Environmental Toxicology

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Cadmium (Cd) is a toxic heavy metal that represents an occupational hazard and environmental pollutant toxic heavy metal, which can cause osteoporosis following accumulation in the body. The purpose of this study was to investigate the effect of Cd on bone tissue osteoclast differentiation in vivo. Female BALB/c mice were randomly divided into three groups and given drinking water with various concentrations of Cd (0, 5, and 25 mg/L) for 16 weeks, after which the mice were sacrificed after collecting urine and blood. The level of Cd, calcium (Ca), phosphorus (P), trace elements, and some biochemical indicators were measured, and the bone was fixed in a 4% formaldehyde solution for histological observation. Bone marrow cells were isolated to determine the expression of osteoclast‐associated mRNA and proteins. Cd was increased in the blood, urine, and bone in response to Cd in drinking water in a dose‐dependent manner. The content of iron (Fe), manganese (Mn), and zinc (Zn) was significantly increased, whereas Ca and P were decreased in bone compared to the control group. Cd affected the histological structure of the bone, and induced the upregulation and downregulation of tartrate‐resistant acid phosphatase 5b (TRACP‐5b) and estradiol in the serum, respectively. Cd had no significant effect on the alkaline phosphatase activity in the serum. The expression of osteoclast marker proteins, including TRACP, cathepsin K, matrix metalloprotein 9, and carbonic anhydrases were all increased in the Cd‐treated bone marrow cells. Cd significantly increased the expression of receptor activator of nuclear factor kappa B ligand (RANKL), but had lower effect on the expression of osteoprotegerin (OPG) in both bone marrow cells and bone tissue. Thus, Cd exposure destroyed the bone microstructure, promoted the formation of osteoclasts in the bone tissue, and accelerated bone resorption, in which the OPG/RANKL pathway may play an important role.

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Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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

Zhuo

Liu

et al. 2019

Environmental Toxicology

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“…Nearly one third of the absorbed Cd accumulates in the kidney, making it the main target of Cd toxicity. Chronic exposure to Cd has been linked to a heightened risk of various kidney disorders, such as proteinuria (Singhania et al, 2017), glomerulonephritis (Nogué et al, 2004), renal failure (Dastan et al, 2019), and kidney impairment (Åkesson et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Low dose cadmium inhibits syndecan‐4 expression in glycocalyx of glomerular endothelial cells

Meng,

Xie,

Liu

et al. 2024

J of Applied Toxicology

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Cadmium (Cd) is one of the most polluting heavy metal in the environment. Cd exposure has been elucidated to cause dysfunction of the glomerular filtration barrier (GFB). However, the underlying mechanism remains unclear. C57BL/6J male mice were administered with 2.28 mg/kg cadmium chloride (CdCl2) dissolved in distilled water by oral gavage for 14 days. The expression of SDC4 in the kidney tissues was detected. Human renal glomerular endothelial cells (HRGECs) were exposed to varying concentrations of CdCl2 for 24 h. The mRNA levels of SDC4, along with matrix metalloproteinase (MMP)‐2 and 9, were analyzed by quantitative PCR. Additionally, the protein expression levels of SDC4, MMP‐2/9, and both total and phosphorylated forms of Smad2/3 (P‐Smad2/3) were detected by western blot. The extravasation rate of fluorescein isothiocyanate–dextran through the Transwell was used to evaluate the permeability of HRGECs. SB431542 was used as an inhibitor of transforming growth factor (TGF)‐β signaling pathway to further investigate the role of TGF‐β. Cd reduced SDC4 expression in both mouse kidney tissues and HRGECs. In addition, Cd exposure increased permeability and upregulated P‐Smad2/3 levels in HRGECs. SB431542 treatment inhibited the phosphorylation of Smad2/3, Cd‐induced SDC4 downregulation, and hyperpermeability. MMP‐2/9 levels increased by Cd exposure was also blocked by SB431542, demonstrating the involvement of TGF‐β/Smad pathway in low‐dose Cd‐induced SDC4 reduction in HRGECs. Given that SDC4 is an essential component of glycocalyx, protection or repair of endothelial glycocalyx is a potential strategy for preventing or treating kidney diseases associated with environmental Cd exposure.

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“…Denkbar wäre die Situation einer erhöhten beruflichen Belastung mit den Knochenstoffwechsel beeinflussenden Substanzen, z. B. Blei oder Kadmium, und einer daraus resultierenden, in der Knochendichtemessung nachgewiesenen Osteoporose[7,8]. Die geschilderte Osteoporose wäre dann in Zusammenhang mit einer Berufskrankheit zu beurteilen.…”

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Begutachtung der Osteoporose und osteoporotischer Frakturen

Maus¹,

Maier²,

Schultz³

et al. 2019

Arthritis und Rheuma

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ZUSAMMENFASSUNGOsteoporose ist eine Erkrankung mit einer verminderten Knochenmasse und Knochenstruktur. Das Frakturrisiko für atraumatische Frakturen ist in Abhängigkeit der Schwere der Erkrankung erhöht. Für den ärztlichen Gutachter stellt die Beurteilung einer osteoporotischen Fraktur eine Herausforderung dar, da in den verschiedenen Versicherungssystemen unterschiedliche Bewertungen hinsichtlich Mitwirkung, Vorinvalidität und Kausalität bestehen. Neben der Klärung der Begrifflichkeiten in der gesetzlichen und privaten Unfallversicherung spielt die Beurteilung der Erkrankung mit klinischen, radiologischen und osteodensitometrischen Parametern eine Rolle. In dem vorliegenden Beitrag werden die Begutachtung der Osteoporose in der gesetzlichen und privaten Unfallversicherung dargestellt und Möglichkeiten zu deren gutachterlichen Beurteilung aufgezeigt.

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Cadmium as a risk factor for osteoporosis in COPD

Cited by 6 publications

References 0 publications

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

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

Low dose cadmium inhibits syndecan‐4 expression in glycocalyx of glomerular endothelial cells

Begutachtung der Osteoporose und osteoporotischer Frakturen

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