Cadmium impact and osteoporosis: mechanism of action

Youness, Eman R.; Mohammed, Nadia A.; Morsy, Fatma A.

doi:10.3109/15376516.2012.702796

Cited by 69 publications

(50 citation statements)

References 36 publications

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“…Interestingly, another in vitro study has also exposed that Cd disrupted active VD 3 cellular actions by mimicking the hormone at its VDR binding sites . However, none of the prior studies measured the hepatic expression of VD‐related molecules with Cd toxicity despite the major roles of the liver in VD homeostasis . This study, to the best of our knowledge, is the first to reveal that chronic Cd toxicity in the PC group was associated with marked inhibitions in hepatic VD‐synthesizing enzymes and VDR alongside increases in the Cyp24a1 enzyme and VDBP.…”

Section: Discussionmentioning

confidence: 70%

“…The interactions between Cd, VD, and Ca 2+ have long been investigated since osteomalacia and renal dysfunction are common features of itai‐itai disease, the most severe form of chronic Cd toxicity . Low abnormal serum VD levels, reduced the production of active VD 3 subsequent to the deactivation of renal Cyp27b1 hydroxylase as well as increased VDBP loss in urine have been documented with Cd toxicity. Interestingly, another in vitro study has also exposed that Cd disrupted active VD 3 cellular actions by mimicking the hormone at its VDR binding sites .…”

Section: Discussionmentioning

confidence: 99%

“…Many reports have shown major declines in systemic VD with chronic Cd toxicity . Moreover, the intestinal absorption of Cd and its toxic effects were enhanced in animals fed with VD 3 or Ca 2+ ‐deficient diets .…”

Section: Introductionmentioning

confidence: 99%

“…[21,22] Many reports have shown major declines in systemic VD with chronic Cd toxicity. [25][26][27] Moreover, the intestinal absorption of Cd and its toxic effects were enhanced in animals fed with VD 3 or Ca 2+deficient diets. [28,29] Cd also deterred the activities of the Cyp27b1 enzyme [25,26] and VDR, [30] thus inhibiting the actions of VD 3 .…”

mentioning

confidence: 99%

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Vitamin D₃ and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti‐inflammatory actions by remodeling cellular calcium pathways

El‐Boshy

Refaat

Almaimani

et al. 2020

J Biochem & Molecular Tox

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Although vitamin D (VD) and calcium (Ca) attenuate cadmium (Cd) metabolism, their combined antioxidant and anti‐inflammatory actions against Cd toxicity have not been previously explored. Hence, this study measured the protective effects of VD ± Ca supplements against Cd hepatotoxicity. Forty adult male rats were distributed to: negative controls (NCs), positive controls (PCs), VD, Ca, and VD3 and Ca (VDC) groups. All groups, except NC, received CdCl2 in drinking water (44 mg/L) for 4 weeks individually or concurrently with intramuscular VD3 (600 IU/kg; three times per week) and/or oral Ca (100 mg/kg; five times per week). The PC group showed abnormal hepatic biochemical parameters and increase in cellular cytochrome C, caspase‐9, and caspase‐3 alongside the apoptotic/necrotic cell numbers by terminal deoxynucleotidyl transferase dUTP nick end labeling technique. The PC hepatic tissue also had substantially elevated pro‐oxidants (malondialdehyde [MDA]/H2O2/protein carbonyls) and inflammatory cytokines (interleukin 1β [IL‐1β]/IL‐6/IL17A/tumor necrosis factor‐α), whereas the anti‐inflammatory (IL‐10/IL‐22) and antioxidants (glutathione [GSH]/GPx/catalase enzyme [CAT]) markers declined. Hypovitaminosis D, low hepatic tissue Ca, aberrant hepatic expression of VD‐metabolizing enzymes (Cyp2R1/Cyp27a1/cyp24a1), receptor and binding protein alongside Ca‐membrane (CaV1.1/CaV3.1), and store‐operated (RyR1/ITPR1) channels, and Ca‐binding proteins (CAM/CAMKIIA/S100A1/S100B) were observed in the PC group. Both monotherapies decreased serum, but not tissue Cd levels, restored the targeted hepatic VD/Ca molecules' expression. However, these effects were more prominent in the VD group than the Ca group. The VDC group, contrariwise, disclosed the greatest alleviations on serum and tissue Cd, inflammatory and oxidative markers, the VD/Ca molecules and tissue integrity. In conclusion, this report is the first to reveal boosted protection for cosupplementing VD and Ca against Cd hepatotoxicity that could be due to enhanced antioxidative, anti‐inflammatory, and modulation of the Ca pathways.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Vitamin D₃ and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti‐inflammatory actions by remodeling cellular calcium pathways

El‐Boshy

Refaat

Almaimani

et al. 2020

J Biochem & Molecular Tox

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“…Cd is toxic to MC3T3 osteoblasts by unknown mechanisms [40] and stimulates osteoclasts, thereby inducing osteoporosis [41]. Cd decreases serum osteocalcin levels in rats [42]. These factors apparently combine to induce calciuria, increase bone resorption and decrease bone mineral density in Cd-exposed children [43].…”

Section: Clinical Toxicitymentioning

confidence: 99%

Cadmium Toxicity and Treatment

Bernhoft¹

2013

The Scientific World Journal

478

270

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Cadmium is a heavy metal of considerable toxicity with destructive impact on most organ systems. It is widely distributed in humans, the chief sources of contamination being cigarette smoke, welding, and contaminated food and beverages. Toxic impacts are discussed and appear to be proportional to body burden of cadmium. Detoxification of cadmium with EDTA and other chelators is possible and has been shown to be therapeutically beneficial in humans and animals when done using established protocols.

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Smoking-Induced Risk of Osteoporosis Is Partly Mediated by Cadmium From Tobacco Smoke: The MrOS Sweden Study

Wallin

Barregård

et al. 2020

Journal of Bone and Mineral Research

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Cigarette smoking is a risk factor for osteoporosis and bone fracture. Moreover, smoking causes exposure to cadmium, which is a known risk factor for osteoporosis. It is hypothesized that part of smoking-induced osteoporosis may be mediated via cadmium from tobacco smoke. We investigated this hypothesis using mediation analysis in a Swedish cohort of elderly men. This study was performed in 886 elderly men from the Swedish cohort of the Osteoporotic Fractures in Men (MrOS) study. Urinary samples, bone mineral density (BMD), smoking data, and other background information were obtained at baseline in 2002-2004. Urinary cadmium was analyzed in baseline samples and adjusted for creatinine. The cohort was followed until August 2018 for fracture incidence, based on the X-ray register. Mediation analysis was conducted to evaluate the indirect effect (via cadmium) of smoking on both BMD and fractures. Time to first fracture was analyzed using the accelerated failure time (AFT) model and Aalen's additive hazard model. The mean level of urinary cadmium was 0.25 μg/g creatinine. There were significant inverse associations between smoking and total body, total hip, and trochanter BMD. The indirect effects via cadmium were estimated to be 43% of the total effects of smoking for whole-body BMD, and even more for total hip and trochanter BMD. Smoking was also associated with higher risk of all fractures and major osteoporosis fractures. The indirect effects via cadmium were largest in nonvertebral osteoporosis fractures and hip fractures, constituting at least one-half of the total effects, in both the AFT and Aalen's model. The findings in this study provide evidence that cadmium exposure from tobacco smoke plays an important role in smoking-induced osteoporosis

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Cadmium impact and osteoporosis: mechanism of action

Cited by 69 publications

References 36 publications

Vitamin D₃ and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti‐inflammatory actions by remodeling cellular calcium pathways

Vitamin D₃ and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti‐inflammatory actions by remodeling cellular calcium pathways

Cadmium Toxicity and Treatment

Smoking-Induced Risk of Osteoporosis Is Partly Mediated by Cadmium From Tobacco Smoke: The MrOS Sweden Study

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Cadmium impact and osteoporosis: mechanism of action

Cited by 69 publications

References 36 publications

Vitamin D3 and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti‐inflammatory actions by remodeling cellular calcium pathways

Vitamin D3 and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti‐inflammatory actions by remodeling cellular calcium pathways

Cadmium Toxicity and Treatment

Smoking-Induced Risk of Osteoporosis Is Partly Mediated by Cadmium From Tobacco Smoke: The MrOS Sweden Study

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Product

Resources

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Vitamin D₃ and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti‐inflammatory actions by remodeling cellular calcium pathways

Vitamin D₃ and calcium cosupplementation alleviates cadmium hepatotoxicity in the rat: Enhanced antioxidative and anti‐inflammatory actions by remodeling cellular calcium pathways