Cadmium osteotoxicity in experimental animals: Mechanisms and relationship to human exposures

Bhattacharyya, Maryka H.

doi:10.1016/j.taap.2009.05.015

Cited by 142 publications

(106 citation statements)

References 83 publications

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“…Since Cd, even at low concentrations, may directly influence bone tissue cell activity and oxidative/antoxidative balance, it seems reasonable to assume that the beneficial impact of AME on the oxidative/antioxidative status of the bone tissue under the higher of the investigated levels of Cd treatment was, at least to some extent, the result of the lower bone concentration of this metal. Thus, via decreasing Cd accumulation in the bone and kidneys, AME might provide protection from the direct and/or indirect impact of this xenobiotic (depending on the exposure level) on the skeleton [22,23,36]. Numerous correlations noted between Cd concentration in the bone tissue and the measured markers of the bone oxidative/antioxidative status in the animals receiving, or not, AME under the treatment with this metal confirm the possibility of such a mechanism.…”

Section: Figmentioning

confidence: 89%

The Mechanism of the Osteoprotective Action of a Polyphenol-Rich Aronia melanocarpa Extract during Chronic Exposure to Cadmium is Mediated by the Oxidative Defense System

et al. 2016

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!Recently, we demonstrated in a rat model that consumption of a polyphenol-rich extract obtained from the berries of Aronia melanocarpa could protect from cadmium-induced disorders in bone turnover and changes in bone mineral status. The aim of this study was to investigate whether the osteoprotective effect of this extract is mediated by the oxidative defense system. Enzymatic and nonenzymatic antioxidants, total antioxidative and oxidative status, hydrogen peroxide, and markers of oxidative protein, lipid, and DNA damage were determined in bone tissue at the distal femoral epiphysis of female Wistar rats receiving 0.1 % aqueous A. melanocarpa extract (prepared from the lyophilized commercial extract containing 65.74 % of polyphenols) as the only drinking fluid and/or cadmium in the diet (1 and 5 mg/kg) for 3, 10, 17, and 24 months. The total oxidative and antioxidative status of the serum was also evaluated. The administration of A. melanocarpa extract provided significant protection from cadmium-induced oxidative stress in the bone and serum, and from lipid peroxidation and oxidative damage to the protein and DNA in the bone tissue. Numerous correlations were noted between indices of the oxidative/antioxidative bone status and markers of bone metabolism previously assayed in the animals receiving A. melanocarpa extract. The results allow the conclusion that the ability of A. melanocarpa extract to mediate the oxidative defense system and prevent oxidative modifications of protein, lipid, and DNA in the bone tissue plays an important role in its osteoprotective action under exposure to cadmium. The findings provide further evidence supporting our suggestion that chokeberry may be a promising natural agent for protection against the toxic action of cadmium in women chronically exposed to this metal. Abbreviations

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Section: Figmentioning

confidence: 89%

The Mechanism of the Osteoprotective Action of a Polyphenol-Rich Aronia melanocarpa Extract during Chronic Exposure to Cadmium is Mediated by the Oxidative Defense System

et al. 2016

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“…Experimental data demonstrate a direct effect of Cd on bone with decreased bone formation and increased bone resorption at Cd concentrations relevant to human exposures (see review by Bhattacharyya (28) ). Cd-exposed osteoblast-like cells decreased their bone-forming activity and secreted prostaglandin E 2 (PGE 2 ), which, in turn, can increase the formation and activity of osteoclasts.…”

Section: Discussionmentioning

confidence: 99%

“…It can be speculated that Cd exposure also results in specific effects on cortical and trabecular bone or in alterations of biomechanical properties that are not detected by DXA; this is also supported by experimental studies. (28,31,32) Other possible mechanisms underlying the effects of Cd on bone in humans include secondary effects owing to Cd-induced kidney damage. Decreased circulating levels of 1,25-dihydroxyvitamin D 3 , however, seem Multivariable-adjusted for age (years), education ( 9 and >9 years; yes/no), body mass index (< or !20 kg/m 2 ), parity (0-6), use of postmenopausal hormones (yes/no), ever use of corticosteroids (yes/no), total physical activity (MET-hours/day), smoking status (never/ever), alcohol intake (g ethanol/day), inflammatory joint diseases (yes/no), kidney diseases (yes/no), liver diseases (yes/no), malabsorption (yes/no).…”

Section: Discussionmentioning

confidence: 99%

Long-term cadmium exposure and the association with bone mineral density and fractures in a population-based study among women

Engström

Michaëlsson

Suwazono

et al. 2010

Journal of Bone and Mineral Research

127

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All people are exposed to cadmium (Cd) via food; smokers are additionally exposed. High Cd exposure is associated with severe bone damage, but the public health impact in relation to osteoporosis and fractures at low environmental exposure remains to be clarified. Within the population-based Swedish Mammography Cohort, we assessed urinary Cd [U-Cd, mg/g of creatinine (cr)] as a marker of lifetime exposure and bone mineral density (BMD) by dual-energy X-ray absorptiometry (DXA) among 2688 women. Register-based information on fractures was retrieved from 1997 to 2009. Associations were evaluated by multivariable regression analyses. In linear regression, U-Cd was inversely associated with BMD at the total body ( p < .001), femoral neck ( p ¼ .025), total hip ( p ¼ .004), lumbar spine ( p ¼ .088), and volumetric femoral neck ( p ¼ .013). In comparison with women with U-Cd < 0.50 mg/g of cr, those with U-Cd ! 0.75 mg/g of cr had odds ratios (ORs) of 2.45 [95% confidence interval (CI) 1.51-3.97] and 1.97 (95% CI 1.24-3.14) for osteoporosis at the femoral neck and lumbar spine, respectively. Among never-smokers, the corresponding ORs were 3.47 (95% CI 1.46-8.23) and 3.26 (95% CI 1.44-7.38). For any first fracture (n ¼ 395), the OR was 1.16 (95% CI 0.89-1.50) comparing U-Cd ! 0.50 mg/g of cr with lower levels. Among never-smokers, the ORs (95% CIs) were 2.03 (1.33-3.09) for any first fracture, 2.06 (1.28-3.32) for first osteoporotic fracture, 2.18 (1.20-3.94) for first distal forearm fracture, and 1.89 (1.25-2.85) for multiple incident fractures. U-Cd at low environmental exposure from food in a general population of women showed modest but significant association with both BMD and fractures, especially in neversmokers, indicating a larger concern than previously known. ß

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“…Subsequent studies identifi ed the kidney as the critical organ of Cd toxicity, although Cd also causes adverse effects on the liver, lungs, pancreas, bones, reproductive organs, placenta, and hematopoietic, nervous, and cardiovascular systems (1,2). In a recent paper Bhattacharyya (18) gave an overview on data that confirm low-level Cd-induced osteotoxicity with decreased bone mineral density and calciotropic hormone levels. The Third US Health and Nutrition Examination Survey (NHANES III) (19), which included 8722 US citizens over the age of 40, showed a signifi cant association between Cd urine content and myocardial infarction.…”

Section: Cadmium Toxicity and Carcinogenicitymentioning

confidence: 99%

Cadmium Toxicity Revisited: Focus on Oxidative Stress Induction and Interactions with Zinc and Magnesium

Matović

Buha

Bulat

et al. 2011

Archives of Industrial Hygiene and Toxicology

184

122

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Discovered in late 1817, cadmium is currently one of the most important occupational and environmental pollutants. It is associated with renal, neurological, skeletal and other toxic effects, including reproductive toxicity, genotoxicity, and carcinogenicity. There is still much to fi nd out about its mechanisms of action, biomarkers of critical effects, and ways to reduce health risks. At present, there is no clinically effi cient agent to treat cadmium poisoning due to predominantly intracellular location of cadmium ions. This article gives a brief review of cadmium-induced oxidative stress and its interactions with essential elements zinc and magnesium as relevant mechanisms of cadmium toxicity. It draws on available literature data and our own results, which indicate that dietary supplementation of either essential element has benefi cial effect under condition of cadmium exposure. We have also tackled the reasons why magnesium addition prevails over zinc and discussed the protective role of magnesium during cadmium exposure. These fi ndings could help to solve the problem of prophylaxis and therapy of increased cadmium body burden.

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Cadmium osteotoxicity in experimental animals: Mechanisms and relationship to human exposures

Cited by 142 publications

References 83 publications

The Mechanism of the Osteoprotective Action of a Polyphenol-Rich Aronia melanocarpa Extract during Chronic Exposure to Cadmium is Mediated by the Oxidative Defense System

The Mechanism of the Osteoprotective Action of a Polyphenol-Rich Aronia melanocarpa Extract during Chronic Exposure to Cadmium is Mediated by the Oxidative Defense System

Long-term cadmium exposure and the association with bone mineral density and fractures in a population-based study among women

Cadmium Toxicity Revisited: Focus on Oxidative Stress Induction and Interactions with Zinc and Magnesium

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