Effect of chromium on vertebrae, femur and calvaria of adult male rats

Sankaramanivel, Sundararaj; Jeyapriya, R; Hemalatha, D; Djody, S. Sitta; Arunakaran, J.; Srinivasan, Narasimhan

doi:10.1191/0960327105ht627oa

Cited by 20 publications

(14 citation statements)

References 33 publications

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“…Brzóska et al [42,43] indicated that low exposure to cadmium (Cd) may affect the mineralization and biomechanical properties of growing bone, thus increasing the risk of fractures. Sankaramanivel et al[44] revealed that a significant increase in the concentration of Chromium can decrease bone formation rate. Benzo(a)pyrene (BaP) and 7,12-dimethylbenz(a)anthracene (DMBA) are polycyclic aromatic hydrocarbons (PAHs) found in the tar fraction of cigarette smoke.…”

Section: Discussionmentioning

confidence: 99%

Bone turnover in passive smoking female rat: relationships to change in bone mineral density

Gao

et al. 2011

BMC Musculoskelet Disord

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BackgroundMany studies have identified smoking as a risk factor for osteoporosis, but it is unclear whether passive smoking has an effect on bone mineral density and bone turnover and if such an effect could cause osteoporosis.The purpose of the study was to investigate the effect of passive smoking on bone mineral density (BMD) and bone turnover and the relationship between BMD and bone turnover in female rat.MethodsForty-eight female Wistar rats were randomized into six groups: 2-month, 3-month,4-month smoke-exposed rats and their controls. A rat model of passive cigarette smoking was prepared by breeding female rats in a cigarette-smoking box for 2, 3 or 4 months. Serums were analyzed for levels of osteocalcin, bone-specific alkaline phosphatase (b-ALP) and Tartrate-resistant acid phosphatase 5b (TRACP 5b). BMD was assessed at lumbar vertebrae and femur by dual energy X-ray absorptiometry in passive smoking rats and in control rats.ResultsBMD of lumbar spine and femur was lower in 4-month smoke-exposed female rats than that in controls. However, there was no significant difference in serum osteocalcin levels between smoke-exposed rats and controls. Significantly lower b-ALP and higher TRACP 5b were found in the 3-month or 4-month smoke-exposed rats compared to controls. Subsequent analysis showed that b-ALP positively correlated with BMD of the lumbar vertebrae(r = 0.764, P = 0.027) and femur(r = 0.899, P = 0.002) in 4-month smoke-exposed female rats. Furthermore, TRACP 5b levels negatively correlated with BMD of lumbar vertebrae (r = -0.871, P = 0.005) and femur (r = -0.715, P = 0.046) in 4-month smoke-exposed female rats.ConclusionOur data suggest that smoke exposure can inhibit bone formation and increase bone resorption. The hazardous effects of passive smoking on bone status are associated with increased bone turnover in female rat.

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Section: Discussionmentioning

confidence: 99%

Bone turnover in passive smoking female rat: relationships to change in bone mineral density

Gao

et al. 2011

BMC Musculoskelet Disord

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“…For histologic scoring of inflammation and bone erosion, sections were stained with either hematoxylin and eosin or tartrate‐resistant acid phosphatase (TRAP). For TRAP staining, sections were incubated in 0.1 M Tris HCl, pH 9.0, for 18 hours, followed by 0.1 M sodium citrate, pH 5.2, for 3 hours (23). Activated sections were incubated for 30 minutes at 37°C in 0.005% Napthol AS‐MX phosphate (Sigma)/0.01% N , N ‐dimethylformamide/0.03% Fast Red Violet LB salt (Sigma)/50 m M sodium tartrate in 0.1 M acetate, pH 5.0 (24, 25) and counterstained with hematoxylin.…”

Section: Methodsmentioning

confidence: 99%

Resolution of inflammation induces osteoblast function and regulates the Wnt signaling pathway

Matzelle

Gallant

Condon

et al. 2012

Arthritis & Rheumatism

126

106

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Objective Inflammation in the bone microenvironment stimulates osteoclast differentiation, resulting in uncoupling of resorption and formation. Mechanisms contributing to the inhibition of osteoblast function in inflammatory diseases, however, have not been elucidated. Rheumatoid arthritis (RA) is a prototype of an inflammatory arthritis that results in focal loss of articular bone. The paucity of bone repair in inflammatory diseases such as RA raises compelling questions regarding the impact of inflammation on bone formation. The aim of this study was to establish the mechanisms by which inflammation regulates osteoblast activity. Methods We characterized an innovative variant of a murine model of arthritis in which inflammation is induced in C57BL/6J mice by transfer of arthritogenic K/B×N serum and allowed to resolve. Results In the setting of resolving inflammation, bone resorption ceased and appositional osteoblast-mediated bone formation was induced, resulting in repair of eroded bone. Resolution of inflammation was accompanied by striking changes in the expression of regulators of the Wnt/β-catenin pathway, which is critical for osteoblast differentiation and function. Down-regulation of the Wnt antagonists secreted frizzled-related protein 1 (sFRP1) and sFRP2 during the resolution phase paralleled induction of the anabolic and pro–matrix mineralization factors Wnt10b and DKK2, demonstrating the role of inflammation in regulating Wnt signaling. Conclusion Repair of articular bone erosion occurs in the setting of resolving inflammation, accompanied by alterations in the Wnt signaling pathway. These data imply that in inflammatory diseases that result in persistent articular bone loss, strict control of inflammation may not be achieved and may be essential for the generation of an anabolic microenvironment that supports bone formation and repair.

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“…Research carried out to-date has shown only negative effects with regard to hexavalent chromium administration [8], yet trivalent chromium administered by gavage as an inorganic salt or an organic complex is considered to be non-toxic for rats, with LD 50 > 2,000 mg/kg BW [11]. In the experiment undertaken by De Lucca et al [12] involving juvenile rats, in which hexavalent chromium was given as 6.25 and 12.5 mg/kg/10 days dosages, toxic effects were noticed on bone formation.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, while there is little information about long-term exposure to the trivalent form, hexavalent chromium overload is known to modify the natural bone metabolism, especially bone formation and resorption, thus having an effect on skeletal growth and condition [4][5][6][7]. These influences may have rebound as changes to some parameters, among these being density and quality of bone [8]. Such effects may be measured tomographically and densitometrically.…”

Section: Introductionmentioning

confidence: 99%

The peripheral quantitative computed tomographic and densitometric analysis of skeletal tissue in male Wistar rats after chromium sulfate treatment

Bieńko¹,

Radzki²,

Wolski³

2017

Ann Agric Environ Med.

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Introduction. This study evaluates the effects of three different doses of chromium sulphate on bone density and the tomographic parameters of skeletal tissue of rats. Materials and method. The experiment was performed on 40 male Wistar rats which received, by gavage, during 90 days, a chromium sulphate in either a daily dose of 400, 600 or 800 µg/kg BW. At the end of experiment, the rats were scanned using the densitometry method (DXA) to determine the bone mineral density, bone mineral content of total skeleton and vertebral column (L2-L4) and parameters of body composition (Lean Mass and Fat Mass). The isolated femora were scanned using peripheral a quantitative computed tomography method (pQCT) for a separate analysis of the trabecular and cortical bone tissue. The ultimate strength, work to ultimate and the Young modulus of femora was also investigated by the threepoint bending test. Results. The negative impact of chromium was observed in relation to bone tissue. All doses significantly decreased total skeleton density and mineral content, and also had impact upon the isolated femora and vertebral column. Trabecular volumetric bone mineral density and trabecular bone mineral content measured by pQCT in distal femur metaphysis were significantly lower in the experimental groups than in the control. Higher doses of chromium also significantly decreased values of ultimate strength and Young modulus in the investigated femora. Conclusions. The results of the experiment demonstrate that chromium sulphate is dose dependent, and exerts a disadvantageous effect on the skeleton, as it decreases bone density and resistance.

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Effect of chromium on vertebrae, femur and calvaria of adult male rats

Cited by 20 publications

References 33 publications

Bone turnover in passive smoking female rat: relationships to change in bone mineral density

Bone turnover in passive smoking female rat: relationships to change in bone mineral density

Resolution of inflammation induces osteoblast function and regulates the Wnt signaling pathway

The peripheral quantitative computed tomographic and densitometric analysis of skeletal tissue in male Wistar rats after chromium sulfate treatment

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