Effects of selenium and iodine deficiency on bone, cartilage growth plate and chondrocyte differentiation in two generations of rats

Ren, Feng-Lin; Guo, Xiong; Zhang, R.J.; Wang, Sh.J.; Zuo, Houjuan; Zhang, Z.T.; Dong, Geng; Yu, Yan; Su, Minggang

doi:10.1016/j.joca.2007.03.013

Cited by 81 publications

(71 citation statements)

References 17 publications

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“…Previous studies have shown that Se deficiency impaired the growth of bone and cartilage [Ren et al, 2007], which has a close relationship with the occurrence of osteoarthritis. In this study, there was higher content of aggrecan and type II collagen in the toxin + Se groups when compared with the toxin groups, suggesting a proanabolic or anticatabolic effect of Se on the ECM component.…”

Section: Discussionmentioning

confidence: 95%

The Effects of Mycotoxins and Selenium Deficiency on Tissue-Engineered Cartilage

Lü

Cao²,

Liu³

et al. 2012

Cells Tissues Organs

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Objective: To investigate the effects of 3 mycotoxins, deoxynivalenol (DON), nivalenol (NIV) and T-2 toxin, in the presence and absence of selenium (Se) on the metabolism of tissue-engineered cartilage to mimic conditions found in Kashin-Beck disease (KBD) environments. Materials and Methods: Chondrocytes were seeded onto bone matrix gelatin (BMG) to construct engineered cartilage. The 3 toxins were added to the culture media for 3 weeks followed by immunhistochemical analyses of collagens type II and X, aggrecan, matrix metalloproteinases 1 and 3 (MMP-1 and MMP-3), MMP inhibitors 1 and 3 (TIMP-1 and TIMP-3) and α₂ macroglobulin (α2M). Results: Type II collagen was decreased while type X collagen was increased in response to DON, NIV and T-2 toxin. Aggrecan was reduced by all 3 mycotoxins. Compared with the control, the 3 toxins decreased the expression of α2M, TIMP-1 and TIMP-3, and increased the expression of MMP-1 and MMP-3. Se could partially inhibit the effects of DON, NIV and T-2 toxins. Conclusion: Under the low Se condition, the 3 mycotoxins produced procatabolic changes in cartilage resulting in the loss of aggrecan and type II collagen and promoted a hypertrophic phenotype of chondrocytes characterized by increasing type-X-collagen expression, enhancing the expression of MMPs, while weakening the TIMPs. Se could partially block the effects mentioned above. These results support the hypothesis that the combination of mycotoxin stress and Se deficiency would be the causative factors for KBD.

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Section: Discussionmentioning

confidence: 95%

The Effects of Mycotoxins and Selenium Deficiency on Tissue-Engineered Cartilage

Lü

Cao²,

Liu³

et al. 2012

Cells Tissues Organs

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“…High mycotoxin content in cereals has been implicated. 47 Additionally, iodine deficiency combined with selenium deficiency have also been suggested. 47 For instance, rats fed a diet with the mycotoxin T2 developed minor signs of cartilage pathology.…”

Section: Selenium and Cartilagementioning

confidence: 99%

Copper, iron, and selenium dietary deficiencies negatively impact skeletal integrity: A review

Medeiros

2016

Exp Biol Med (Maywood)

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Nutrients have been known to have a significant role in maintaining the health of the skeleton, both bone and cartilage. The nutrients that have received the majority of the attention are Vitamin D and calcium. However, limited attention has been directed toward three trace elements that may have mechanistic impact upon the skeletal tissues and could compromise skeletal health resulting from inadequate intakes of copper, iron, and selenium. The role of copper and selenium has been known, but the role of iron has only received recent attention. Copper deficiency is thought to impact bone health by a decrease in lysyl oxidase, a copper-containing enzyme, which facilitates collagen fibril crosslinking. Iron deficiency impact upon bone has only recently been discovered but the exact mechanism on how the deficient states enhance bone pathology is speculative. Selenium deficiency has an impact on cartilage thereby having an indirect impact on bone. However, several studies suggest that a mycotoxin when consumed by humans is the culprit in some cartilage disorders and the presence of selenium could attenuate the pathology. This review summarizes the current knowledge base with respect to skeletal integrity when each of these three trace elements are inadequate in diets of both animals and humans.

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“…The hormone thyroxine also plays an important role in the regulation of bone growth and chondrocyte differentiation (Ren et al, 2007). Although plasma thyroxine concentrations were not significantly lower in the iodine-deficient freshwater reference colony and the iodine-sufficient marine colony, concentrations in gulls from lakes Erie, Ontario, and Huron and the Detroit River were markedly lower than those from both the reference colonies (Fox et al, 2007b).…”

Section: Locationmentioning

confidence: 95%

Health of Herring Gulls (Larus argentatus) in Relation to Breeding Location in the Early 1990s. III. Effects on the Bone Tissue

Fox¹,

Lundberg²,

Wejheden³

et al. 2008

Journal of Toxicology and Environmental Health, Part A

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Health effects associated with the Great Lakes environment were assessed in adult herring gulls (Larus argentatus) in the early 1990s, including the size and quality of their bones. Femurs were excised from 140 individuals from 10 colonies distributed throughout the Great Lakes and 2 reference colonies in Lake Winnipeg (freshwater) and the Bay of Fundy (marine). Femurs of gulls from the Great Lakes differed from the freshwater or marine reference for 9 of 12 variables of size, composition, and strength assessed using peripheral quantitative computed tomography (pQCT) and biomechanical testing. Femurs of Great Lakes gulls were significantly smaller in length (−2.9%), periosteal circumference (−2.4%), and crosssectional area (−5.4%) than freshwater reference birds. Femurs of the Great Lakes gulls had a lower significant cortical bone mineral content (−8.1%) and density (−2%) than the marine reference. A significant increase in the amount the bone could bend before it broke (+34%) and the energy required to break it (+44%) and a significant decrease (−16.3%) in stiffness during three-point biomechanical bending test were also detected in Great Lakes versus the freshwater gulls. These differences are indicative of impaired mineralization. When divided into high and low 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity equivalent (TCDD-TEQ) colonies, the amount the bone could bend before it broke and the energy required to break it were significantly higher in the high TEQ colonies, but not high polychlorinated biphenyl (PCB) colonies. Breeding location and dietary choices of Great Lakes herring gulls in the early 1990s resulted in modulations of physiological processes that affected the size, mineralization, and biomechanical properties of bone.

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Effects of selenium and iodine deficiency on bone, cartilage growth plate and chondrocyte differentiation in two generations of rats

Abstract: Combined selenium and iodine deficiency impaired the growth of bone and cartilage. The changes in the expression of ColX and PTHrP induced by combined selenium and iodine deficiency were compatible to measurements of ColX and PTHrP in Kashin-Beck osteoarthropathy.

Cited by 81 publications

References 17 publications

The Effects of Mycotoxins and Selenium Deficiency on Tissue-Engineered Cartilage

The Effects of Mycotoxins and Selenium Deficiency on Tissue-Engineered Cartilage

Copper, iron, and selenium dietary deficiencies negatively impact skeletal integrity: A review

Health of Herring Gulls (Larus argentatus) in Relation to Breeding Location in the Early 1990s. III. Effects on the Bone Tissue

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