Oxidative stress and status of antioxidant enzymes in children with Kashin–Beck disease

Wang, W.; Wei, Shuqin; Luo, Mai; Yu, Bin; Cao, Jing; Zhou, Yang; Wang, Zhi; Goldring, Mary B.; Chen, J.

doi:10.1016/j.joca.2013.08.002

Cited by 47 publications

(31 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These chemicals are produced in response to oxidative stress, which suggest the disease is oxidative stress related. 51 Another human study on subjects with either Kashin-Beck or osteoarthritis revealed downregulation of the expression and synthesis of two important mRNAs and and corresponding enzymes, respectively. The first enzyme was chondroitin sulfate N-acetylgalactosoaminyl-transferase I.…”

Section: Selenium and Cartilagementioning

confidence: 99%

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

Medeiros

2016

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

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.

show abstract

Section: Selenium and Cartilagementioning

confidence: 99%

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

Medeiros

2016

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

show abstract

“…Previously, we demonstrated that KBD is an oxidative stress‐related disease, and oxidative stress has been shown to lead to necrosis in hypertrophic chondrocytes in in vitro studies . The necrosis in the deep zone of the cartilage was caused by oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Death of chondrocytes in Kashin‐Beck disease: Apoptosis, necrosis or necroptosis?

Zhang

et al. 2018

Int J Experimental Path

View full text Add to dashboard Cite

Summary The purpose of this paper was to investigate chondrocyte distribution and death in the cartilage in Kashin‐Beck disease (KBD). Apoptotic chondrocytes were detected by TUNEL assay. Ultrastructural changes were examined by transmission electron microscope (TEM). Biochemical markers associated with apoptosis (eg, caspase‐3) and necroptosis (eg, RIP3) were investigated by immunohistochemistry. In KBD cartilage chondrocyte death was characterized by paler staining of the cells. Multiple chondral cell clusters surrounded the areas lacking cells in the deep zone. The per cent of TUNEL‐positive and RIP3‐positive chondrocytes were higher in the middle zones of KBD samples; however, there was some positive staining for TUNEL but negative staining for caspase‐3. Immunohistochemistry failed to detect significant differences in caspase‐3 levels in KBD children compared to controls, suggesting that beside apoptosis necroptosis dominates as a cell death mechanism in the middle zone of cartilage from KBD children. To clarify further the presence of chondrocyte necroptosis in KBD, we performed TUNEL, caspase‐3 and RIP3 staining in a rat KBD model which is based upon T‐2 toxin treatment under selenium‐deficient conditions. Apoptosis and necroptosis co‐existed in the middle zone in this rat KBD model. Ultrastructural analysis of chondrocyte from deep cartilage revealed abnormal cells with numerous morphological changes, such as plasma membrane breakdown, generalized swelling of the cytoplasm and loss of identifiable organelles. Chondrocyte death by necrosis in the deep zone of cartilages in KBD may be a result of exposure to T‐2 toxin from bone marrow or bloodstream under selenium‐deficient nutrition status in KBD endemic areas. Chondrocyte death plays a key role in either the initiation or the progression of KBD pathogenesis.

show abstract

“…In KBD children, the involved glutathione peroxidase members were GPX4, GPX6, GPX7 (expression ratio = 2.12±0.43, 0.34±0.04, 2.20±0.86, respectively). KBD is an oxidative stress-related disease [19] and members of the glutathione peroxidase family are responsible for antioxidant function of organism. More glutathione peroxidase members are involved in adult KBD.…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Analysis Suggests Bone Development-Related Genes GDF5 and DIO2 Are Involved in the Development of Kashin-Beck Disease in Children Rather than Adults

Wen

Zhang

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

ObjectiveTo investigate the differences in gene expression between children and adults with Kashin-Beck disease (KBD).Methods12 children with KBD and 12 healthy children were selected and divided into 4 KBD vs. control pairs matched according to age and gender, with each pair having 3 KBD children and 3 healthy children. Additionally, 15 adults with KBD and 15 healthy adults were selected and divided into 5 KBD vs. control pairs matched according to age and gender, with each pair having 3 KBD adults and 3 healthy adults. Total RNA was isolated from peripheral blood mononuclear cells (PBMCs) respectively. A total of 367 target genes were selected based on previous genome-wide gene expression profile analysis. Expression levels of the 367 genes were evaluated by customized oligonucleotide microarray and the differentially expressed genes were identified. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was conducted to validate the microarray data.ResultsA total of 95 (25.9%) genes in KBD children and 158 (43.1%) genes in KBD adults were found to exhibit more than two-fold change in gene expression level relative to healthy controls. By comparing differentially expressed genes identified in KBD children to those of KBD adults, 42 genes were found to be differentially expressed only in KBD children. And 105 genes were found to be differentially expressed only in KBD adults. Further, 16 differentially expressed genes common to both KBD children and adults were found to be asynchronously expressed in KBD children compared to KBD adults.ConclusionSignificant differences in gene expression pattern were identified between KBD children and KBD adults, indicating different molecular mechanisms underlying cartilage lesions of KBD children and KBD adults. In addition, bone development-related genes GDF5 (expression ratio = 2.14±0.02) and DIO2 (expression ratio = 0.11±0.05) may contribute to the development of KBD in children rather than in adults.

show abstract

Oxidative stress and status of antioxidant enzymes in children with Kashin–Beck disease

Abstract: KBD is an oxidative stress-related disease, and the oxidative stress in cartilage contributes to the pathology of cartilage damage in KBD.

Cited by 47 publications

References 33 publications

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

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

Death of chondrocytes in Kashin‐Beck disease: Apoptosis, necrosis or necroptosis?

Gene Expression Analysis Suggests Bone Development-Related Genes GDF5 and DIO2 Are Involved in the Development of Kashin-Beck Disease in Children Rather than Adults

Contact Info

Product

Resources

About