Promotion of the articular cartilage proteoglycan degradation by T-2 toxin and selenium protective effect

Liu, Siyuan; Cao, Junling; Shi, Zhijun; Chen, Jinghong; Zhang, Zengtie; Hughes, Claire E.; Caterson, Bruce

doi:10.1631/jzus.b071322

Cited by 38 publications

(25 citation statements)

References 23 publications

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“…Therefore, the T-2 toxin contamination was proposed as a possible cause of KBD (424). In support of this hypothesis, cell culture studies demonstrated that T-2 toxin can inhibit aggrecan synthesis in human chondrocytes, promote aggrecanases and pro-inflammatory cytokines expression, and aggrecan degradation; selenium can inhibit the effects of T-2 toxin (222). A previous study by the same group showed that selenium can partly block T-2 toxin-induced apoptosis in chondrocytes (82).…”

Section: Clinical Disordersmentioning

confidence: 82%

Selenium in Human Health and Disease

Fairweather‐Tait

Bao

Broadley

et al. 2011

Antioxidants & Redox Signaling

1,072

820

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This review covers current knowledge of selenium in the environment, dietary intakes, metabolism and status, functions in the body, thyroid hormone metabolism, antioxidant defense systems and oxidative metabolism, and the immune system. Selenium toxicity and links between deficiency and Keshan disease and Kashin-Beck disease are described. The relationships between selenium intake/status and various health outcomes, in particular gastrointestinal and prostate cancer, cardiovascular disease, diabetes, and male fertility, are reviewed, and recent developments in genetics of selenoproteins are outlined. The rationale behind current dietary reference intakes of selenium is explained, and examples of differences between countries and/or expert bodies are given. Throughout the review, gaps in knowledge and research requirements are identified. More research is needed to improve our understanding of selenium metabolism and requirements for optimal health. Functions of the majority of the selenoproteins await characterization, the mechanism of absorption has yet to be identified, measures of status need to be developed, and effects of genotype on metabolism require further investigation. The relationships between selenium intake/status and health, or risk of disease, are complex but require elucidation to inform clinical practice, to refine dietary recommendations, and to develop effective public health policies.

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Section: Clinical Disordersmentioning

confidence: 82%

Selenium in Human Health and Disease

Fairweather‐Tait

Bao

Broadley

et al. 2011

Antioxidants & Redox Signaling

1,072

820

View full text Add to dashboard Cite

show abstract

“…These effects could be reversed by the addition of selenium. The effects of T-2 toxin have also been studied on aggrecan metabolism in human chondrocytes and cartilage in vitro (Li et al 2008). The perturbed balance between aggrecan synthesis and degradation in cartilage might be an important step in the initiation of the cartilage degradation.…”

Section: Kashin-beck Diseasementioning

confidence: 99%

Public Health Impacts of Foodborne Mycotoxins

Groopman

Pestka

2014

Annu. Rev. Food Sci. Technol.

481

314

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Mycotoxins are toxic and carcinogenic metabolites produced by fungi that colonize food crops. The most agriculturally important mycotoxins known today are aflatoxins, which cause liver cancer and have also been implicated in child growth impairment and acute toxicoses; fumonisins, which have been associated with esophageal cancer (EC) and neural tube defects (NTDs); deoxynivalenol (DON) and other trichothecenes, which are immunotoxic and cause gastroenteritis; and ochratoxin A (OTA), which has been associated with renal diseases. This review describes the adverse human health impacts associated with these major groups of mycotoxins. First, we provide background on the fungi that produce these different mycotoxins and on the food crops commonly infected. Then, we describe each group of mycotoxins in greater detail, as well as the adverse effects associated with each mycotoxin and the populations worldwide at risk. We conclude with a brief discussion on estimations of global burden of disease caused by dietary mycotoxin exposure.

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“…Production of TNF-α results in high level of nitric oxide (NO), which in turn induces chondrocyte apoptosis (Clancy et al, 2004). Our previous study showed that T-2 toxin increased the production of TNF-α (Li et al, 2008). Therefore, TNF-α could play an important role in triggering and modulating of T-2 toxin-induced apoptosis.…”

Section: Rt-pcr Detection Of Bax Bcl-xl Bcl-2 P53 Fas and Caspasementioning

confidence: 99%

T-2 toxin-induced apoptosis involving Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 signaling pathways in human chondrocytes

Chen

Cao

Chu

et al. 2008

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To investigate the effects of T-2 toxin on expressions of Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 on human chondrocytes. Methods: Human chondrocytes were treated with T-2 toxin (1~20 ng/ml) for 5 d. Fas, p53 and other apoptosis-related proteins such as Bax, Bcl-2, Bcl-xL, caspase-3 were determined by Western blot analysis and their mRNA expressions were determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: Increases in Fas, p53 and the pro-apoptotic factor Bax protein and mRNA expressions and a decrease of the anti-apoptotic factor Bcl-xL were observed in a dose-dependent manner after exposures to 1~20 ng/ml T-2 toxin, while the expression of the anti-apoptotic factor Bcl-2 was unchanged. Meanwhile, T-2 toxin could also up-regulate the expressions of both pro-caspase-3 and caspase-3 in a dose-dependent manner. Conclusion: These data suggest a possible underlying molecular mechanism for T-2 toxin to induce the apoptosis signaling pathway in human chondrocytes by regulation of apoptosis-related proteins.

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Promotion of the articular cartilage proteoglycan degradation by T-2 toxin and selenium protective effect

Cited by 38 publications

References 23 publications

Selenium in Human Health and Disease

Selenium in Human Health and Disease

Public Health Impacts of Foodborne Mycotoxins

T-2 toxin-induced apoptosis involving Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 signaling pathways in human chondrocytes

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