Effects of moniliformin and selenium on human articular cartilage metabolism and their potential relationships to the pathogenesis of Kashin-Beck disease

Zhang, An; Cao, Junling; Yang, Bo; Chen, Jinghong; Zhang, Zengtie; Liu, Siyuan; Fu, Qiang; Hugnes, Clare E.; Caterson, Bruce

doi:10.1631/jzus.b0900074

Cited by 27 publications

(11 citation statements)

References 32 publications

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“…Similar in vitro effects have also been reported by Zhang et al [18] where an exposure of human fetal chondrocytes for 5 days to MON (1000, 2000, 4000, 8000, 16,000 and 32,000 µg L −1 ) was enough to significantly decrease cell viability. The same authors have shown through immunohistochemistry that MON (4000 µg L −1 ) triggered the expression of MMP-13, and promoted the catabolism of aggrecan and Coll II in human chondrocytes exposed for 16 days.…”

Section: Discussionsupporting

confidence: 87%

Preliminary Evaluation of Moniliformin as a Potential Threat for Teleosts

Gonçalves¹,

Tarasco

Schatzmayr³

et al. 2018

Fishes

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Aquaculture feed manufacturers and producers increasingly recognize the importance of mycotoxins, which contaminate plant-based meals used in compound aquafeeds, and their potential to negatively impact production. Though data on the worldwide occurrence of legislated mycotoxins e.g., trichothecenes and zearalenone (ZEN) are well documented, relatively little information is available regarding other mycotoxins also produced by Fusarium, notably moniliformin (MON). Given that MON is known to affect the survival, growth, skeletal formation and bone mineralization in terrestrial species, its widespread occurrence on maize and maize by-products typically used in aquaculture makes it relevant to study these parameters in teleost fish. In the present work we have tested the effect of MON exposure on survival, bone development and mineralization using zebrafish (Danio rerio) as a model species and fish derived osteo-chondroprogenitor cell line for in vitro studies. Moniliformin exposure did not decrease bone mineralization in zebrafish larvae or extracellular matrix mineralization in the mineralogenic cell line VSa13. Here, the minimal in vitro cytotoxicity concentration was found to be 1000 µg L −1 MON. Incidence of deformities was also not altered by MON at the concentration tested (450 µg L −1 ) although larval growth was affected, as shown by a decrease in the standard length of exposed specimens at 20 days post fertilization. Survival decreased significantly in larvae exposed to MON concentrations higher than 900 µg L −1 . Influence of MON on survival and growth might be relevant for aquaculture industry. As MON is a water-soluble mycotoxin, its leaching from feed is highly probable, so MON assimilation into the surrounding aqueous environment should also be considered. Tested levels in fish larvae are within the reported occurrence levels of MON in commercial feed and plant meals.

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Section: Discussionsupporting

confidence: 87%

Preliminary Evaluation of Moniliformin as a Potential Threat for Teleosts

Gonçalves¹,

Tarasco

Schatzmayr³

et al. 2018

Fishes

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“…Zhao et al reported that polysaccharide extracted from selenium-enriched Ganoderma lucidum had a DNAprotective effect against oxidative damage by hydroxyl radicals and that a high selenium concentration had a much stronger effect against hydroxyl and superoxide radicals 30 . In addition, Zhang et al reported that moniliformin toxin promoted the catabolism of aggrecan and type II collagen in cultured human chondrocytes and that selenium could partially alleviate the damage of aggrecan induced by moniliformin toxin 37 . Moreover, in China, endemic selenium deficiency is often accompanied by endemic iodine deficiency; all selenium-deficient areas of China are also areas of iodine deficiency disease 38 .…”

Section: Discussionmentioning

confidence: 99%

An animal model of Kashin–Beck disease induced by a low-nutrition diet and exposure to T-2 toxin

Kang

Yao

Yang

et al. 2013

Osteoarthritis and Cartilage

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“…It is also involved in the regulation of HSP27 26. CRK can promote cell motility by a Rho and hyaluronan‐CD44‐dependent signaling mechanism 27, and may be relevant in KBD chondrocytes, since increased expression of CD44 has been shown in KBD cartilage 28, and in mycotoxin moniliformin‐affected cartilage 29. Keratin 1 (K2C1) contributes to signal transduction as a signal receptor complex by binding with integrin.…”

Section: Discussionmentioning

confidence: 99%