The Role of Mitochondria in T-2 Toxin-Induced Human Chondrocytes Apoptosis

Liu, Jiangtao; Wang, Linlin; Guo, Xiong; Pang, Qiuxiang; Wu, Shixun; Wu, Cuiyan; Xu, Peng; Bai, Yidong

doi:10.1371/journal.pone.0108394

Cited by 55 publications

(33 citation statements)

References 34 publications

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“…However, when selenium was added to these cultures, this partly blocked the pathologies including mitochondrial dysfunction observed in T2-treated cultures and reduced oxidative damage and chondrocyte apoptosis. 53 This study in addition to the previous study above 48 could suggest that the toxin is the primary cause of Kashin-Beck disease, but in the presence of selenium, the pathology is attenuated and possibly absent.…”

Section: Selenium and Cartilagesupporting

confidence: 58%

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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Section: Selenium and Cartilagesupporting

confidence: 58%

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

Medeiros

2016

Exp Biol Med (Maywood)

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“…For example, in human chondrocytes, T-2 toxin (1, 10, 20, 100 ng/ml) treatment for 1-5 days decreased the viabilities in concentration-and time-dependent manners. T-2 toxin (10 and 20 ng/ml) also significantly reduced the ΔΨm and decreased the cellular ATP levels by 20% and 27%, respectively [32].…”

Section: Trichothecenes Induce Mitochondria-dependent Apoptosismentioning

confidence: 92%

“…Interestingly, T-2 toxin in higher doses of 100-200 μM increased the activity of mitochondrial complex I (NADH dehydrogenase), but decreased the oxygen consumption of whole cells and purified mitochondria of yeast cells [46]. In human chondrocytes, T-2 toxin (42.87 nM) treatment for 5 days significantly decreased the activities of mitochondrial complex III (coenzyme Q-cytochrome c reductase), complex IV (cytochrome c oxidase) and complex V (ATP synthase), and induced loss of ΔΨm, decrease of ATP levels, and ROS generation, which however, were reversed by selenium [32]. Similarly, T-2 toxin and DON significantly decreased the respiration rate of electron transport systems of rat liver cells.…”

Section: Trichothecenes Inhibit Mitochondrial Functionmentioning

confidence: 96%

WITHDRAWN: Mitochondria: a critical target in the toxicity of trichothecenes and potential treatment strategies

Huang¹,

Cui²,

Wu³

et al. 2018

Oncotarget

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Copyright: Huang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACTTrichothecenes are secondary metabolites produced by fungi of genus Fusarium. It was known that trichothecenes can bind to the 60S subunit of the eukaryotic ribosomes, resulting in inhibition of protein synthesis. However, emerging evidences suggest that trichothecenes can target the mitochondria to induce mitochondrial dysfunction and mitochondria-dependent apoptosis. Numerous studies have investigated the mitochondria-associated toxicities induced by trichothecenes. Here, we mainly collected the data associated with mitochondria and its relationship with trichothecene-induced toxic effects. We showed that mitochondria are the main site of reactive oxygen species production and mediate the trichothecene-induced apoptosis in various cells. The mitochondrial membrane permeabilization plays critical roles in this apoptotic process. Trichothecenes can penetrate the mitochondrial membrane due to its amphiphilic property, and inhibit the activities of mitochondrial respiratory chain complexes and electron transfer in mitochondria. Besides, trichothecenes reduce the mitochondrial biogenesis and mitochondrial transcription and translation. Peroxisome proliferator-activated receptor-γ co-activator 1α and mammalian target of rapamycin pathway are closely linked to this process. Trichothecenes can activate various microRNAs that may mediate the protein synthesis inhibition. These microRNAs may have a crosstalk with mitochondria to mediate the mitochondrial dysfunction and transcription repression in mitochondrial genome. Numerous natural compounds have been tested for their effective antioxidant and anti-inflammatorycapacities. Specially, mitochondria-targeted antioxidants and mitophagy exhibit outstanding cytoprotective abilitysince they can reduce the mitochondrial reactive oxygen species and maintain the mitochondrial quality. This review may shed some new light on the mitochondriaassociated mechanism underlying the toxicity of trichothecenes and new preventive ways to combat these mycotoxins. www.impactjournals.com/oncotarget/

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“…13) Alle CPPs haben zwei gemeinsa- Zinkfingernukleasen, Transcription-activator-like-effector-Nuklease (Talen) und Clustered-regularly-interspaced-shortpalindromic-repeat(Crispr)-Systeme in Zellen einzuschleusen. [14][15][16][17] Lange galten kationische Sequenzen bei CPPs als unerlässlich, um von der Zelle aufgenommen zu werden. Allerdings widerlegte die Entdeckung des PepNeg-Peptids diese Annahme.…”

Section: Transporthelferunclassified