Nitric oxide mediates apoptosis and mitochondrial dysfunction and plays a role in growth hormone deficiency by nivalenol in GH3 cells

Huang, Deyu; Cui, Luqing; Guo, Ping; Xue, Xi-Juan; Wu, Qinghua; Hussain, Hamid; Wang, Xu; Zhang, Yuan

doi:10.1038/s41598-017-16908-y

Cited by 16 publications

(6 citation statements)

References 56 publications

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“…Earlier study have indicated that trichothecenes could be rapidly absorbed by the mitochondria from rat liver as early as 2 minutes at 37 °C in a dose-dependent manner [19]. T-2 toxin and DON were shown to change the normal ultrastructural morphology of mitochondria, including formation of megamitochondria, mitochondrial swelling and collapse in mitochondrial cristae in various mammal cells in vitro after exposure to these myctoxins [17,[20][21][22]. In consideration of the fatal role of mitochondria in the oxidative phosphorylation (OXPHOS), Ca 2+ and redox homeostasis and coordination of apoptotic signals, the serious damage to mitochondria is almost lethal to the cells.…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Mitochondria: a critical target in the toxicity of trichothecenes and potential treatment strategies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

confidence: 99%

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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“…However, most antioxidant therapies were applied for at least 12 weeks 15 – 18 . Growth hormone (GH), a peptide secreted by adenohypophysis cells, can reduce OS in some types of cells 19 , 20 ; for this reason, GH has been widely applied to treat pathologies associated with OS, such as burns over large areas, obesity, Alzheimer’s disease and multiple sclerosis 21 . GH bound to the GH receptor (GHR) augments the effects of gonadotropin on GCs and thecal cells, and may improve follicle development and steroidogenesis 22 .…”

Section: Introductionmentioning

confidence: 99%

Growth hormone alleviates oxidative stress and improves oocyte quality in Chinese women with polycystic ovary syndrome: a randomized controlled trial

Gong

Luo

Fan

et al. 2020

Sci Rep

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Oxidative stress (OS) is associated with poor oocyte quality and in vitro fertilization and embryo transfer (IVF-ET) outcomes for patients with polycystic ovary syndrome (PCOS). Growth hormone (GH) can function to reduce OS in some types of cells. Therefore, this prospective randomized study investigated whether GH can significantly improve OS and oocyte quality in women with PCOS. This study enrolled 109 and 50 patients with and without PCOS (controls), respectively. The patients with PCOS were randomly assigned to receive treatment with GH (PCOS-T) or not (PCOS-C). The primary outcome included markers of OS in serum and FF, and secondary outcomes were mitochondrial function in granulosa cells (GCs) and IVF-ET outcomes. The PCOS groups showed higher basal serum total oxidant status (TOS) and OS index (OSI) levels. The follicle fluid (FF) TOS and OSI and GC apoptosis rate were significantly higher, whereas the GC mitochondrial membrane potential (MMP) was significantly lower in the PCOS-C group than in the PCOS-T and non-PCOS control groups (P < 0.05). Significantly more oocytes were fertilised and cleavage stage embryos were produced in the PCOS-T group than in the PCOS-C group (P < 0.05). GH also improved the rates of implantation and clinical pregnancy, but not significantly (P > 0.05). This study showed that GH alleviated the TOS and OSI level in FF and improved GC mitochondrial dysfunction and oocyte quality in patients with PCOS. Clinical Trial Registration Number: This project was prospectively registered on the Chinese Clinical Trial Registry on October 20, 2018. (ChiCTR1800019437) (https://www.chictr.org.cn/edit.aspx?pid=28663&htm=4).

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“…Amplified ROS and RNS actions and oxidative stress have been regarded as critical contributors in the pathogenesis of PitNETs (124)(125)(126)(127)(128)(129)(130). Furthermore, mitochondrial dysfunction has been described showing morphological and functional changes, such as bigger mitochondria with irregular swelling and fragmented cristaes (124).…”

Section: Cellular Bioenergeticsmentioning

confidence: 99%

Architects of Pituitary Tumour Growth

2022

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The pituitary is a master gland responsible for the modulation of critical endocrine functions. Pituitary neuroendocrine tumours (PitNETs) display a considerable prevalence of 1/1106, frequently observed as benign solid tumours. PitNETs still represent a cause of important morbidity, due to hormonal systemic deregulation, with surgical, radiological or chronic treatment required for illness management. The apparent scarceness, uncommon behaviour and molecular features of PitNETs have resulted in a relatively slow progress in depicting their pathogenesis. An appropriate interpretation of different phenotypes or cellular outcomes during tumour growth is desirable, since histopathological characterization still remains the main option for prognosis elucidation. Improved knowledge obtained in recent decades about pituitary tumorigenesis has revealed that this process involves several cellular routes in addition to proliferation and death, with its modulation depending on many signalling pathways rather than being the result of abnormalities of a unique proliferation pathway, as sometimes presented. PitNETs can display intrinsic heterogeneity and cell subpopulations with diverse biological, genetic and epigenetic particularities, including tumorigenic potential. Hence, to obtain a better understanding of PitNET growth new approaches are required and the systematization of the available data, with the role of cell death programs, autophagy, stem cells, cellular senescence, mitochondrial function, metabolic reprogramming still being emerging fields in pituitary research. We envisage that through the combination of molecular, genetic and epigenetic data, together with the improved morphological, biochemical, physiological and metabolically knowledge on pituitary neoplastic potential accumulated in recent decades, tumour classification schemes will become more accurate regarding tumour origin, behaviour and plausible clinical results.

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Nitric oxide mediates apoptosis and mitochondrial dysfunction and plays a role in growth hormone deficiency by nivalenol in GH3 cells

Cited by 16 publications

References 56 publications

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

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

Growth hormone alleviates oxidative stress and improves oocyte quality in Chinese women with polycystic ovary syndrome: a randomized controlled trial

Architects of Pituitary Tumour Growth

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