Individual and combined effects of  Fusarium  toxins on apoptosis in PK15 cells and the protective role of  N -acetylcysteine

Zhang, Wei; Zhang, Shihua; Zhang, Meiling; Yang, Lige; Cheng, Baohua; Li, Jianping; Shan, Anshan

doi:10.1016/j.fct.2017.10.057

Cited by 46 publications

(27 citation statements)

References 46 publications

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“…In this experiment, our data clearly demonstrated that the activities of Gpx and GR were significantly increased after NAC pretreatment, and that ROS was significantly reduced. Our study showed that NAC preconditioning could alleviate the activity of antioxidant enzymes in SIEC02 cells, and this result is also consistent with another team's results on the pig kidney PK15 cells [ 49 ]. In addition, pretreatment with NAC positively reduced ROS generation, suggesting a potential antioxidant for NAC, which is conformed to reduce cellular ROS by adding NAC in Jurkat T cells [ 50 ].…”

Section: Discussionsupporting

confidence: 92%

“…SYBR Green I RT-PCR kit (Takara, Dalian, China) was used to measure the mRNA expression of apoptosis-related genes (Bcl-2, Bax, cyto c, caspase-9, caspase-3), and β-actin was used as the internal control gene to correct for differences. The sequences of the specific primers used were as follows in Table 1 [ 49 ]. The sequences of the specific primers in this study used were designed from published GenBank sequences, and they were synthesized by Sangon (Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

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Protective Effect of N-Acetylcysteine against Oxidative Stress Induced by Zearalenone via Mitochondrial Apoptosis Pathway in SIEC02 Cells

Wang

Zhang

et al. 2018

Toxins

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Zearalenone (ZEN), a nonsteroidal estrogen mycotoxin, is widely found in feed and foodstuffs. Intestinal cells may become the primary target of toxin attack after ingesting food containing ZEN. Porcine small intestinal epithelial (SIEC02) cells were selected to assess the effect of ZEN exposure on the intestine. Cells were exposed to ZEN (20 µg/mL) or pretreated with (81, 162, and 324 µg/mL) N-acetylcysteine (NAC) prior to ZEN treatment. Results indicated that the activities of glutathione peroxidase (Gpx) and glutathione reductase (GR) were reduced by ZEN, which induced reactive oxygen species (ROS) and malondialdehyde (MDA) production. Moreover, these activities increased apoptosis and mitochondrial membrane potential (ΔΨm), and regulated the messenger RNA (mRNA) expression of Bax, Bcl-2, caspase-3, caspase-9, and cytochrome c (cyto c). Additionally, NAC pretreatment reduced the oxidative damage and inhibited the apoptosis induced by ZEN. It can be concluded that ZEN-induced oxidative stress and damage may further induce mitochondrial apoptosis, and pretreatment of NAC can degrade this damage to some extent.

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Section: Discussionsupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

Protective Effect of N-Acetylcysteine against Oxidative Stress Induced by Zearalenone via Mitochondrial Apoptosis Pathway in SIEC02 Cells

Wang

Zhang

et al. 2018

Toxins

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“…NAC, a well-known thiol antioxidant that acts as a glutathione precursor was widely used in clinical practice [ 108 ]. Studies have demonstrated that NAC could partially reverse the damages including oxidative damage and apoptosis induced by Fusarium toxin in PK15 cells [ 20 ]. What’s more, studies have showed that ZEA induced epigenetic effects and genotoxic including inhibiting GJIC, chromosome aberrations and DNA lesions through oxidative process, which was partially prevented by using Vitamin E [ 53 , 57 ].…”

Section: What Can Protect the Damage Or Cell Death Induced By Zeamentioning

confidence: 99%

“…In addition, many studies have revealed that ZEA could cause cell apoptosis and necrosis. ZEA induced obvious apoptosis in endometrial stromal cells (ESCs), PK15 cells, Leydig cells, Sertoli cells, raw 264.7 macrophages and porcine granulosa cells [ 18 , 20 , 21 , 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

Zearalenone Promotes Cell Proliferation or Causes Cell Death?

Zheng

Wang

et al. 2018

Toxins

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Zearalenone (ZEA), one of the mycotoxins, exerts different mechanisms of toxicity in different cell types at different doses. It can not only stimulate cell proliferation but also inhibit cell viability, induce cell apoptosis, and cause cell death. Thus, the objective of this review is to summarize the available mechanisms and current evidence of what is known about the cell proliferation or cell death induced by ZEA. An increasing number of studies have suggested that ZEA promoted cell proliferation attributing to its estrogen-like effects and carcinogenic properties. What’s more, many studies have indicated that ZEA caused cell death via affecting the distribution of the cell cycle, stimulating oxidative stress and inducing apoptosis. In addition, several studies have revealed that autophagy and some antioxidants can reverse the damage or cell death induced by ZEA. This review thoroughly summarized the metabolic process of ZEA and the molecular mechanisms of ZEA stimulating cell proliferation and cell death. It concluded that a low dose of ZEA can exert estrogen-like effects and carcinogenic properties, which can stimulate the proliferation of cells. While, in addition, a high dose of ZEA can cause cell death through inducing cell cycle arrest, oxidative stress, DNA damage, mitochondrial damage, and apoptosis.

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“…With a primary focus on combinations of mycotoxins with comparably high prevalence but different modes of action (e.g., DON and ZEN), a vast number of different mycotoxin combinations have already been tested in vitro. The majority of these studies investigated primarily cytotoxic effects and/or related readouts in different cell models (e.g., Ren et al 2017 ; Smith et al 2017a , b , 2018 ; Wang et al 2014 ; Zhang et al 2018 ; Zhou et al 2017 ). Based on these studies, it appears that the impact of the combination of DON and ZEN varies substantially depending on the ratio of test compounds applied, the concentration range, and the cell model, ranging from antagonistic to additive and even synergistic effects.…”

Section: Current Status Of Combinatory Effects Of Zen and Its Modifiementioning

confidence: 99%

A critical evaluation of health risk assessment of modified mycotoxins with a special focus on zearalenone

et al. 2018

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A comprehensive definition introducing the term "modified mycotoxins" to encompass all possible forms in which mycotoxins and their modifications can occur was recently proposed and has rapidly gained wide acceptance within the scientific community. It is becoming increasingly evident that exposure to such modified mycotoxins due to their presence in food and feed has the potential to pose a substantial additional risk to human and animal health. Zearalenone (ZEN) is a well-characterized Fusarium toxin. Considering the diversity of modified forms of ZEN occurring in food and feed, the toxicologically relevant endocrine activity of many of these metabolites, and the fact that modified forms add to a dietary exposure which approaches the tolerable daily intake by free ZEN alone, modified forms of ZEN present an ideal case study for critical evaluation of modified mycotoxins in food safety. Following a summary of recent scientific opinions of EFSA dealing with health risk assessment of ZEN alone or in combination with its modified forms, uncertainties and data gaps are highlighted. Issues essential for evaluation and prioritization of modified mycotoxins in health risk assessment are identified and discussed, including opportunities to improve exposure assessment using biomonitoring data. Further issues such as future consideration of combinatory effects of the parent toxin with its modified forms and also other compounds co-occurring in food and feed are addressed. With a particular focus on ZEN, the most pressing challenges associated with health risk assessment of modified mycotoxins are identified and recommendations for further research to fill data gaps and reduce uncertainties are made.

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Individual and combined effects of Fusarium toxins on apoptosis in PK15 cells and the protective role of N -acetylcysteine

Cited by 46 publications

References 46 publications

Protective Effect of N-Acetylcysteine against Oxidative Stress Induced by Zearalenone via Mitochondrial Apoptosis Pathway in SIEC02 Cells

Protective Effect of N-Acetylcysteine against Oxidative Stress Induced by Zearalenone via Mitochondrial Apoptosis Pathway in SIEC02 Cells

Zearalenone Promotes Cell Proliferation or Causes Cell Death?

A critical evaluation of health risk assessment of modified mycotoxins with a special focus on zearalenone

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