Deoxynivalenol-induced oxidative stress and Nrf2 translocation in maternal liver on gestation day 12.5 d and 18.5 d

Yu, Miao; Zhao, Peng; Liao, Yixiang; Wang, Liangliang; Li, Dan; Qin, Chenyuan; Hu, Jiawei; Wang, Zhenting; Cai, Mengyao; Cai, Qiang; Zhang, Feng; Shi, Shaojun; Yang, Wei

doi:10.1016/j.toxicon.2019.02.018

Cited by 27 publications

(17 citation statements)

References 30 publications

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“…A previous study found that after 14 days of exposure to DON (28 mg/kg bw/day), the antioxidant enzyme activities in the liver of mice decreased [ 8 ]. Yu et al also reported similar conclusions [ 9 ]. Oxidative stress is an important mechanism involved in the toxicity of DON [ 8 ].…”

Section: Introductionsupporting

confidence: 69%

The Protective Effect of Heme Oxygenase-1 on Liver Injury Caused by DON-Induced Oxidative Stress and Cytotoxicity

Meng

Wang

Liao

et al. 2021

Toxins

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Deoxynivalenol (DON) is a kind of Fusarium toxin that can cause a variety of toxic effects. Oxidative stress and DNA damage play a critical role in the toxicity of DON. However, previous studies focused more on acute toxicity in vivo/vitro models and lacked subchronic toxicity study in vivo. The potentially harmful effect of DON given at doses comparable to the daily human consumption in target organs, especially the liver, which is the main detoxification organ of DON, is also still not fully understood. Otherwise, Heme Oxygenase-1 (HO-1) has also reduced cell damage under the DON condition according to our previous study. Therefore, we used a rodent model that mimicked daily human exposure to DON and further explored its mechanism of toxic effects on liver tissue and Hepa 1–6 cell line. We also used adeno-associated virus (AAV)-modified HO-1 expressing by tail vein injection and constructed lentivirus-Hepa 1–6 cell line for mimicking HO-1 protective ability under the DON condition. The main results showed that both 30 d and 90 d exposures of DON could cause low-grade inflammatory infiltration around hepatic centrilobular veins. The reactive oxygen species (ROS) and 8-hydroxy-2 deoxyguanosine (8-OHdG) increased during DON exposure, indicating oxidation stress and DNA damage. Significantly, AAV-mediated liver-specific overexpression of HO-1 reduced DON-induced liver damage and indirectly protected the abilities of antioxidant enzyme/DNA damage repair system, while AAV-mediated silence of HO-1 produced the opposite effect. In addition, we found that overexpression of HO-1 could enhance autophagy and combined it with an antioxidant enzyme/DNA damage repair system to inhibit DON-induced hepatocyte damage. Altogether, these data suggest that HO-1 reduces the oxidative stress and DNA damage caused by DON sub-chronic exposure through maintaining DNA repair, antioxidant activity, as well as autophagy.

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Section: Introductionsupporting

confidence: 69%

The Protective Effect of Heme Oxygenase-1 on Liver Injury Caused by DON-Induced Oxidative Stress and Cytotoxicity

Meng

Wang

Liao

et al. 2021

Toxins

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“…Nrf2 is a transcription factor which plays a crucial role in cellular defense. The nuclear translocation of Nrf2 accelerates the removal of ROS thus relieving oxidative stress (41) . In the present study, the nuclear translocation of Nrf2 and upregulation of UCP2 may function as alternate adaptive responses to the overproduction of ROS from mitochondria.…”

Section: Discussionmentioning

confidence: 99%

High glucose induces apoptosis, glycogen accumulation and suppresses protein synthesis in muscle cells of olive flounder Paralichthys olivaceus

et al. 2021

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The effect and the mechanism of high glucose on fish muscle cells are not fully understood. In the present study, muscle cells of olive flounder (Paralichthys olivaceus) were treated with high glucose (33 mM) in vitro. Cells were incubated in three kinds of medium containing 5 mM glucose, 5 mM glucose and 28 mM mannitol (as an isotonic contrast) or 33 mM glucose named the Control group, the Mannitol group and the HG (high glucose) group, respectively. Results showed that high glucose increased the ADP/ATP ratio and the reactive oxygen species (ROS) level, decreased mitochondrial membrane potential (MMP), induced the release of cytochrome C (CytC) and cell apoptosis. High glucose also led to cell glycogen accumulation by increasing the glucose uptake ability and affecting the mRNA expressions of glycogen synthase and glycogen phosphorylase. Meanwhile, it activated AMP-activated protein kinase (AMPK), inhibited the activity of mammalian target of rapamycin (mTOR) signaling pathway and the expressions of myogenic regulatory factors (MRFs). The expressions of myostatin-1 (mstn-1) and E3 ubiquitin ligases including muscle RING-finger protein 1 (murf-1) and muscle atrophy F-box protein (mafbx) were also increased by the high glucose treatment. No difference was found between the Mannitol group and the Control group. These results demonstrate that high glucose has the effects of inducing apoptosis, increasing glycogen accumulation and inhibiting protein synthesis on muscle cells of olive flounder. The mitochondria mediated apoptotic signaling pathway, AMPK and mTOR pathways participated in these biological effects.

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“…This hypothesis seems to be confirmed by subsequent studies in which DON causes maternal liver damage during pregnancy. However, increased expression of Nrf2/HO-1 reduces the amount of reactive oxygen species and thus protect hepatocytes against toxicity of this mycotoxin (Yu et al 2019 ). Taken together, although ribotoxic stress is believed to be the main cellular response of DON in cells, this literature study allows to conclude that oxidative stress and activation of its main response element, i.e., the Nrf2 signaling pathway, is always associated with the influence of DON on different cells and different individuals.…”

Section: Mycotoxinsmentioning

confidence: 99%

Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

Kozieł

Kowalska

Piastowska-Ciesielska

2021

Arch Toxicol

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Nuclear factor erythroid 2-like 2 (Nrf2) is a transcription factor participating in response to cellular oxidative stress to maintain the redox balance. Generation of reactive oxygen species (ROS) and, in consequence, oxidative stress, are physiological as well as pathological processes which take place in almost all types of cells. Nrf2, in response to oxidative stress, activates expression and production of antioxidant enzymes to remove free radicals. However, the role of Nrf2 seems to be more sophisticated and its increased expression observed in cancer cells allows to draw a conclusion that its role is tissue—and condition—dependent. Interestingly, Nrf2 might also play a crucial role in response to environmental factors like mycotoxins. Thus, the aim of the study is to review the role of Nrf2 in cells exposed to most common mycotoxins to check if the Nrf2 signaling pathway serves as the main response element to mycotoxin-induced oxidative stress in human and animal cells and if it can be a target of detoxifying agents.

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Deoxynivalenol-induced oxidative stress and Nrf2 translocation in maternal liver on gestation day 12.5 d and 18.5 d

Cited by 27 publications

References 30 publications

The Protective Effect of Heme Oxygenase-1 on Liver Injury Caused by DON-Induced Oxidative Stress and Cytotoxicity

The Protective Effect of Heme Oxygenase-1 on Liver Injury Caused by DON-Induced Oxidative Stress and Cytotoxicity

High glucose induces apoptosis, glycogen accumulation and suppresses protein synthesis in muscle cells of olive flounder Paralichthys olivaceus

Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

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Deoxynivalenol-induced oxidative stress and Nrf2 translocation in maternal liver on gestation day 12.5 d and 18.5 d

Cited by 27 publications

References 30 publications

The Protective Effect of Heme Oxygenase-1 on Liver Injury Caused by DON-Induced Oxidative Stress and Cytotoxicity

The Protective Effect of Heme Oxygenase-1 on Liver Injury Caused by DON-Induced Oxidative Stress and Cytotoxicity

High glucose induces apoptosis, glycogen accumulation and suppresses protein synthesis in muscle cells of olive flounder Paralichthys olivaceus

Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

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Deoxynivalenol-induced oxidative stress and Nrf2 translocation in maternal liver on gestation day 12.5 d and 18.5 d