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Toxins 2018, 10(10), 407; https://doi.org/10.3390/toxins10100407

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

Institute of Animal Nutrition, Northeast Agricultural University, Harbin 150030, China
These authors contributed equally to the paper.
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Authors to whom correspondence should be addressed.
Received: 5 August 2018 / Revised: 27 September 2018 / Accepted: 2 October 2018 / Published: 9 October 2018
(This article belongs to the Special Issue Effects of Mycotoxins on the Intestine)
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Abstract

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. View Full-Text
Keywords: Zearalenone; N-acetylcysteine; SIEC02 cells; Mitochondrial apoptosis Zearalenone; N-acetylcysteine; SIEC02 cells; Mitochondrial apoptosis
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Wang, J.; Li, M.; Zhang, W.; Gu, A.; Dong, J.; Li, J.; Shan, A. Protective Effect of N-Acetylcysteine against Oxidative Stress Induced by Zearalenone via Mitochondrial Apoptosis Pathway in SIEC02 Cells. Toxins 2018, 10, 407.

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