Response of selenoproteins gene expression profile to mercuric chloride exposure in chicken kidney

Chu, Jia-Hong; Yan, Yu-Xue; Gao, Pei-Chao; Chen, Xuewei; Fan, Rui-Feng

doi:10.1016/j.rvsc.2020.08.020

Cited by 9 publications

(1 citation statement)

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“…Selenium constitutes one of the indispensable trace elements found in both humans and animals, including pigs. Selenium, serving as a constituent of mammalian enzymes like glutathione peroxidase and other selenoproteins, assumes a crucial role in numerous physiological reactions, such as augmenting immunity, fortifying stress resistance, detoxification, and cancer prevention [ 8 , 9 , 10 ]. In the realm of pig feed, the supplementation of selenium takes place through the inclusion of both inorganic and organic forms [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Selenomethionine Alleviates Deoxynivalenol-Induced Oxidative Injury in Porcine Intestinal Epithelial Cells Independent of MAPK Pathway Regulation

Huang,

Zhong,

et al. 2024

Antioxidants

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Deoxynivalenol (DON) is a prevalent contaminant in feed and food, posing a serious threat to the health of both humans and animals. The pig stands as an ideal subject for the study of DON due to its recognition as the most susceptible animal to DON. In this study, the IPEC-J2 cells were utilized as an in vitro model to explore the potential of SeMet in alleviating the intestinal toxicity and oxidative injury in intestinal epithelial cells when exposed to DON. Cells were treated either with or without 4.0 μM SeMet, in combination with or without a simultaneous treatment with 0.5 μg/mL DON, for a duration of 24 h. Then, cells or related samples were analyzed for cell proliferation, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) level, gene expressions, and protein expressions. The results showed that SeMet mitigated the cellular toxicity caused by DON, evidenced by elevated cell proliferation and the reduced LDH release of IPEC-J2 cells in the SeMet + DON group vs. the DON group. Moreover, the SeMet treatment markedly promoted antioxidant functions and decreased the oxidative injury in IPEC-J2 cell, which is indicated by the decreased ROS level and up-regulated mRNA levels of GPX1, TXNRD1, Nrf2, and GCLC in IPEC-J2 cells in the SeMet + DON group vs. the DON group. However, in both the absence and presence of exposure to DON, the SeMet treatment did not affect the protein expression of MAPK (JNK, Erk1/2, and P38) and phosphorylated MAPK (p-JNK, p-Erk1/2, and p-P38) in IPEC-J2 cells. Collectively, SeMet alleviated the DON-induced oxidative injury in porcine intestinal epithelial cells independent of the MAPK pathway regulation.

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