Research Papers:

Toxicity assessment of hydrogen peroxide on Toll-like receptor system, apoptosis, and mitochondrial respiration in piglets and IPEC-J2 cells

Jie Yin, Miaomiao Wu, Yuying Li, Wenkai Ren, Hao Xiao, Shuai Chen, Chunyong Li, Bie Tan, Hengjia Ni, Xia Xiong, Yuzhe Zhang, Xingguo Huang, Rejun Fang, Tiejun Li and Yulong Yin _

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Oncotarget. 2017; 8:3124-3131. https://doi.org/10.18632/oncotarget.13844

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Jie Yin1,2,*, Miaomiao Wu1,*, Yuying Li1,2,*, Wenkai Ren1,2, Hao Xiao1, Shuai Chen1,2, Chunyong Li1, Bie Tan1, Hengjia Ni1, Xia Xiong1, Yuzhe Zhang1, Xingguo Huang3,4, Rejun Fang3, Tiejun Li1,4, Yulong Yin1,4,5

1Scientific Observing and Experimental Station of Animal Nutrition and Feed Science in South-Central, Ministry of Agriculture, Hunan Provincial Engineering Research Center of Healthy Livestock, Key Laboratory of Agro-ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences, Changsha, Hunan 410125, China

2University of Chinese Academy of Sciences, Beijing 100039, China

3Department of Animal Science, Hunan Agriculture University, Changsha, Hunan 410125, China

4Hunan Co-Innovation Center of Animal Production Safety, Changsha, Hunan 410128, China

5College of Animal Science of South China Agricultural University, Guangzhou 510642, China

*These authors contributed equally to this work

Correspondence to:

Tiejun Li, email: [email protected]

Yulong Yin, email: [email protected]

Keywords: H2O2, TLRs, apoptosis, mitochondrial respiration, piglet

Received: September 28, 2016     Accepted: November 24, 2016     Published: December 09, 2016


In this study, expressions of toll-like receptors (TLRs) and apoptosis-related genes in piglets and mitochondrial respiration in intestinal porcine epithelial cells were investigated after hydrogen peroxide (H2O2) exposure. The in vivo results showed that H2O2 influenced intestinal expressions of TLRs and apoptosis related genes. H2O2 treatment (5% and 10%) downregulated uncoupling protein 2 (UCP2) expression in the duodenum (P < 0.05), while low dosage of H2O2 significantly increased UCP2 expression in the jejunum (P < 0.05). In IPEC-J2 cells, H2O2 inhibited cell proliferation (P < 0.05) and caused mitochondrial dysfunction via reducing maximal respiration, spare respiratory, non-mitochondrial respiratory, and ATP production (P < 0.05). However, 50 uM H2O2 significantly enhanced mitochondrial proton leak (P < 0.05). In conclusion, H2O2 affected intestinal TLRs system, apoptosis related genes, and mitochondrial dysfunction in vivo and in vitro models. Meanwhile, low dosage of H2O2 might exhibit a feedback regulatory mechanism against oxidative injury via increasing UCP2 expression and mitochondrial proton leak.

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