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

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 (H(2)O(2)) exposure. The in vivo results showed that H(2)O(2) influenced intestinal expressio...

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Detalles Bibliográficos
Autores principales: Yin, Jie, Wu, Miaomiao, Li, Yuying, Ren, Wenkai, Xiao, Hao, Chen, Shuai, Li, Chunyong, Tan, Bie, Ni, Hengjia, Xiong, Xia, Zhang, Yuzhe, Huang, Xingguo, Fang, Rejun, Li, Tiejun, Yin, Yulong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356869/
https://www.ncbi.nlm.nih.gov/pubmed/27966452
http://dx.doi.org/10.18632/oncotarget.13844
Descripción
Sumario: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 (H(2)O(2)) exposure. The in vivo results showed that H(2)O(2) influenced intestinal expressions of TLRs and apoptosis related genes. H(2)O(2) 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, H(2)O(2) 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 H(2)O(2) significantly enhanced mitochondrial proton leak (P < 0.05). In conclusion, H(2)O(2) affected intestinal TLRs system, apoptosis related genes, and mitochondrial dysfunction in vivo and in vitro models. Meanwhile, low dosage of H(2)O(2) might exhibit a feedback regulatory mechanism against oxidative injury via increasing UCP2 expression and mitochondrial proton leak.