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Nonylphenol Induces Pancreatic Damage in Rats through Mitochondrial Dysfunction and Oxidative Stress


The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of widely diffused and stable environmental contaminants. Due to its hydrophobicity and long half-life, NP can easily accumulate in living organisms, including humans, where it displays a series of toxic effects. It has been widely reported that NP affects male reproduction. In addition, there is increasing evidence suggesting that NP is detrimental to various organs, including the pancreas. This study investigated the adverse effects of NP exposure on the pancreas. Sprague-Dawley rats were treated with different doses of NP for 90 consecutive days. The data suggested that the body weights of the rats with NP treatments decreased, and highest dose of NP treatment (180 mg/kg) dramatically increased water consumption. Meanwhile, H&E staining and immuno-histochemistry indicated that islets in the pancreases shrunk when the rats were treated with the indicated doses of NP. TUNEL staining demonstrated that NP exposure up-regulated the level of apoptosis in the pancreases in a dose-dependent manner. Besides that, NP exposure inhibited the secretion of insulin and disrupted glucose tolerance. The levels of reactive oxygen species (ROS) and intracellular calcium ([Ca2+]i) in the islets were up-regulated in the groups of rats with NP treatments, but the levels of Mitochondria Membrane Potential (MMP) were down-regulated. These results suggest that NP-induced pancreatic damage in rats occurs through mitochondrial dysfunction and oxidative stress, which caused glucose tolerance disruption and insulin secretion decrease.

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Publication details

The article was received on 26 Dec 2016, accepted on 16 Mar 2017, published on 17 Mar 2017 and first published online on 17 Mar 2017

Article type: Paper
DOI: 10.1039/C6TX00450D
Citation: Toxicol. Res., 2017, Accepted Manuscript
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    Nonylphenol Induces Pancreatic Damage in Rats through Mitochondrial Dysfunction and Oxidative Stress

    X. Li, L. Zhou, Y. Ni, A. Wang, M. Hu, Y. Lin, C. Hong, J. Wan, B. Chen, L. Fang, J. Tong, X. Tong, S. Tao and H. Tian, Toxicol. Res., 2017, Accepted Manuscript , DOI: 10.1039/C6TX00450D

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