The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the 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 treated with NP decreased, and the highest dose of NP treatment (180 mg kg-1) dramatically increased water consumption by rats. Meanwhile, H&E staining and immunohistochemistry 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 this, 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 treated with NP, but the levels of Mitochondrial Membrane Potential (MMP) were down-regulated. These results suggest that NP-induced pancreatic damage in rats occurs through mitochondrial dysfunction and oxidative stress, which causes disruption of glucose tolerance and decrease in insulin secretion.

中文翻译：

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壬基酚通过线粒体功能障碍和氧化应激诱导大鼠胰腺损伤。

有机烷基酚4-壬基酚（NP）被认为是一种破坏内分泌的化学物质（EDC），它是一种广泛扩散且稳定的环境污染物。由于其疏水性和长的半衰期，NP可以很容易地在包括人类在内的活生物体中积累，并在其中表现出一系列的毒性作用。据广泛报道，NP影响雄性生殖。另外，越来越多的证据表明，NP对包括胰腺在内的各种器官都是有害的。这项研究调查了NP暴露对胰腺的不利影响。连续90天用不同剂量的NP处理Sprague-Dawley大鼠。数据表明，NP处理的大鼠体重下降，而最大剂量的NP处理（180 mg kg-1）显着增加了大鼠的耗水量。同时，H＆E染色和免疫组织化学表明，当使用指定剂量的NP处理大鼠时，胰岛中的胰岛缩小。TUNEL染色表明，NP暴露以剂量依赖的方式上调了胰腺细胞凋亡的水平。除此之外，NP暴露会抑制胰岛素分泌并破坏葡萄糖耐量。NP处理的大鼠组胰岛中的活性氧（ROS）和细胞内钙（[Ca2 +] i）的水平上调，但线粒体膜电位（MMP）的水平下调。这些结果表明，NP诱导的大鼠胰腺损伤是通过线粒体功能障碍和氧化应激引起的，这会破坏葡萄糖耐量并降低胰岛素分泌。E染色和免疫组织化学表明，当用指定剂量的NP治疗大鼠时，胰岛中的胰岛缩小。TUNEL染色表明，NP暴露以剂量依赖的方式上调了胰腺细胞凋亡的水平。除此之外，NP暴露会抑制胰岛素分泌并破坏葡萄糖耐量。NP处理的大鼠组胰岛中的活性氧（ROS）和细胞内钙（[Ca2 +] i）水平上调，但线粒体膜电位（MMP）水平下调。这些结果表明，NP诱导的大鼠胰腺损伤是通过线粒体功能障碍和氧化应激引起的，这会破坏葡萄糖耐量并降低胰岛素分泌。E染色和免疫组织化学表明，当用指定剂量的NP治疗大鼠时，胰岛中的胰岛缩小。TUNEL染色表明，NP暴露以剂量依赖的方式上调了胰腺细胞凋亡的水平。除此之外，NP暴露会抑制胰岛素分泌并破坏葡萄糖耐量。NP处理的大鼠组胰岛中的活性氧（ROS）和细胞内钙（[Ca2 +] i）水平上调，但线粒体膜电位（MMP）水平下调。这些结果表明，NP诱导的大鼠胰腺损伤是通过线粒体功能障碍和氧化应激引起的，这会破坏葡萄糖耐量并降低胰岛素分泌。