کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
575213 | 1453040 | 2016 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Potential hepatic toxicity of buprofezin at sublethal concentrations: ROS-mediated conversion of energy metabolism
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کلمات کلیدی
MRCSCO1Cox17lactate dehydrogenase BLDHBPFKFB3OGDHIDH2MMPMitochondrial DNA - DNA میتوکندریاROS - ROSBuprofezin - بوپروفیزینmtDNA - دیانای میتوکندریاییMitochondrial respiratory chain - زنجیره تنفسی mitochondrialHepatic toxicity - سمیت کبدیCitrate synthase - سیترات سیتواستاتFumarase - فومارازEnergy metabolism - متابولیسم انرژیMitochondrial membrane potential - پتانسیل غشای میتوکندریTCA cycle - چرخه TCAtricarboxylic acid cycle - چرخه اسید تریکاربوکیلیکReactive oxygen species (ROS) - گونه های اکسیژن واکنشی (ROS)Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
مهندسی و علوم پایه
مهندسی شیمی
بهداشت و امنیت شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Buprofezin is known for its broad-spectrum action and environmental safety. The popularity of buprofezin has raised concerns about its potentially adverse effects on human health and risk to the environment. In this study, we first identified the liver as one of the major organs in which buprofezin accumulated, and we detected a severe oxidative stress response. Next, we demonstrated that sublethal concentrations of buprofezin promoted the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Importantly, reactive oxygen species (ROS) generation partially accounted for the shunting of the energy metabolism through the buprofezin-mediated inhibition of cytochrome c oxidase activity. ROS directly perturbed the activities of several key TCA cycle enzymes, stimulated glycolysis, and indirectly disturbed the activity of the respiratory chain complex by altering mitochondrial DNA (mtDNA). These findings clarify the potential mechanisms of buprofezin toxicity and provide biomarkers for buprofezin-mediated hepatotoxicity at sublethal concentrations.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Hazardous Materials - Volume 320, 15 December 2016, Pages 176-186
Journal: Journal of Hazardous Materials - Volume 320, 15 December 2016, Pages 176-186
نویسندگان
Xiaotong Ji, Tingting Ku, Na Zhu, Xia Ning, Wei Wei, Guangke Li, Nan Sang,