Effect of co-exposure to nickel and particulate matter on insulin resistance and mitochondrial dysfunction in a mouse model

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• 作者：Xiaohua Xu (1)
  Xiaoquan Rao (2)
  Tse-Yao Wang (2)
  Silis Y Jiang (2)
  Zhekang Ying (1)
  Cuiqing Liu (1) (3)
  Aixia Wang (1)
  Mianhua Zhong (4)
  Jeffrey A Deiuliis (1)
  Andrei Maiseyeu (1)
  Sanjay Rajagopalan (1) (5)
  Morton Lippmann (4)
  Lung-Chi Chen (4)
  Qinghua Sun (1) (2) (5)
  
• 关键词：Nickel ; Inflammation ; Insulin resistance ; Air pollution
• 刊名：Particle and Fibre Toxicology
• 出版年：2012
• 出版时间：December 2012
• 年：2012
• 卷：9
• 期：1
• 全文大小：609KB
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• 作者单位：Xiaohua Xu (1)
  Xiaoquan Rao (2)
  Tse-Yao Wang (2)
  Silis Y Jiang (2)
  Zhekang Ying (1)
  Cuiqing Liu (1) (3)
  Aixia Wang (1)
  Mianhua Zhong (4)
  Jeffrey A Deiuliis (1)
  Andrei Maiseyeu (1)
  Sanjay Rajagopalan (1) (5)
  Morton Lippmann (4)
  Lung-Chi Chen (4)
  Qinghua Sun (1) (2) (5)
  
  1. Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Columbus, Ohio, USA
  2. Division of Environmental Health Sciences, College of Public Health, The Ohio State University, Columbus, Ohio, USA
  3. Department of Physiology, Hangzhou Normal University, Hangzhou, China
  4. Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York, USA
  5. Division of Cardiology, College of Medicine, The Ohio State University, Columbus, Ohio, USA
  

文摘

Background It has been well recognized that toxicity of fine ambient air particulate matter (PM2.5) may depend on its chemical constituents, including components such as soluble metals that may theoretically exert distinctive effects. We have recently demonstrated an important effect of PM2.5 on metabolic function. Since transition metals, such as nickel (Ni), represent an important component of exposure in certain environments, and may significantly influence the toxicity of inhalational exposure, we investigated the effects of Ni as a variable component of ambient PM2.5 exposure. Methods Male ApoE knockout mice were exposed to filtered air (FA), fine-sized nickel sulfate particles alone (Ni) at 0.44 μg/m3, concentrated ambient air PM2.5 (CAPs) at a mean of 70 μg/m3, or CAPs+Ni in Tuxedo, NY, 6 hours/day, 5 days/week, for 3 months. Results Exposure to Ni, irrespective of co-exposure to CAPs, resulted in body weight gain, while exposure to CAPs+Ni significantly enhanced fasting glucose and worsened insulin resistance measures (HOMA-IR), when compared with exposure to CAPs alone. CAPs+Ni exposure induced a significant decrease in phosphorylation of AMP-activated protein kinase (AMPK) α. Exposure to Ni or CAPs+Ni significantly induced microcirculatory dysfunction and increased monocytic cell infiltration into lung and adipose, and decreased uncoupling protein 1 expression at gene and protein levels and several brown adipocyte-specific genes in adipose tissue. Conclusions Ni exposure has effects on metabolic and inflammatory parameters that are comparable to that of CAPs. Additionally, Ni synergistically exacerbates CAPs-induced adverse effects on some of, but not all of, these parameters, that may be mediated via the AMPK signaling pathway. These findings have important implications for inhaled transition metal toxicity that may exert synergistic effects with other PM2.5 components.