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

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

Particle and fibre toxicology (2012-11-07)
Xiaohua Xu, Xiaoquan Rao, Tse-Yao Wang, Silis Y Jiang, Zhekang Ying, Cuiqing Liu, Aixia Wang, Mianhua Zhong, Jeffrey A Deiuliis, Andrei Maiseyeu, Sanjay Rajagopalan, Morton Lippmann, Lung-Chi Chen, Qinghua Sun
摘要

It has been well recognized that toxicity of fine ambient air particulate matter (PM(2.5)) 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 PM(2.5) 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 PM(2.5) exposure. Male ApoE knockout mice were exposed to filtered air (FA), fine-sized nickel sulfate particles alone (Ni) at 0.44 μg/m(3), concentrated ambient air PM(2.5) (CAPs) at a mean of 70 μg/m(3), or CAPs+Ni in Tuxedo, NY, 6 hours/day, 5 days/week, for 3 months. 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. 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 PM(2.5) components.

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Sigma-Aldrich
硫酸镍(II) 六水合物, ACS reagent, ≥98%
Sigma-Aldrich
硫酸镍(II), anhydrous, 99.99% trace metals basis
Sigma-Aldrich
硫酸镍(II) 六水合物, ReagentPlus®, powder or crystals
Supelco
硫酸镍(II) 六水合物, ≥99.99% trace metals basis
Sigma-Aldrich
硫酸镍(II) 七水合物, purum p.a., crystallized, ≥99.0% (KT)
Sigma-Aldrich
硫酸镍(II) 七水合物, 99.999% trace metals basis
Sigma-Aldrich
硫酸镍(II)六水合物 七水合物, for nickel plating, DIN 50970 H, ≥20.6% Ni and Co basis
Sigma-Aldrich
硫酸镍(II) 六水合物, puriss. p.a., ACS reagent, 99-102.0%