Chronic Al2O3-nanoparticle exposure causes neurotoxic effects on locomotion behaviors by inducing severe ROS production and disruption of ROS defense mechanisms in nematode Caenorhabditis elegans
Chronic Al2O3-nanoparticle exposure causes neurotoxic effects on locomotion behaviors by inducing severe ROS production and disruption of ROS defense mechanisms in nematode Caenorhabditis elegans
复制标题
慢性 Al2O3 纳米颗粒暴露通过诱导严重的 ROS 产生和破坏线虫的 ROS 防御机制,对运动行为产生神经毒性作用
DOI:
10.1016/j.jhazmat.2012.03.083
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发表时间:
2012-06-15
影响因子:
13.6
通讯作者:
Wang, Dayong
中科院分区:
文献类型:
--
作者:
Li, Yinxia;Yu, Shunhui;Wang, Dayong
To date, knowledge on mechanisms regarding the chronic nanotoxicity is still largely minimal. In the present study, the effect of chronic (10-day) Al2O3-nanoparticles (NPs) toxicity on locomotion behavior was investigated in the nematode Caenorhabditis elegans. Exposure to 0.01-23.1 mg/L of Al2O3-NPs induced a decrease in locomotion behavior, a severe stress response, and a severe oxidative stress; however, these effects were only detected in nematodes exposed to 23.1 mg/L of bulk Al2O3. Formation of significant oxidative stress in nematodes exposed to Al2O3-NPs was due to both the increase in ROS production and the suppression of ROS defense mechanisms. More pronounced increases in ROS, decreases in SOD activity, and decrease in expression of genes encoding Mn-SODs (sod-2 and sod-3) were detected in nematodes exposed to Al2O3-NPs compared with bulk Al2O3. Moreover, treatment with antioxidants or SOD-3 overexpression not only suppressed oxidative stress but also prevented adverse effects on locomotion behaviors from Al2O3-NPs exposure. Thus, chronic exposure to Al2O3-NPs may have adverse effects on locomotion behaviors by both induction of ROS production and disruption of ROS defense mechanisms. Furthermore, sod-2 and sod-3 mutants were more susceptible than the wild-type to chronic Al2O3-NPs-induced neurotoxicity inhibition. (C) 2012 Elsevier B.V. All rights reserved.