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

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• 作者：Yinxia Li^a ; ¹ ; Shunhui Yu^b ; ¹ ; Quili Wu^a ; ¹ ; Meng Tang^c ; Yuepu Pu^c ; Dayong Wang^a ; ^{dayongw@seu.edu.cn}
• 关键词：Al2O3-nanoparticles ; Chronic exposure ; Neurotoxicity ; Locomotion behavior ; Oxidative stress ; Caenorhabditis elegans
• 刊名：Journal of Hazardous Materials
• 出版年：2012
• 期刊代码：50_03043894
• 类别：ce
• 出版时间：15 June, 2012
• 卷：219-220
• 期：Complete
• 页码：221-230
• 文件大小：1359 K

摘要

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.