中文摘要：

目的：研究重金属暴露对秀丽线虫脂肪积累的急性中毒效应,鉴定重金属暴露秀丽线虫中发生表达模式改变的与脂肪酸代谢相关的基因。方法：银、镉、铬、铜、汞、锰和锌作为测试重金属,Nile Red荧光探针染色分析重金属暴露线虫肠道的脂肪酸含量变化,并测定重金属暴露线虫中脂肪酸代谢相关基因的转录水平变化。结果：在所分析重金属中,高浓度银、铬和铜暴露可以显著诱导线虫肠道脂肪积累的增加,而高浓度镉暴露可以显著降低线虫肠道脂肪的积累。而且,与对照组相比,高浓度的银和铬暴露不明显影响基因pod-2、gei-7、lbp-8、gpd-3、W05G11.6、C03H5.4和C07E3.9的表达水平,而在暴露的线虫动物中,基因fat-5、fat-6和fat-7的表达水平显著升高,lbp-1、acs-2和ech-1的表达水平显著降低。结论：高浓度银、铬、铜和镉暴露可以导致异常的秀丽线虫肠道的脂肪积累变化,其中高浓度银和铬暴露导致线虫脂肪积累增加的主要原因可能归因于暴露动物体内脂肪酸去饱和与线粒体β-氧化代谢途径以及脂肪酸结合能力的异常。

英文摘要：

Objective：To investigate the acute toxicity of metal exposure on fat storage,and to identify the sensitive genes required for the metabolism of fatty acid in metal exposed nematode Caenorhabditis elegans.Method：Silver（Ag）,cadmium（Cd）,chromium（Cr）,copper（Cu）,mercury（Hg）,manganese（Mn）,and zinc（Zn） were chosen as test metals.Nile Red staining was used to evaluate the content of fatty acid in control and metal exposed nematodes.The transcription levels of genes required for fatty acid metabolism were further examined in control and metal exposed nematodes.Results：Among the examined metals,exposure to Ag and Cr at the concentrations of 75 and 200 μmol·L-1 and exposure to Cu at the concentration of 75 μmol·L-1 significantly increased the fat storage,and exposure to Cd at the concentration of 200 μmol·L-1 significantly decreased the fat storage in intestine of nematodes.Moreover,exposure to Ag and Cr at the concentration of 200 μmol·L-1 did not affect the expression levels of pod-2,gei-7,lbp-8,gpd-3,W05G11.6,C03H5.4 and C07E3.9 compared with control.In contrast to this,the fat-5,fat-6,and fat-7 expression was dramatically increased,and the expression of lbp-1,acs-2 and ech-1 was significantly decreased in 200 μmol·L-1 Ag and Cr exposed nematodes compared with control.Conclusion：The abnormal fat storage can be observed in nematodes exposed to high levels of Ag,Cr,Cu,and Cd,and the observed formation of increased fat storage in Ag and Cr exposed nematodes was largely due to the abnormalities of fatty acid desaturation,mitochondrial β-oxidation,and fatty acid binding.