کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6315761 | 1619161 | 2016 | 10 صفحه PDF | دانلود رایگان |
- Root tips of CuO NPs-treated Arabidopsis suffered oxidative stress and cell damage.
- CuO NPs (10Â mg/L) caused 1035 up-regulated genes and 623 down-regulated genes.
- 47 up-regulated genes response to oxidative stress were analyzed.
- RT-PCR results of oxidative stress-related genes supported microarray findings.
- Oxidative stress was caused by CuO NPs themselves rather than the released Cu2+.
Microarray analysis of toxicogenomic effects of CuO NPs on Arabidopsis thaliana was conducted. Arabidopsis growth was significantly inhibited by CuO NPs (10 and 20 mg/L). CuO NPs (10 and 20 mg/L) caused significant root damage after short-time (0-2 h) exposure while their corresponding Cu2+ ions (0.80 and 1.35 mg/L) did not show any root damage. After longer exposure times (1 and 2 days), Cu2+ ions induced obvious root damage, indicating that released Cu2+ ions from CuO NPs contributed partial toxicity during CuO NPs exposure. After CuO NPs (10 mg/L) exposure for 2 h, reactive oxygen species (ROS) generation in root tips was much higher than that in the corresponding Cu2+ ions (0.8 mg/L) treatment. The gene ontology categories identified from microarray analysis showed that CuO NPs (10 mg/L) caused 1658 differentially expressed genes (p < 0.01, fold change>3). Of these, 1035 and 623 genes were up-regulated and down-regulated, respectively. 47 genes among all the up-regulated genes were response to oxidative stress, in which 19 genes were also related to “response to abiotic stimulus” and 12 genes were involved in the phenylpropanoid biosynthesis of the KEGG metabolic pathway. The expression of all the selected genes (RHL41, MSRB7, BCB, PRXCA, and MC8) measured using quantitative RT-PCR was consistent with the microarray analysis. CuO NPs contributed much stronger up-regulation of oxidative stress-related genes than the corresponding Cu2+ ions.
Journal: Environmental Pollution - Volume 212, May 2016, Pages 605-614