Functional disruption in epidermal barrier enhances toxicity and accumulation of graphene oxide

被引：8
作者：
Ding, Xuecheng [1 ,2 ]
Rui, Qi [1 ]
Wang, Dayong [2 ]
机构：
[1] Nanjing Agr Univ, Coll Life Sci, Nanjing 210095, Jiangsu, Peoples R China
[2] Southeast Univ, Med Sch, Minist Educ, Key Lab Environm Med Engn, Nanjing 210009, Jiangsu, Peoples R China
来源：
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY | 2018年 / 163卷
关键词：
Epidermal barrier; Molecular basis; Nanotoxicity; Graphene oxide; Caenorhabditis elegans; NEMATODE CAENORHABDITIS-ELEGANS; WALLED CARBON NANOTUBES; INNATE IMMUNE-RESPONSE; C-ELEGANS; NANOPOLYSTYRENE PARTICLES; DEFENSE SYSTEM; COLLAGEN GENES; CELL ADHESION; NANOPARTICLES; PROTEIN;
D O I：
10.1016/j.ecoenv.2018.07.102
中图分类号：
X [环境科学、安全科学];
学科分类号：
08 ; 0830 ;
摘要：
In Caenorhabditis elegans, mutation of mit-7 causes the deficits in epidermal barrier. Using the nematodes with epidermal-specific RNA interference (RNAi) knockdown of mlt-7 as a genetic tool, we found that epidermal-specific RNAi knockdown of mIt-7 resulted in a susceptibility to graphene oxide (GO) toxicity, and enhanced GO accumulation in the body. Epidermal-development related proteins of BLI-1 and IFB-1 acted as downstream targets of MLT-7, and mediated the function of MLT-7 in maintaining the epidermal barrier. Antimicrobial proteins of NLP-30 and CNC-2 also acted as downstream targets of MLT-7 in the regulation of GO toxicity. Epidermal-specific RNAi knockdown of nlp-30 or cnc-2 enhanced GO toxicity and accumulation in bli-1(RNAi) or ifb-1(RNAi) nematodes. Our data highlights the importance of maintaining normal epidermal barrier for nematodes against the GO toxicity.
引用
收藏
页码：456 / 464
页数：9
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