Gopalakrishnan Nair Prakash M, Chung Ill Min
Department of Applied Biosciences, College of Life and Environmental Sciences, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 143-701, Seoul, South Korea.
Comp Biochem Physiol B Biochem Mol Biol. 2015 Dec;190:1-7. doi: 10.1016/j.cbpb.2015.08.004. Epub 2015 Aug 14.
Zinc oxide nanoparticles (ZnONPs) are widely used in several commercial products due to their unique physicochemical properties. However, their release into the aquatic environments through various anthropogenic activities will lead to toxic effect in aquatic organisms. Although several investigations have been reported on the effect of ZnONPs in aquatic organisms using traditional end points such as survival, growth, and reproduction, the molecular level end points are faster and sensitive. In this study, the expression of different genes involved in oxidative stress response, detoxification, and cellular defense was studied in an ecotoxicologically important bio-monitoring organism Chironomus riparius in order to understand the subcellular effects of ZnONPs. The fourth instar larvae were exposed to 0, 0.2, 2, 10, and 20 mg/L of ZnONPs and Zn ions (in the form of ZnSO4.7H2O) for 24 and 48 h period. The expression of CuZn superoxide dismutase, manganese superoxide dismutase, catalase, phospholipid hydroperoxide glutathione peroxidase, thioredoxin reductase 1 and delta-3, sigma-4 and epsilon-1 classes of glutathione S-transferases, cytochrome p4509AT2, and heat shock protein 70 were studied using real-time polymerase chain reaction method. Gene expression results showed that the expression of genes related to oxidative stress response was more pronounced as a result of ZnONPs exposure as compared to Zn ions. The mRNA expression of genes involved in detoxification and cellular protection was also modulated. Significantly higher expression levels of oxidative stress-related genes shows that oxidative stress is an important mechanism of toxicity as a result of ZnONPs exposure in C. riparius.
氧化锌纳米颗粒(ZnONPs)因其独特的物理化学性质而被广泛应用于多种商业产品中。然而,通过各种人为活动将其释放到水生环境中会对水生生物产生毒性作用。尽管已经有多项研究报道了使用传统终点指标(如生存、生长和繁殖)来研究ZnONPs对水生生物的影响,但分子水平的终点指标更快且更敏感。在本研究中,为了了解ZnONPs的亚细胞效应,对生态毒理学上重要的生物监测生物摇蚊(Chironomus riparius)中参与氧化应激反应、解毒和细胞防御的不同基因的表达进行了研究。将四龄幼虫暴露于0、0.2、2、10和20 mg/L的ZnONPs和锌离子(以ZnSO4·7H2O的形式)中24小时和48小时。使用实时聚合酶链反应方法研究了铜锌超氧化物歧化酶、锰超氧化物歧化酶、过氧化氢酶、磷脂氢过氧化物谷胱甘肽过氧化物酶、硫氧还蛋白还原酶1以及谷胱甘肽S-转移酶的δ-3、σ-4和ε-1类、细胞色素p4509AT2和热休克蛋白70的表达。基因表达结果表明,与锌离子相比,ZnONPs暴露导致与氧化应激反应相关的基因表达更为明显。参与解毒和细胞保护的基因的mRNA表达也受到了调节。氧化应激相关基因的显著更高表达水平表明,氧化应激是ZnONPs暴露导致摇蚊毒性的重要机制。