Oxidative stress and apotosis to Zebrafish (Danio rerio) embryos exposed to perfluorooctane sulfonate (PFOS) and ZnO nanoparticles

Abstract

Objectives: Perfluorooctane sulfonate (PFOS) and zinc oxide nanoparticles (ZnO-NPs) are frequently detected in the environment but few studies have assessed the joint toxicity of them. Oxidative stress and apoptosis to zebrafish (Danio rerio) embryos induced by the PFOS and ZnO-NPs were investigated in this study. Material and Methods: The embryos were exposed to the PFOS (0, 0.4, 0.8 and 1.6 mg/l), 25, 50 mg/l) and PFOS plus ZnO-NPs (0.4+12.5, 0.8+25 and 1.6+50 mg/l) mixture solutions until 96 h post-fertilization. Activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (Gpx) and malondialdehyde (MDA) content were measured in zebrafish embryos after exposure lasting for 96 h. At the same time, the genes expression related to reactive oxygen species (ROS) generation, oxidative damage and apoptosis were also measured. Results: A significant induction of the ROS accompanied by the increase in the activity of the Gpx and MDA contents were found in co-treatment groups. Furthermore, several apoptosis pathway related genes such as Bax, p53, caspase-3 and caspase-9 were significantly up-regulated in the PFOS plus ZnO-NPs exposure groups, while anti-apoptotic gene Bcl-2 was significantly down-regulated in the PFOS plus ZnO-NPs exposure groups. In addition, some oxidative stress-related genes such as Cat, GSH peroxidase 1 (Gpx1a) and superoxide dismutase 1 (Sod1) were also significantly down-regulated after the PFOS plus ZnO-NPs co-treatments. Conclusions: The results demonstrated that the PFOS plus ZnO-NPs co-exposure could cause more serious oxidative stress and apoptosis than the PFOS and ZnO-NPs exposure alone at the exposure concentrations above. The synergistic effects of the PFOS and ZnO-NPs may be the important mechanisms of their toxicity to zebrafish embryos. Int J Occup Med Environ Health 2017;30(2):213-229

Toxicity of microwave-assisted biosynthesized zinc nanoparticles in mice: a preliminary study

“…Silver nanoparticles (AgNPs) have been shown to induce OS in human colon cancer cells through increased LPO and reduced GSH levels with the induction of mitochondria-involved apoptosis via the elevated levels of Bcl and caspase-3 proteins [34]. ZnO NPs have also proved to induce the expression of the genes attributed to ROS generation, OS damage and apoptosis such as Bax, p53, caspase-3 and caspase-9 [35]. Another study has also demonstrated that biogenic NPs (tellurium nanorods) induced necrosis or late apoptosis without altering the activity of caspase pathway [22].…”

Comparative analysis of the toxicity of gold nanoparticles in zebrafish

“…Nanoparticles can induce oxidative stress in human fibroblasts, erythrocytes, vascular endothelial cells, mesenchymal stem cells and a variety of tumour cells (Abdal Dayem et al, ). Nanoparticles have also been shown to cause oxidative stress in zebrafish embryos and in the liver of adult zebrafish (Choi et al, ; Du, Cai, Wang, & You, ; Faria et al, ; Zhao et al, ). Catalase, glutathione peroxidase (GPX) and superoxide dismutase (SOD) are detoxifying enzymes for ROS that regulate redox homeostasis (Abdal Dayem et al, ).…”

“…Bcl2 plays an important role in the regulation of ROS generation and maintenance of the redox status (Hockenbery, Oltvai, Yin, Milliman, & Korsmeyer, ). Du et al () showed that zinc oxide nanoparticle treatment resulted in significant increases in SOD and GPX activities in zebrafish embryos. Zhao et al () also demonstrated significantly increased SOD activity in zebrafish embryos treated with zinc oxide nanoparticles.…”

“…Nanoparticles have been reported to cause apoptosis in zebrafish embryos and tissues of adult zebrafish (Choi et al, ; Du et al, ; Zhao et al, ). We examined the apoptotic effects of nanoparticle exposure (0.05 n m ) and found the most common feature being the crowded bright spots in the heart and eye areas (Figure ), representing the accumulation of toxic substances ultimately leading to apoptosis.…”

Hedgehog pathway inhibition causes primary follicle atresia and decreases female germline stem cell proliferation capacity or stemness

“…Malondialdehyde (MDA), a representative lipid peroxide, is generated in cells when oxygen radical levels increase [29]. The activity of SOD2 and GPx, as well as the concentration of GSH and MDA, was used to measure the oxidative stress level in this study [30,31]. Bcl-2 is a mitochondrial membrane protein that blocks the apoptotic cell death [32].…”