Combined toxicity of amorphous silica nanoparticles and methylmercury to human lung epithelial cells

Yu, Yizhi; Duan, Junchao; Yang, Li; Yu, Yang; Jin, Minghua; Li, Chenxu; Wang, Yapei; Sun, Zhiwei

doi:10.1016/j.ecoenv.2014.10.026

Cited by 53 publications

(32 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although nano-SiO 2 exerted low toxic effects in mice, exposure to both nano-SiO 2 and CdCl 2 significantly enhanced CdCl 2 -induced oxidative damage in mice livers. A recent study, which is similar to our study, showed that exposure of A549 cells to a combination of nano-SiO 2 and methylmercury (MeHg) exerted additive effects on cell viability, ROS generation, SOD activity, DNA damage and apoptosis, and synergistic effects on MDA content and GSH-Px activity (Yu et al, 2015).…”

Section: Discussionsupporting

confidence: 83%

“…Guo et al (2013) showed that exposure to the combination of low toxic dose of nano-SiO 2 and CdCl 2 markedly increased cadmium accumulation in the liver and induced significant hepatic oxidative stress. Yu et al (2015) recently investigated the combined toxicity of amorphous nanoSiO 2 and MeHg on human lung epithelial cells. They found that A549 cells exposed to the combination of nano-SiO 2 and MeHg showed higher intracellular MeHg concentration than cells exposed to MeHg alone, suggesting that nano-SiO 2 facilitated the cellular uptake of MeHg.…”

Section: Discussionmentioning

confidence: 99%

“…Human lung cell lines are routinely used to assess the toxicities of PM and mixture of ambient air pollutants (Deng et al, 2014;Líbalová et al, 2014;Michael et al, 2013;Yu et al, 2015). However, effects of exposure to a combination of Pb, a typical air pollutant, and silica, a typical UFP, are unclear.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Combined exposure to nano-silica and lead induced potentiation of oxidative stress and DNA damage in human lung epithelial cells

Yuan

et al. 2015

Ecotoxicology and Environmental Safety

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Combined exposure to nano-silica and lead induced potentiation of oxidative stress and DNA damage in human lung epithelial cells

Yuan

et al. 2015

Ecotoxicology and Environmental Safety

View full text Add to dashboard Cite

“…While two factorial analysis of variance (ANOVA) was used to determine SiNPs and B[a]P interactions, an F value greater than a F (4,10) = 3.4780 critical value indicates that there is a deference between the treatment groups. Their marginal means were compared using profile plots (interaction plots), as described by Ennos [26] and Yu, et al [27]. The interaction plots of estimated marginal means for visual exploration of interactions involving combinations of between-subjects and/or within-subjects factors, was constructed using the General Linear Model (GLM) command in SPSS.…”

Section: Methodsmentioning

confidence: 99%

Combined Effect of Silica Nanoparticles and Benzo[a]pyrene on Cell Cycle Arrest Induction and Apoptosis in Human Umbilical Vein Endothelial Cells

Asweto

et al. 2017

IJERPH

Self Cite

View full text Add to dashboard Cite

Particulate matter (PM) such as ultrafine particulate matter (UFP) and the organic compound pollutants such as polycyclic aromatic hydrocarbon (PAH) are widespread in the environment. UFP and PAH are present in the air, and their presence may enhance their individual adverse effects on human health. However, the mechanism and effect of their combined interactions on human cells are not well understood. We investigated the combined toxicity of silica nanoparticles (SiNPs) (UFP) and Benzo[a]pyrene (B[a]P) (PAH) on human endothelial cells. Human umbilical vascular endothelial cells (HUVECs) were exposed to SiNPs or B[a]P, or a combination of SiNPs and B[a]P. The toxicity was investigated by assessing cellular oxidative stress, DNA damage, cell cycle arrest, and apoptosis. Our results show that SiNPs were able to induce reactive oxygen species generation (ROS). B[a]P, when acting alone, had no toxicity effect. However, a co-exposure of SiNPs and B[a]P synergistically induced DNA damage, oxidative stress, cell cycle arrest at the G2/M check point, and apoptosis. The co-exposure induced G2/M arrest through the upregulation of Chk1 and downregulation of Cdc25C, cyclin B1. The co-exposure also upregulated bax, caspase-3, and caspase-9, the proapoptic proteins, while down-regulating bcl-2, which is an antiapoptotic protein. These results show that interactions between SiNPs and B[a]P synergistically potentiated toxicological effects on HUVECs. This information should help further our understanding of the combined toxicity of PAH and UFP.

show abstract

“…However, exposure to SiNPs could also result in injury to various systems, such as respiratory system, cardiovascular system, and so on. 1,2 In addition, SiNPs are the main constituents of atmospheric particulate matter, 3 while lead (Pb) is another well-known toxic environmental air pollutant derived from anthropogenic activities. 4 Nanoparticles possess a unique feature wherein heavy metals could be adsorbed on the surface and subsequently result in adverse toxicity.…”

Section: Introductionmentioning

confidence: 99%

Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system

Lin

Yang

Shi

et al. 2018

IJN

Self Cite

View full text Add to dashboard Cite

BackgroundThe harmful effects following the release of nanomaterials into environment are of great concern today.PurposeIn this study, subacute effect due to co-exposure to low-dose silica nanoparticles (SiNPs) and lead acetate (Pb) on cardiovascular system was detected in Sprague Dawley male rats.Materials and MethodsHistopathological and ultrastructural changes of heart, aortic arch and abdominal aorta were detected. Blood routine and blood biochemistry examinations were used to show the changes of blood components. The fibrinolytic and plasmin factors, inflammation-related factors and myocardial-related enzyme in serum were analysised by ELISA and Western blot assay.ResultsHistopathological and ultrastructural examination of heart, aortic arch, and abdominal aorta showed that serious damage occurred in co-exposure group (n=6/group). Blood routine examination showed that leukocytosis and thrombocytopenia increased markedly, while changes in the erythrocyte count were not obvious in the co-exposure group. The expression of alanine transaminase (ALT) decreased obviously in co-exposure group, while no significant changes were noted in the expression of aspartate aminotransferase (AST), cholesterol (CHO), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C) in the co-exposure group on blood biochemistry analysis. In addition, data from ELISA analysis showed that the levels of fibrinolytic and plasmin factors, including thrombin time (TT), prothrombin time (PT), activated partial thromboplastin time (APTT), tissue-type plasminogen activator (t-PA), tissue factor pathway inhibitor (TFPI), and antithrombin III (AT III), were decreased, while those of human fibrinogen (FIB) and D-dimer (D2D) increased significantly in the co-exposure group. Moreover, the myocardial-related enzyme in serum, tested by ELISA, and cardiovascular-related protein expression of atrial natriuretic peptide and brain natriuretic peptide, tested by Western blot assay, was increased in the heart. Furthermore, the expression of inflammation factors such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) was increased in heart tissue subjected to combined exposure, which was manifested by Western blot assay, while the protein levels of angiotensin II (ANG II) and endothelin 1 were (ET-1) elevated in blood vessels in the co-exposure group.ConclusionIn conclusion, the major interactions involved in subacute toxicity due to co-exposure to low doses of SiNPs and Pb on cardiovascular system were expected to be additive and synergistic in nature. Co-exposure to SiNPs and Pb could aggravate the cardiovascular toxicity via endothelial damage, hypercoagulation, and cardiac injury in vivo.

show abstract

Combined toxicity of amorphous silica nanoparticles and methylmercury to human lung epithelial cells

Cited by 53 publications

References 62 publications

Combined exposure to nano-silica and lead induced potentiation of oxidative stress and DNA damage in human lung epithelial cells

Combined exposure to nano-silica and lead induced potentiation of oxidative stress and DNA damage in human lung epithelial cells

Combined Effect of Silica Nanoparticles and Benzo[a]pyrene on Cell Cycle Arrest Induction and Apoptosis in Human Umbilical Vein Endothelial Cells

Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system

Contact Info

Product

Resources

About