Silver Nanocolloids Disrupt Medaka Embryogenesis through Vital Gene Expressions

Abstract

Silver nanomaterials are the major components of healthcare products largely because of their antimicrobial effects. However, their unintended toxicity to biological organisms and its mechanism are not well understood. Using medaka fish embryo model, the toxic effects and corresponding mechanisms of silver nanocolloids (SNC, particle size 3.8 ± 1.0-diameter nm) were investigated. SNC caused morphological changes in embryos including cardiovascular malformations, ischemia, underdeveloped central nervous system and eyes, and kyphosis at exposures of 0.5 mg/L. Interestingly, SNC were observed inside the eggs at a level of 786.1 ± 32.5 pg/mg egg weight, and TEM analysis showed that SNC adhered to the surface and inside of the chorion. Meanwhile, medaka oligo DNA microarray and qRT-PCR were used for gene expression analysis in the embryos exposed to 0.05 mg/L SNC for 48 h. As a result, expressions of six of the oxidative stress-, embryogenesis- and morphogenesis-related genes, ctsL, tpm1, rbp, mt, atp2a1, and hox6b6, were affected by the SNC exposure, and these genes' involvement in those malformations was implied. Thus, SNC could potentially cause malformations in the cardiovascular and central nervous systems in developing medaka embryo through SNC-induced differential expression of the genes related to oxidative stress, embryonic cellular proliferation, and morphological development.

Assessment of silver nanoparticle toxicity for common carp (Cyprinus carpio) fish embryos using a novel method controlling the agglomeration in the aquatic media

“…In addition-and as we also discuss elsewhere-the effects observed are unlikely to be related to freely dissolved silver ions because none of the samples had Ag in concentrations higher than analytical LOD (10 μg L −1 ). Also, existing studies on toxicity of silver to fish revealed much higher effective (LOEC) concentrations of 50 and 500 μg L −1 for Japanese medaka (Kashiwada et al 2012) and zebrafish ( Bar-Ilan et al 2009), respectively.…”

Significance of adverse outcome pathways in biomarker-based environmental risk assessment in aquatic organisms

“…AgNP-exposed zebrafish also exhibited upregulation of the expression of a number of apoptosis-related genes, including p53, bcl2-associated X protein, phophatidylinositol glycan C, phosphatidylinositol glycan P, and insulin-like growth factor binding-protein 3 (Yeo and Pak, 2008). Embryo deformities have also been reported in AgNP-exposed Japanese medaka, in addition to altered expression patterns of six oxidative stress-related, embryogenesis-related, and morphogenesis-related genes (ctsL, tpm1, rbp, mt, atp2a, and hox6b6) (Kashiwada et al, 2012). Zebrafish also show AgNPinduced phenotypic abnormalities, including spinal deformities, cardiac malformation, yolk sac edema, head edema, and eye malformation Asharani et al, 2008).…”

“…The release of NPs into the aquatic environment is of particular concern due to their potential ecological and environmental health risks (Robichaud et al, 2009;Maurer-Jones et al, 2013). Out of all the NPs in use, silver nanoparticles (AgNPs) are of the greatest concern due to their extensive use for their antimicrobial properties and their release into the aquatic environment, which poses a hazard (Kashiwada et al, 2012;Kwok et al, 2012;Maurer-Jones et al, 2013). In recent study, AgNPs have been shown to be lethal to fish embryos in a concentration-dependent manner and AgNPtreated fish embryos exhibit delayed hatching (Asharani et al, 2008; Bar-Ilan et al, 2009).…”

Predicting the environmental impact of nanosilver

“…Kashiwada et al (2012) reported that Japanese medaka (Oryzias latipes) embryos exposed to 0.5-1 mg/L AgNPs (unspecified capping agent) up to 14 days demonstrated cardiovascular defects, ischemia, an underdeveloped central nervous system, and differential expression of genes related to oxidative stress, embryogenesis, and morphogenesis. Fathead minnow (Pimephales promelas) embryos exposed to NanoAmor and Sigma AgNPs with unspecified capping agent (0.625-25 mg/L) for 4 days showed increased mortality and developmental abnormalities; the uptake of AgNPs was also noted (Laban et al, 2010).…”