Potential of biofluid components to modify silver nanoparticle toxicity

Abstract

Establishing realistic exposure scenarios is critical for cytotoxic investigation of silver (Ag) nanoparticles in the gastrointestinal tract. This study investigated the potential interaction with and effect of biofluid components, namely cholic acid, deoxycholic acid and ursodeoxycholic acid, on AgNP toxicity. Two cell lines corresponding to organs related to the biofluid components were employed. These were HepG-2 a hepatocellular carcinoma derived from liver tissue and Hep2 an epithelial cell line. Physiochemical and cytotoxic screening was performed and the ability of biofluid components to modify AgNP cytotoxicity was explored. No alteration to the physiochemical characteristics of AgNP by biofluid components was demonstrated. However, biofluid component addition resulted in alteration of AgNP toxicity. Greater ROS induction was noted in the presence of CA and DCA. UDCA demonstrated no modification of toxicity in HEpG-2 cells however significant modification was noted in Hep2 cells. It is concluded that biofluid components can modify AgNP toxicity but this is dependent on the biofluid component itself and the location where it acts. Short AbstractSilver nanoparticle (AgNP) interaction with biofluids upon entry to the body is important for accurate toxicological investigation. A number of toxicological tests were performed and demonstrated modification of AgNP toxicity by the chosen biofluid components cholic acid, deoxycholic acid and ursodeoxycholic acid. It is concluded that the influence on AgNP toxicity by biofluid components is dependent on the biofluid component itself and the location where it acts.

Liposomal encapsulation of silver nanoparticles enhances cytotoxicity and causes induction of reactive oxygen species‐independent apoptosis

“…In contrast, this was not the same for Lipo‐AgNP where there was a slight reduction in recorded sizes (140.1 nm in water and 138.9 nm in media). Previous studies have reported an increase in AgNP size in culture media and this increase in size has been proposed to be due to an association of AgNP with proteins (Hansen & Thunemann, ; Mukherjee, O'Claonadh, Casey, & Chambers, ; Murphy, Sheehy, Casey, & Chambers, ; Shannahan et al, ). The interaction of AgNP with protein in culture media was most likely prevented by Lipo‐AgNP due to the presence of the protective lipid layer, preventing the encapsulated AgNP from directly interacting with biomolecules in the milieu of the culture media.…”

In vitro comparative cytotoxicity study of aminated polystyrene, zinc oxide and silver nanoparticles on a cervical cancer cell line

“…The mechanism of cell death caused by NPs has been attributed to oxidative stress, with ROS generation indicated as a primary mechanism of NP related apoptotic cell death (Sastre et al 2000, Piao et al 2011, Yu et al 2013, Murphy et al 2015a, Saini et al 2016, Zhao et al 2016, Zhu et al 2016. ROS generation in the cells is regulated by protective enzymes and antioxidant mechanisms.…”

Silver nanoparticles induce pro‐inflammatory gene expression and inflammasome activation in human monocytes

“…The proinflammatory cytokine expression detected after AgNP exposure and the amplified expression noted after exposure to AgNP and LPS combined may result from ROS production. These AgNP have previously been shown to be potent inducers of ROS in liver, epithelial, keratinocyte and cervical cell lines, Hep-G2, Hep2, HaCaT and HeLa, respectively (Gupta Mukherjee et al, 2012;Murphy et al, 2015). Further investigation is required to determine if a similar ROS-driven mechanism occurs after exposure to these specific AgNP.…”

“…Upon entry, nanoparticles associate with various biomolecules producing a surface coating. The variety of biomolecules within the body leads to any number of combinations coating the particle surface, making it an important contributory factor of a cellular response to nanoparticles and the extent of toxicity (Lynch et al, 2006;Monopoli et al, 2012;Murphy et al, 2015;Dubey et al, 2015). A nanoparticles biomolecule surface coating can induce a Trojan horse effect whereby toxicity appears delayed only to occur days later, resulting from dissolution of the biomolecule coating within the lysosome after cellular internalization .…”

“…When suspended in RPMI-1640, data indicated a slight shift in hydrodynamic radius but the particle size fell within the range of 34-40 nm. Further detailed characterization together with representative particle images and DLS data were described in our previous paper (Murphy et al, 2015).…”