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. 2024 Aug 29:15:1447046.
doi: 10.3389/fmicb.2024.1447046. eCollection 2024.

Toxicity of gold nanoparticles complicated by the co-existence multiscale plastics

Lan Zhang  1 , Yuyang Ma  1   2 , Zhiliang Wei  3 , Luyang Wang  1
Affiliations

Toxicity of gold nanoparticles complicated by the co-existence multiscale plastics

Lan Zhang et al. Front Microbiol. .

Abstract

Introduction: Gold nanoparticles (AuNPs) have been developed as treatment materials for various diseases and shown magnificent potential. By contrast to the broad toxicological studies on the single exposure (AuNPs), how the other health risks modulate the toxicological profile of AuNPs remains to be investigated. Plastics are among the most common health risks in daily life due to the broad utilization of plastic products. Therefore, in this study, we aimed to reveal the toxicological effects induced by co-exposure of gold nanorod (AuR) and polystyrene micro- and nano-plastics (hereinafter, referred to as AuRmPS and AuRnPS, respectively) in mice.

Methods: Systematic biochemical characterizations were performed to investigate the hepatotoxicity, nephrotoxicity, neurotoxicity, inflammatory responses, alterations in gut microbiota induced by co-exposure, and to analyze the toxicological phenomena from the roles of reactive oxygen species and gut-organ axis.

Results: It has been found that hepatotoxicity, nephrotoxicity, neurotoxicity, and inflammation were exacerbated in AuRnPS and AuRmPS, and gut microbiota composition was more severely altered in AuRnPS exposure. These results suggest the necessity of reducing plastics exposure in AuNPs-based therapies. Moreover, protection against the nano-sized plastic particles holds higher priority.

Conclusion: These findings will facilitate the explorations of methods to reduce therapeutic toxicity and improve biosafety for specific treatments by referring to the orders of importance in protecting different organs.

Keywords: gold nanoparticles; gut microbiota; microplastics; nanoplastics; toxicity.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Schematic illustration for the fates of micro−/nanoplastics and gold nanoparticles (AuNPs). Macroplastic are fragmented and degraded into micro−/nano-plastic due to various mechanical, chemical and biological processes in the environment. Micro−/nano-plastics can enter the human bodies and coexist with AuNPs.
Figure 2
Figure 2
Characterizations of the AuR and PS used in this study. TEM image (A) and extinction spectra (B) of AuR. SEM images of 500 nm PS (C) and 5 μm PS (D).
Figure 3
Figure 3
Histopathological results of liver (A–D), and of kidney (E–H) for the Con, AuR, AuRnPS, and AuRmPS groups. Effects of single exposure (AuR) and co-exposures (AuRnPS and AuRmPS) on hepatotoxicity (I–M), nephrotoxicity (N,O), and neurotoxicity (P,Q). (I) shows the comparisons among four groups for ALT; (J) for AST; (K) for SOD; (L) for GSH; (M) for CAT; (N) for MDA; (O) for BUN; (P) for CRE, (Q) for AChE, and for (R) NO. Green and blue arrows indicate inflammatory cell infiltration and fat vacuoles, respectively. *p < 0.05; **p < 0.01; ***p < 0.001.
Figure 4
Figure 4
Effects of single exposure (AuR) and co-exposures (AuRnPS and AuRmPS) on inflammatory response (A–C) and lipid metabolism (D–F). (A) shows the comparisons among four groups for TNF-α; (B) for IL-6; (C) for TG; (D) for T-CHO; (E) HDL-C, and (F) for HDL-C. *p < 0.05; **p < 0.01.
Figure 5
Figure 5
Effects of single exposure (AuR) and co-exposures (AuRmPS and AuRnPS) on community distribution and compositions of fecal microbiota. (A) Alpha index rarefaction curve. (B) Venn diagram for OTUs. (C) Shannon, (D) Simpson, (E) Chao, and (F) Ace indexes of OTU level; (G) Principal co-ordinates analysis (PCoA); and (H) Changes in the fecal microbiota composition at the family level. *p < 0.05.
Figure 6
Figure 6
(A) Correlations between biomarkers and relative abundance of gut microbiota at the family level. (B) Heatmap of gut microbial genes involved in human diseases at the Level 3 of the KEGG pathway annotation. *p < 0.05, **p < 0.01, **p < 0.001.
Figure 7
Figure 7
(A) Entry and translocation pathways of micro−/nano- particles. (B) Schematic illustration of the ROS-activated Keap1-Nrf2/ARE signaling pathway induced by the co-exposure of AuR with PS micro−/nanoplastics. (C) Different pathways for nanoparticles to generate ROS. (D) Bidirectional or multidirectional communication links (axes) between the gut microbiota and liver, kidney, or brain, respectively. GIT, gastrointestinal tract. ROS, Reactive oxygen species. Keap 1, Kelch-like ECH-associated protein 1. Nrf2, nuclear factor etythroid-2 related factor 2. ARE, antioxidant response element. NP, nanoparticles. NF-kB, nuclear factor-kappa B.
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Grants and funding

The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. The authors gratefully acknowledge funding from a Special Fund for the Qingdao Science and Technology Program of Public Wellbeing (22–3-7-cspz-4-nsh).

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