Developmental Toxicity of Surface-Modified Gold Nanorods in the Zebrafish Model

Zain Zaki Zakaria; Nouf N Mahmoud; Fatiha M Benslimane; Huseyin C Yalcin; Ala-Eddin Al Moustafa; Maha Al-Asmakh

doi:10.1021/acsomega.2c01313

Developmental Toxicity of Surface-Modified Gold Nanorods in the Zebrafish Model

ACS Omega. 2022 Aug 16;7(34):29598-29611. doi: 10.1021/acsomega.2c01313. eCollection 2022 Aug 30.

Authors

Zain Zaki Zakaria^{1

2}, Nouf N Mahmoud^{1

3}, Fatiha M Benslimane², Huseyin C Yalcin², Ala-Eddin Al Moustafa^{2

4}, Maha Al-Asmakh^{1

2}

Affiliations

¹ Department of Biomedical Sciences, College of Health Sciences, QU Health, Qatar University, Doha 122104, Qatar.
² Biomedical Research Center, Qatar University, PO Box 2713, Doha 122104, Qatar.
³ Faculty of Pharmacy, Al-Zaytoonah University of Jordan, Amman 11733, Jordan.
⁴ College of Medicine, QU Health, Qatar University, PO Box 2713, Doha 122104, Qatar.

Abstract

Background: nanotechnology is one of the fastest-growing areas, and it is expected to have a substantial economic and social impact in the upcoming years. Gold particles (AuNPs) offer an opportunity for wide-ranging applications in diverse fields such as biomedicine, catalysis, and electronics, making them the focus of great attention and in parallel necessitating a thorough evaluation of their risk for humans and ecosystems. Accordingly, this study aims to evaluate the acute and developmental toxicity of surface-modified gold nanorods (AuNRs), on zebrafish (Danio rerio) early life stages.

Methods: in this study, zebrafish embryos were exposed to surface-modified AuNRs at concentrations ranging from 1 to 20 μg/mL. Lethality and developmental endpoints such as hatching, tail flicking, and developmental delays were assessed until 96 h post-fertilization (hpf).

Results: we found that AuNR treatment decreases the survival rate in embryos in a dose-dependent manner. Our data showed that AuNRs caused mortality with a calculated LC50 of EC_50,24hpf of AuNRs being 9.1 μg/mL, while a higher concentration of AuNRs was revealed to elicit developmental abnormalities. Moreover, exposure to high concentrations of the nanorods significantly decreased locomotion compared to untreated embryos and caused a decrease in all tested parameters for cardiac output and blood flow analyses, leading to significantly elevated expression levels of cardiac failure markers ANP/NPPA and BNP/NPPB.

Conclusions: our results revealed that AuNR treatment at the EC₅₀ induces apoptosis significantly through the P53, BAX/BCL-2, and CASPASE pathways as a suggested mechanism of action and toxicity modality.