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AuthorZakaria, Zain Z
AuthorMahmoud, Nouf N
AuthorBenslimane, Fatiha M
AuthorYalcin, Huseyin C.
AuthorAl Moustafa, Ala-Eddin
AuthorAl-Asmakh, Maha
Available date2022-08-24T07:21:54Z
Publication Date2022-08-20
Publication NameACS Omega
Identifierhttp://dx.doi.org/10.1021/acsomega.2c01313
CitationZakaria, Z. Z., Mahmoud, N. N., Benslimane, F. M., Yalcin, H. C., Al Moustafa, A. E., & Al-Asmakh, M. (2022). Developmental Toxicity of Surface-Modified Gold Nanorods in the Zebrafish Model. ACS Omega.
URIhttp://hdl.handle.net/10576/33400
AbstractBackground: 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 surfacemodified 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 EC50,24hpf 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.
SponsorThis research was funded by the Qatar University–internal grant, grant number QUCP-CHS-2022-483 for M.A. and financial funding of the Deanship of Scientific Research at the Al-Zaytoonah University of Jordan (2020-2019/12/28) for N.M.
Languageen
PublisherAmerican Chemical Society
Subjectzebrafish
gold
nanorod
toxicity
cardiotoxicity
TitleDevelopmental Toxicity of Surface-Modified Gold Nanorods in the Zebrafish Model
TypeArticle
ESSN2470-1343
dc.accessType Open Access


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