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Aouey, B.* ; Boukholda, K.* ; Gargouri, B.* ; Bhatia, H.S. ; Attaai, A.* ; Kebieche, M.* ; Bouchard, M.* ; Fetoui, H.*

Silica nanoparticles induce hepatotoxicity by triggering oxidative damage, apoptosis, and bax-Bcl2 signaling pathway.

Biol. Trace Elem. Res. 200, 1688-1698 (2021)
Verlagsversion DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
The increase in the usage of silica nanoparticles (SiNPs) in the industrial and medical fields has raised concerns about their possible adverse effects on human health. The present study aimed to investigate the potential adverse effects of SiNPs at daily doses of 25 and 100 mg/kg body weight intraperitoneally (i.p.) for 28 consecutive days on markers of liver damage in adult male rats. Results revealed that SiNPs induced a marked increase in serum markers of liver damage, including lactate dehydrogenase (LDH), alanine aminotransferase (ALAT), and aspartate aminotransferase (ASAT). SiNPs also induced an elevation of reactive oxygen species (ROS) production in liver, along with an increase in oxidative stress markers (NO, MDA, PCO, and H2O2), and a decrease in antioxidant enzyme activities (CAT, SOD, and GPx). Quantitative real-time PCR showed that SiNPs also induced upregulation of pro-apoptotic gene expression (including Bax, p53, Caspase-9/3) and downregulation of anti-apoptotic factors Bcl-2. Moreover, histopathological analysis revealed that SiNPs induced hepatocyte alterations, which was accompanied by sinusoidal dilatation, Kupffer cell hyperplasia, and the presence of inflammatory cells in the liver. Taken together, these data showed that SiNPs trigger hepatic damage through ROS-activated caspase signaling pathway, which plays a fundamental role in SiNP-induced apoptosis in the liver.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Apoptosis ; Caspase ; Hepatotoxicity ; Ros ; Silica Nanoparticles; Subchronic Toxicity; Gold Nanoparticles; Therapeutic Target; Vivo; Stress; Silver; P53
ISSN (print) / ISBN 0163-4984
e-ISSN 1559-0720
Zeitschrift Biological Trace Element Research
Quellenangaben Band: 200, Heft: 4, Seiten: 1688-1698 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort 999 Riverview Drive Suite 208, Totowa, Nj 07512 Usa
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Tissue Engineering and Regenerative Medicine (ITERM)
Förderungen MSERS