Hexagonal boron nitride nanoparticles trigger oxidative stress by modulating thiol/disulfide homeostasis

Kar F., Hacıoğlu C., Göncü Y., Şentürk H., Erel Ö., Ay N., ...More

Human & Experimental Toxicology, vol.40, no.9, pp.1572-1583, 2021 (SCI-Expanded)

  • Publication Type: Article / Article
  • Volume: 40 Issue: 9
  • Publication Date: 2021
  • Doi Number: 10.1177/09603271211002892
  • Journal Name: Human & Experimental Toxicology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, BIOSIS, CAB Abstracts, Chimica, CINAHL, EMBASE, Environment Index, Food Science & Technology Abstracts, MEDLINE, Pollution Abstracts, Veterinary Science Database
  • Page Numbers: pp.1572-1583
  • Kütahya Health Sciences University Affiliated: Yes


Background: Hexagonal boron nitride nanoparticles (hBN NPs) are encouraging nanomaterials with unique

chemical properties in medicine and biomedical fields. Until now, the optimal hBN NP’s dosage and biochemical

mechanism that can be used for in vivo systems has not been fully revealed. The main aim of this article is to

reveal characteristics, serum and tissue interactions and any acute cytotoxic effect of different dose of hBN

NPs for the first time.

Methods: hBN NPs at concentrations varying between 50–3200 mg/kg was administered by intravenous

injection to Wistar albino rats (n ¼ 80) divided into seven dosage and control groups. Blood and tissue samples

were taken after 24 hours.

Results: Our findings suggested that higher doses hBN NPs caused oxidative stress on the serum of rats dosedependently.

However, hBN NPs did not affect thiol/disulfide homeostasis on kidney, liver, spleen, pancreas and

heart tissue of rats. Furthermore, hBN NPs increased serum disulfide formation by disrupting the thiol/disulfide

balance in rats. Also, LOOH and MPO levels increased at high doses, while CAT levels decreased statistically.

Conclusion: The results revealed that hBN NPs induce oxidative stress in a dose-dependent manner by

modulating thiol/disulfide homeostasis in rats at higher concentrations